Assignment Level: Advanced

Board-level postgraduate nephrology self-assessment.

Complete all 10 single-best-answer questions to receive detailed clinical explanations on the results page.

Renal Pharmacology, Dosing, and Drug Safety

Board-level MRCP-style single-best-answer MCQs covering dosing adjustments, drug safety, pharmacokinetics in renal replacement therapy, acute and chronic management, and recognition of drug-induced kidney injury.

1 / 10

A 72-year-old man with a new diagnosis of pulmonary embolism is admitted with acute kidney injury. Estimated creatinine clearance is 18 mL/min. Which anticoagulation strategy is most appropriate while renal function remains severely reduced and reversible?

Therapeutic enoxaparin 1 mg/kg subcutaneously every 12 hours (standard dosing)

Therapeutic enoxaparin 1 mg/kg subcutaneously once daily (reduced-frequency regimen)

Unfractionated heparin infusion with APTT monitoring

Fondaparinux (synthetic pentasaccharide) at therapeutic dose

Commence rivaroxaban oral therapy at the standard initial dose for pulmonary embolus

Correct answer: Unfractionated heparin infusion with APTT monitoring. In significant renal impairment (CrCl <30 mL/min) low molecular weight heparins (LMWHs) such as enoxaparin accumulate, increasing bleeding risk; dosing regimens that rely on once-daily administration are inadequate to guarantee safe therapeutic exposure in severe AKI. Unfractionated heparin (UFH) has a shorter half-life, is not renally cleared to the same degree, and is rapidly reversible, making it the preferred initial agent while renal function is unstable or likely reversible. Fondaparinux is predominantly renally excreted and is contraindicated or used with extreme caution in severe renal impairment. Direct oral anticoagulants (eg rivaroxaban) are not appropriate in severe AKI because of reduced clearance, variable exposure and inability to rapidly reverse anticoagulation if needed. Reduced-frequency enoxaparin (eg once daily) does not reliably avoid accumulation in severe renal impairment and is not the preferred strategy in acute reversible AKI. Why alternatives are less appropriate: - A (enoxaparin 1 mg/kg q12h): standard therapeutic LMWH dosing commonly results in accumulation and bleeding in CrCl <30 mL/min. - B (enoxaparin 1 mg/kg once daily): reduced-frequency regimens may still cause accumulation and are not the safest choice when rapid reversal or titration may be needed. - D (fondaparinux): cleared renally and unsuitable in severe renal impairment. - E (rivaroxaban): DOACs have significant renal clearance and are generally avoided in acute severe AKI.

2 / 10

A 64-year-old man on thrice-weekly high-flux haemodialysis is admitted with MRSA bacteraemia. You plan vancomycin therapy. Which initial strategy is most appropriate?

Give an IV loading dose (15–20 mg/kg) then measure trough and provide supplemental doses after each dialysis session guided by levels

Start a continuous infusion without a loading dose and do not measure levels because dialysis protects against accumulation

Administer a low fixed vancomycin dose after each dialysis without measuring serum levels

Avoid vancomycin and use linezolid because it does not require level monitoring

Give vancomycin orally to achieve systemic concentrations for MRSA bacteraemia

Correct answer: Give an IV loading dose (15–20 mg/kg) then measure trough and provide supplemental doses after each dialysis session guided by levels. Vancomycin is dialysable depending on dialysis membrane and modality (high-flux membranes remove significant drug). Best practice is to give an appropriate weight-based loading dose to reach therapeutic concentrations, then monitor serum concentrations and supplement dosing after dialysis sessions as required. Trough or AUC-guided monitoring informs re-dosing; in haemodialysis patients, supplementary post-dialysis dosing is commonly required.

Why alternatives are less appropriate:
- B (continuous infusion without loading/levels): continuous infusion without loading is likely to result in subtherapeutic initial exposure; dialysis alters clearance and therapeutic monitoring is required.
- C (low fixed doses without levels): fixed low dosing risks undertreatment and toxicity; monitoring is necessary.
- D (avoid vancomycin and use linezolid): linezolid is an alternative for some MRSA infections, but for bloodstream infections vancomycin remains a first-line agent in many cases; switching merely to avoid monitoring is not appropriate.
- E (oral vancomycin): oral vancomycin is not absorbed and is ineffective for systemic bacteraemia.

3 / 10

A 58-year-old critically ill patient on continuous venovenous haemodiafiltration (effluent rate approximately 25 mL/kg/h) requires broad-spectrum Gram-negative coverage. Which meropenem dosing regimen is most appropriate initially?

Meropenem 500 mg IV every 8 hours

Meropenem 1 g IV every 12 hours

Meropenem 2 g IV once daily

Meropenem continuous infusion 3 g over 24 hours without a loading dose

Meropenem 1 g IV every 8 hours (standard critically ill dosing)

Correct answer: Meropenem 1 g IV every 8 hours. Continuous renal replacement therapy (CRRT) increases antibiotic clearance compared with non-dialysed patients; in critically ill patients on CRRT, meropenem dosing often needs to approximate standard or increased dosing (eg 1 g IV q8h) to achieve pharmacodynamic targets (time above MIC). Reduced doses (eg 500 mg q8h) or prolonged intervals risk underexposure. Continuous infusion can be used after a loading dose to optimise time-dependent killing, but should be used with an initial loading dose and therapeutic context; a single high daily dose is not appropriate for meropenem’s pharmacodynamics.

Why alternatives are less appropriate:
- A (500 mg q8h): may under-dose in CRRT and critical illness.
- B (1 g q12h): extended interval may not maintain time > MIC in severe infections on CRRT.
- C (2 g once daily): single daily dosing is inappropriate for time-dependent beta-lactams.
- D (continuous infusion without loading dose): continuous infusion can be effective but requires an initial loading dose to rapidly achieve therapeutic concentrations; without a loading dose, delays in reaching target exposures occur.

4 / 10

A 68-year-old woman with long-standing hypertension and new acute kidney injury has been taking an ACE inhibitor for blood-pressure control. Serum creatinine rose from 120 to 175 µmol/L within two weeks of initiation. Which is the most likely mechanism by which ACE inhibitors can acutely raise creatinine in this context?

Direct tubular epithelial cell toxicity leading to acute tubular necrosis

Inhibition of prostaglandin synthesis causing reduced afferent arteriolar vasodilatation

Inhibition of angiotensin II–mediated efferent arteriolar constriction reducing glomerular filtration pressure

Immune-mediated interstitial nephritis with eosinophilia and rash

Formation of obstructing uric acid crystals in renal tubules

Correct answer: Inhibition of angiotensin II–mediated efferent arteriolar constriction reducing glomerular filtration pressure. ACE inhibitors (and ARBs) reduce angiotensin II activity, which normally constricts the efferent arteriole to maintain glomerular filtration pressure especially when renal perfusion is reduced (eg renal artery stenosis, volume depletion). Blocking this effect causes a fall in intraglomerular pressure with a rise in serum creatinine; a modest rise (<30%) may be acceptable, but larger rises suggest bilateral renal artery stenosis or severe renal hypoperfusion. Why alternatives are less appropriate: - A (direct tubular toxicity): ACE inhibitors are not typical causes of acute tubular necrosis. - B (prostanoid inhibition): that describes NSAID mechanism (inhibition of prostaglandin-mediated afferent vasodilatation), not ACE inhibitors. - D (immune interstitial nephritis): this is drug-induced by beta-lactams, NSAIDs, PPIs, etc., not a recognised common ACE inhibitor mechanism. - E (uric acid crystals): not a mechanism of ACE inhibitor–induced creatinine rise.

5 / 10

An 82-year-old woman with non-valvular atrial fibrillation is on maintenance haemodialysis, weighs 58 kg, and is being considered for apixaban for stroke prevention. How should apixaban be dosed under the dose-reduction criteria used in this question?

Apixaban contraindicated in dialysis — do not prescribe

Apixaban 5 mg twice daily irrespective of age or weight in dialysis patients

Apixaban 2.5 mg once daily

Apixaban 2.5 mg twice daily (dose reduction applies)

Start apixaban at 10 mg twice daily for 7 days then reduce

Under the dose-reduction criteria specified for this question, age 80 years or older and body weight 60 kg or less are two criteria for reducing apixaban to 2.5 mg twice daily. Dosing in dialysis is jurisdiction- and label-dependent, so local prescribing guidance must be followed; the key educational point is to apply the stated criteria consistently rather than assume either an absolute contraindication or an unchanged dose.

6 / 10

A 60-year-old man with bilateral renal artery stenosis was started on lisinopril. His serum creatinine increased by 45% within 5 days. What is the most appropriate immediate action?

Continue lisinopril and monitor renal function weekly because small increases are expected

Increase the lisinopril dose to achieve better blood-pressure control

Stop lisinopril immediately and arrange imaging of the renal arteries

Start intravenous fluids aggressively to reverse the creatinine rise

Add a loop diuretic to reduce intravascular volume and improve renal perfusion

Correct answer: Stop lisinopril immediately and arrange imaging of the renal arteries. A rise in serum creatinine of >30% after commencing an ACE inhibitor suggests impaired ability to maintain intraglomerular pressure (eg bilateral renal artery stenosis). The recommended immediate action is to stop the ACE inhibitor and investigate for renal artery stenosis (eg duplex, CT angiography) rather than continue treatment. If the ACE inhibitor is responsible for the substantial decline in GFR, stopping it commonly leads to improved renal function.

Why alternatives are less appropriate:
- A (continue and monitor): a >30% rise is clinically significant and should prompt cessation and investigation.
- B (increase lisinopril dose): would likely worsen renal function.
- D (start IV fluids): unless there is evidence of hypovolaemia, aggressive fluids are not indicated and could cause harm.
- E (add loop diuretic): reducing intravascular volume will further reduce renal perfusion and is inappropriate.

7 / 10

A 74-year-old man with CKD stage 4 (eGFR 22 mL/min/1.73 m2) presents with muscle weakness and peaked T waves on ECG. What is the single most important immediate therapy to reduce the risk of lethal arrhythmia?

Give intravenous calcium gluconate (or calcium chloride if central access) to stabilise the cardiac membrane

Administer oral sodium polystyrene sulfonate (cation-exchange resin) to lower serum potassium

Start immediate haemodialysis without any temporising measures

Give oral magnesium oxide to correct hypomagnesaemia which is causing ECG changes

Give oral potassium-restricted diet counselling and arrange outpatient follow-up

Correct answer: Give intravenous calcium gluconate (or calcium chloride if central access) to stabilise the cardiac membrane. In hyperkalaemia with ECG changes, immediate membrane stabilisation with IV calcium is the priority because it rapidly reduces the risk of fatal arrhythmia, though it does not lower serum potassium. Other measures to shift potassium intracellularly (insulin with glucose, nebulised salbutamol, sodium bicarbonate if acidotic) should follow, and definitive removal (eg dialysis) should be arranged if necessary.

Why alternatives are less appropriate:
- B (oral sodium polystyrene sulfonate): onset is delayed and it's not appropriate as the immediate life-saving therapy.
- C (immediate haemodialysis without temporising): dialysis is definitive but arranging access and dialysis takes time; membrane stabilisation must be given immediately.
- D (oral magnesium oxide): magnesium is not the first-line treatment for ECG changes due to hyperkalaemia.
- E (dietary advice/outpatient follow-up): grossly inadequate and dangerously slow in the presence of ECG changes.

8 / 10

A 35-year-old man started a proton-pump inhibitor 3 weeks ago for dyspepsia and now presents with malaise, rising creatinine and a maculopapular rash. Urinalysis shows modest proteinuria and eosinophiluria. Which drug is the most likely cause of his acute kidney injury?

Amoxicillin–clavulanate

Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen

Rifampicin

Allopurinol

Proton-pump inhibitor (eg omeprazole)

Correct answer: Proton-pump inhibitor (eg omeprazole). The presentation is typical for acute interstitial nephritis (AIN): recent drug exposure (commonly within days to weeks), rash, systemic symptoms, eosinophiluria/pyuria and rising creatinine. Proton-pump inhibitors are a well-recognised and increasingly common cause of AIN. NSAIDs can cause AIN but classically are more associated with nephrotic-range proteinuria and a different time course; beta-lactam antibiotics (eg penicillins) and rifampicin can also cause AIN, but in this vignette the timing and classic PPI association make PPI the most likely culprit.

Why alternatives are less appropriate:
- A (amoxicillin–clavulanate): can cause AIN but less likely given the recent PPI start and typical epidemiology.
- B (NSAIDs): can cause AIN but often with different features (eg nephrotic syndrome) and are a common cause but PPI is classically implicated in subacute AIN.
- C (rifampicin): can cause AIN but is usually associated with anti-tuberculous therapy history.
- D (allopurinol): can cause hypersensitivity syndromes including renal injury but less commonly presents with classic AIN histology compared with PPIs.

9 / 10

A 62-year-old patient with eGFR 22 mL/min/1.73 m2 is started on gentamicin (an aminoglycoside) for severe sepsis. Which initial dosing and monitoring strategy is most appropriate?

Give a single high-dose once-daily aminoglycoside (eg 5–7 mg/kg) and perform therapeutic drug monitoring (peak and trough/AUC) to adjust the dosing interval and dose

Give 1 mg/kg every 8 hours without monitoring because frequent small doses reduce toxicity

Avoid any aminoglycoside dosing until renal function recovers

Give 5 mg/kg once and repeat dosing only if clinical deterioration occurs

Start continuous infusion without any monitoring because steady exposure reduces nephrotoxicity

Aminoglycosides are concentration-dependent antibiotics with a post-antibiotic effect. In severe infection they may be given as a high initial dose with therapeutic drug monitoring, using measured concentrations and kidney function to adjust the dose and dosing interval. AUC-guided monitoring is preferred where available; peak/trough-based protocols remain used in some settings. Repeated unmonitored small doses risk accumulation and nephrotoxicity, while avoiding an indicated aminoglycoside or giving an unmonitored single dose risks treatment failure or toxicity.

10 / 10

A 70-year-old man with stage 4 CKD requires an urgent contrast-enhanced CT. Which prophylactic measure is supported by guideline-level recommendations to reduce the risk of contrast-associated acute kidney injury?

Administer oral N-acetylcysteine the day before and after the procedure

Use heparin anticoagulation prophylactically to improve renal perfusion

Schedule immediate prophylactic haemodialysis after contrast to prevent injury

Provide peri-procedural intravenous isotonic crystalloid (saline) and minimise contrast volume

Administer high-dose intravenous mannitol to protect renal tubules

Correct answer: Provide peri-procedural intravenous isotonic crystalloid (saline) and minimise contrast volume. Current guideline guidance emphasises adequate volume expansion with isotonic crystalloid (eg normal saline) for patients at increased risk of contrast-associated AKI, and minimising contrast dose and use of low-/iso-osmolar contrast media where possible. Routine use of N-acetylcysteine is not supported as standard prophylaxis by high-quality evidence and is no longer routinely recommended. Prophylactic haemodialysis to remove contrast is not recommended. Heparin and mannitol are not recommended prophylactic measures for contrast-associated AKI.

Why alternatives are less appropriate:
- A (oral N-acetylcysteine): evidence is inconsistent; not routinely recommended as a substitute for hydration.
- B (heparin prophylaxis): no evidence that anticoagulation prevents contrast nephropathy and it risks bleeding.
- C (prophylactic haemodialysis): studies do not support routine post-contrast dialysis to prevent AKI and it is impractical and risky.
- E (mannitol): not recommended and may be harmful.

Your score is

The average score is 70%

By Wordpress Quiz plugin

Board-level postgraduate nephrology self-assessment.

Complete all 10 single-best-answer questions to receive detailed clinical explanations on the results page.

Renal Pathology and Biopsy Interpretation

Renal biopsy interpretation — advanced clinical vignettes, diagnosis, management decisions and complications relevant to nephrology trainees and exam candidates.

1 / 10

A 66-year-old patient on CRRT following septic shock is improving: vasopressor dose is being weaned and mean arterial pressure has been stable >65 mmHg without escalation for 24 hours. Urine output remains low but creatinine is not rising further. What is the most appropriate next step regarding RRT modality?

Continue CRRT indefinitely until renal recovery is complete

Switch immediately to peritoneal dialysis to facilitate mobilization

Transition to intermittent haemodialysis when haemodynamics are stable and vasopressor support minimal

Stop all dialysis now because creatinine has plateaued

Change to high-dose CRRT (increased effluent) to accelerate renal recovery

This question tests recognition of the appropriate timing to change modality. The best answer is to transition to intermittent haemodialysis when the patient is haemodynamically stable with minimal vasopressor support (option 3). Continuing CRRT unnecessarily prolongs intensive use of resources; peritoneal dialysis is not the usual next step in this setting. Stopping dialysis immediately is unsafe because the patient remains oliguric and may still require solute/volume control. Increasing CRRT dose has not been shown to accelerate renal recovery. Therefore transitioning to intermittent haemodialysis as haemodynamics permit is the correct action.

2 / 10

A 45-year-old patient with nephrotic syndrome undergoes a percutaneous renal biopsy. The pathologist reports 6 glomeruli on light microscopy. Which statement is most accurate regarding sample adequacy and diagnostic reliability?

Six glomeruli are adequate for definitive exclusion of focal segmental glomerulosclerosis (FSGS).

A minimum of about 10 glomeruli is generally required to reduce sampling error for focal lesions such as FSGS.

Any number of glomeruli is acceptable if electron microscopy is performed.

At least 30 glomeruli are universally required for routine native kidney biopsy interpretation.

The number of glomeruli is irrelevant if immunofluorescence is strongly positive.

Correct answer: B. Focal glomerular diseases (for example FSGS) can be missed if sampling is small because only a subset of glomeruli are involved. Most textbooks and pathology guidance state that ~10 glomeruli is a practical minimum for reasonable sensitivity; 20 or more is ideal. A sample with only 6 glomeruli risks false-negative results for focal lesions. Option A is incorrect because 6 glomeruli are insufficient to exclude focal pathology confidently. Option C is incorrect: electron microscopy provides ultrastructural detail but cannot compensate fully for insufficient numbers of glomeruli when lesions are segmental/focal. Option D is incorrect because 30 glomeruli is not a universal requirement for routine native biopsies (it may be desirable in research or lupus categorisation but is not a standard minimum). Option E is incorrect because immunofluorescence positivity does not negate the importance of glomerular sampling for assessing the distribution and chronicity of disease.

3 / 10

A patient presents with rapidly progressive renal failure. Renal biopsy shows extensive crescent formation on light microscopy and immunofluorescence reveals smooth, linear IgG deposition along glomerular basement membranes. Which diagnosis is most likely?

Immune complex (post-infectious) crescentic glomerulonephritis

Granulomatosis with polyangiitis (pauci-immune ANCA-associated GN)

Anti-glomerular basement membrane (anti-GBM) disease

Membranous nephropathy

IgA nephropathy with crescents

Correct answer: C. Linear IgG staining of the GBM on immunofluorescence is characteristic of anti-GBM disease (Goodpasture's), which often presents with rapidly progressive glomerulonephritis with crescents. Option A (immune complex GN) typically shows granular (‘lumpy-bumpy’) immune complex deposition rather than smooth linear staining. Option B (pauci-immune ANCA-associated GN) is defined by little or no immune deposition on IF (pauci-immune), not linear IgG. Option D (membranous nephropathy) classically shows granular subepithelial immune deposits with a granular IF pattern. Option E (IgA nephropathy) shows dominant/codominant mesangial IgA deposition, not diffuse linear GBM IgG.

4 / 10

Light microscopy is otherwise normal, and electron microscopy of a nephrotic patient shows diffuse (near-complete) podocyte foot-process effacement with no immune complex deposits. The most likely primary diagnosis is:

Minimal change disease (MCD)

Membranous nephropathy

Diabetic nephropathy

Amyloidosis

IgA nephropathy

Diffuse foot-process effacement with otherwise normal light microscopy and no immune-complex deposits is classic for minimal change disease in the appropriate nephrotic clinical context. Primary FSGS can also show foot-process effacement, but would be supported by segmental sclerosis on light microscopy. Membranous nephropathy has subepithelial immune deposits, diabetic nephropathy has mesangial expansion/GBM thickening, amyloidosis has Congo-red-positive fibrils, and IgA nephropathy has mesangial immune deposits.

5 / 10

A 62-year-old man presents with rapidly progressive renal impairment and a renal biopsy showing extensive crescentic glomerulonephritis but little or no immune deposition on immunofluorescence (pauci-immune pattern). Which is the most appropriate immediate step in management?

Wait for ANCA results before initiating therapy, as immunosuppression can be harmful if diagnosis uncertain.

Start oral ACE inhibitor and conservative management only, unless dialysis required.

Commence plasma exchange as sole therapy while awaiting serology.

Start high‑dose corticosteroids immediately and request ANCA testing (with view to add further immunosuppression once ANCA results available).

Perform urgent repeat biopsy to confirm findings before treatment.

Correct answer: D. Pauci-immune crescentic GN most often reflects ANCA-associated vasculitis; this is a rapidly progressive condition where early high‑dose corticosteroids (often IV methylprednisolone followed by oral prednisolone) are started promptly while diagnostic serology (ANCA) is obtained and decisions about additional induction therapy (cyclophosphamide or rituximab) are made. Option A is unsafe—delaying steroids pending serology risks further irreversible renal injury. Option B is inadequate for rapidly progressive GN. Option C (plasma exchange as sole therapy) is not routinely the correct initial sole therapy for ANCA-associated GN; plasma exchange may be considered in specific scenarios (e.g. concomitant severe pulmonary haemorrhage or certain severe presentations) but steroids and induction immunosuppression are the first steps. Option E (repeat biopsy) is unnecessary and delays urgent treatment.

6 / 10

Which biopsy feature is most characteristic of acute T-cell–mediated (cellular) rejection in a renal transplant?

Diffuse C4d staining of peritubular capillaries without significant inflammatory infiltrate.

Segmental granular immune complex deposition in glomeruli.

Extensive thrombotic microangiopathy affecting glomerular capillaries.

Prominent neutrophilic infiltration with bacterial colonies.

Dense interstitial mononuclear infiltrates with tubulitis (lymphocytes invading tubular epithelium).

Correct answer: E. Acute T-cell–mediated rejection is defined histologically by dense interstitial mononuclear (mostly T cell) infiltrates accompanied by tubulitis—lymphocytes infiltrating and damaging tubular epithelium. Option A (diffuse C4d in peritubular capillaries) is a marker suggestive of antibody-mediated rejection. Option B (granular immune complex deposition) suggests immune-complex glomerulonephritis, not acute cellular rejection. Option C (TMA) can be seen in many contexts, including antibody-mediated rejection or drug toxicity, but is not the defining feature of acute cellular rejection. Option D indicates acute pyelonephritis or severe infection rather than rejection. The Banff classification uses the degree of interstitial inflammation and tubulitis to grade cellular rejection.

7 / 10

A 58-year-old man with nephrotic-range proteinuria and biopsy-proven membranous nephropathy has renal histology showing 70% cortical interstitial fibrosis and tubular atrophy with 60% globally sclerosed glomeruli. Which management approach is most appropriate?

Start aggressive immunosuppression (cyclophosphamide plus steroids) to preserve renal function.

Proceed with conservative, supportive renal care and consider non-immunosuppressive measures; immunosuppression is unlikely to restore function.

Immediate plasmapheresis to remove immune complexes.

Begin high-dose calcineurin inhibitor therapy to reduce proteinuria and reverse fibrosis.

Perform repeat biopsy in 6 weeks before making management decisions.

Correct answer: B. Extensive chronic changes—high proportion of interstitial fibrosis/tubular atrophy and global glomerulosclerosis—predict poor potential for recovery with immunosuppression; risks of aggressive immunosuppression often outweigh benefits. Management should focus on supportive measures (blood pressure and proteinuria control with RAAS blockade, salt restriction, diuretics as needed, and preparation for renal replacement therapy if progressive). Option A is incorrect because substantial chronic irreversible damage reduces likelihood of benefit from aggressive immunosuppression. Option C (plasmapheresis) is not standard for primary membranous nephropathy without specific indications (e.g. severe anti-GBM disease or refractory cases). Option D (calcineurin inhibitors) carry nephrotoxicity risk and are unlikely to reverse established fibrosis. Option E (repeat biopsy) is unnecessary and would delay appropriate supportive care.

8 / 10

A renal biopsy submitted in formalin only yields negative immunofluorescence despite clinical features strongly suggestive of IgA nephropathy. What is the best next step to identify mesangial IgA deposition without re-biopsy if the laboratory resources allow?

Accept the negative IF and diagnose non-immune nephropathy.

Request serum IgA level as a substitute for tissue diagnosis.

Treat empirically for IgA nephropathy without further tissue testing.

Ask the pathology laboratory to perform immunostaining on paraffin-embedded tissue after antigen retrieval (for example pronase digestion) to unmask deposits.

Send the paraffin blocks for electron microscopy only.

Correct answer: D. If fresh/frozen tissue for direct immunofluorescence is not available because the specimen was fixed in formalin, paraffin immunofluorescence or immunohistochemistry after protease (pronase) antigen retrieval can often recover masked immune deposits, including mesangial IgA. This approach avoids re-biopsy. Option A is incorrect because a negative IF in a specimen fixed incorrectly may be a false negative. Option B (serum IgA) is neither sensitive nor specific for tissue deposition and cannot replace tissue diagnosis. Option C (empiric treatment) without confirmation may subject the patient to unnecessary risks. Option E (EM only) will not reliably demonstrate IgA immune complexes—EM can show electron-dense deposits but without immunostaining it may not distinguish IgA deposits definitively.

9 / 10

A middle-aged patient with progressive nephrotic syndrome has renal IF showing strong linear staining of tubular basement membranes and glomerular basement membranes for a single light chain (kappa) and IgG isotype restriction. Which diagnosis is most consistent with these findings?

Membranous nephropathy secondary to immune complexes

Monoclonal immunoglobulin deposition disease (MIDD)

Amyloidosis (AL type)

IgA nephropathy

Post-infectious glomerulonephritis

Correct answer: B. MIDD (often light-chain deposition disease) characteristically shows linear, nodular, or diffuse deposition along the glomerular and tubular basement membranes with restriction to a single light chain (kappa or lambda) and a single heavy-chain isotype—evidence of monoclonality. Option A (secondary membranous) shows granular subepithelial deposits and is typically polyclonal. Option C (amyloidosis) shows Congo red–positive deposits and nonbranching fibrils on EM rather than linear monoclonal staining along basement membranes. Option D (IgA nephropathy) shows mesangial-dominant IgA deposition. Option E (post-infectious GN) shows granular 'lumpy-bumpy' deposits and hypocomplementaemia, not monoclonal linear TBM/GBM staining.

10 / 10

Two hours after an ultrasound-guided native renal biopsy the patient becomes hypotensive and has gross haematuria. What is the most appropriate immediate response?

Observe the patient closely and repeat vital signs in one hour, as post-biopsy haematuria is usually self-limiting.

Start intravenous antibiotics for presumed infected haematoma and plan elective imaging next day.

Administer intravenous tranexamic acid and discharge once haematuria reduces.

Resuscitate (IV fluids ± blood transfusion as indicated), stop anticoagulants/antiplatelets, cross-match blood and arrange urgent imaging (CT angiography) with interventional radiology available for possible embolisation.

Arrange elective outpatient CT scan the following week to look for haematoma size.

Correct answer: D. Significant haematuria with hypotension after renal biopsy suggests active bleeding; immediate resuscitation, correction/cessation of anticoagulation, blood crossmatch and urgent imaging (contrast CT angiography) to localise bleeding with a view to urgent angioembolisation are appropriate. Option A is unsafe because delay risks ongoing haemodynamic compromise. Option B (start antibiotics) is not the immediate priority for an acute bleed. Option C (tranexamic acid and discharge) is inappropriate in a haemodynamically unstable patient—the antifibrinolytic alone is insufficient and discharge would be unsafe. Option E (elective imaging next week) dangerously delays urgent intervention.

Your score is

The average score is 17%

By Wordpress Quiz plugin

Board-level postgraduate nephrology self-assessment.

Complete all 10 single-best-answer questions to receive detailed clinical explanations on the results page.

Pediatric Nephrology for Adult Examinations

Ten MRCP/board-style single-best-answer questions on paediatric nephrology topics that adult physicians must recognise: diagnosis, interpretation, acute and chronic management, complications and investigations.

1 / 10

A term neonate (24 hours old) is noted to have urine output <0.5 mL/kg/h, low blood pressure after an episode of perinatal hypoxia and required neonatal resuscitation. Serum creatinine is rising compared with cord value. Which is the most likely cause of the oliguria?

Ischaemic acute tubular necrosis from perinatal hypoperfusion

Bilateral renal agenesis

Posterior urethral valves

Congenital nephrotic syndrome

Maternal creatinine still dominating neonatal value

In neonates with perinatal asphyxia and early oliguria/creatinine rise the most likely cause is ischaemic ATN; reckon with supportive management and nephrology input.

This neonate has oliguria in the first day of life together with perinatal hypoxia and hypotension. Ischaemic (ischemic) acute tubular necrosis (ATN) from severe perinatal hypoperfusion is the commonest cause of early neonatal acute kidney injury (AKI) in this context. Bilateral renal agenesis presents with anhydramnios antenatally and is incompatible with life; it would be apparent earlier and not present with rising neonatal creatinine after a resuscitation event. Posterior urethral valves cause obstructive uropathy that typically presents with bladder distension, poor stream or progressive renal impairment rather than a sudden rise in creatinine immediately after perinatal hypoxia; antenatal hydronephrosis may be present. Congenital nephrotic syndrome presents later with heavy proteinuria, oedema and hypoalbuminaemia rather than immediate oliguria with perinatal hypoxia. Maternal creatinine influences neonatal values for the first 24–48 hours but would not explain progressive rise in creatinine with oliguria after hypoxic insult; the clinical context points to intrinsic AKI (ATN).

2 / 10

An 18-month-old boy has had two febrile urinary tract infections in the past 6 months. Renal ultrasound shows unilateral moderate hydronephrosis. What is the next most appropriate investigation to define the likely cause?

Repeat ultrasound in 6 weeks

Dimercaptosuccinic acid (DMSA) renal cortical scan

Micturating cystourethrogram (MCUG/VCUG)

Serum immunoglobulin levels

Renal biopsy

In young children (especially boys) with recurrent febrile UTIs and hydronephrosis, perform an MCUG/VCUG to look for vesicoureteric reflux or posterior urethral valves.

In a young boy with recurrent febrile UTIs and ultrasound evidence of hydronephrosis, a micturating cystourethrogram (MCUG/VCUG) is indicated to assess for vesicoureteric reflux and to exclude posterior urethral valves (PUV), particularly because boys are more likely to have obstructive pathology. A DMSA scan assesses renal cortical scarring but does not identify the cause of hydronephrosis or bladder outlet obstruction and is not the first investigation to define anatomic cause. Repeating the ultrasound without functional/voiding imaging delays diagnosis of reflux/PUV. Serum immunoglobulins are only indicated if there is concern about recurrent unusual infections or immunodeficiency; they do not define structural urinary tract pathology. Renal biopsy is not indicated to investigate recurrent UTIs or hydronephrosis.

3 / 10

An 8-year-old child presents with new-onset nephrotic syndrome and responds completely to an initial course of oral corticosteroids. He then has frequent relapses despite alternate-day prednisolone. Which is the most appropriate next step as a steroid-sparing agent in a frequently relapsing, steroid-sensitive child?

Immediate renal biopsy and start cyclophosphamide

Begin cyclophosphamide as a steroid-sparing agent

Switch to low-dose long-term prednisolone only

Start angiotensin-converting enzyme (ACE) inhibitor alone

Proceed directly to rituximab

For frequently relapsing steroid-sensitive nephrotic syndrome in children, consider a steroid‑sparing immunosuppressant such as cyclophosphamide (or alternatives) rather than prolonged high‑dose steroids or immediate biologic therapy.

In children with steroid-sensitive nephrotic syndrome who have frequent relapses despite alternate-day steroids, steroid-sparing agents are indicated to reduce steroid exposure. Oral cyclophosphamide (or levamisole in some contexts) has traditionally been used as a first-line steroid-sparing agent for frequently relapsing steroid-sensitive disease. Immediate renal biopsy is not routinely required in steroid-sensitive, typical minimal-change–type presentations before using a steroid-sparing agent. Continuing only low‑dose prednisolone perpetuates steroid toxicity and is not the preferred long-term strategy if frequent relapses occur. ACE inhibitors reduce proteinuria and are useful adjuncts but are not primary steroid-sparing immunosuppressants in this setting. Rituximab is effective for difficult steroid-dependent or frequently relapsing disease refractory to first‑line steroid‑sparing agents and is generally reserved for patients who have failed conventional agents or have contraindications.

4 / 10

A 3-year-old is admitted with bloody diarrhoea from an antecedent diarrhoeal illness, pallor, rising creatinine, thrombocytopenia and schistocytes on blood film. What is the most appropriate immediate management step?

Start broad‑spectrum IV antibiotics immediately

Urgent plasma exchange

Supportive care including fluid management and prepare for renal replacement if required

Immediate platelet transfusion because of thrombocytopenia

Start eculizumab straight away

Typical STEC-HUS is managed primarily with careful supportive care and renal replacement therapy when needed; antibiotics and platelet transfusion are not routine and eculizumab is reserved for complement-mediated disease.

This presentation is typical of typical (Shiga-toxin–associated) haemolytic uraemic syndrome (STEC-HUS). The mainstay of initial management is supportive care: careful fluid balance, blood pressure control, correction of electrolyte disturbances and timely initiation of renal replacement therapy if indicated. Antibiotics for diarrhoeal illness are generally avoided because some antibiotics may increase Shiga toxin release and worsen HUS risk or severity. Plasma exchange is not beneficial for typical STEC-HUS; it may be considered in rare circumstances of severe neurologic involvement but is not routine. Platelet transfusion is avoided unless there is life‑threatening bleeding or an invasive procedure is required because it may exacerbate microthrombosis. Eculizumab (complement C5 inhibitor) is indicated for complement-mediated (atypical) HUS in selected cases but is not standard immediate therapy for typical STEC-HUS.

5 / 10

A 6-year-old boy has persistent microscopic haematuria and a family history of hearing loss. Which investigation is the most appropriate next test to confirm the diagnosis?

Genetic testing for COL4A5/COL4A3/COL4A4 mutations

Urine culture

Doppler renal ultrasound

Serum complement C3 and C4 levels

Immediate renal biopsy with electron microscopy

Suspected Alport syndrome should be investigated first with genetic testing for type IV collagen genes to establish diagnosis and guide counselling.

The clinical picture (familial persistent haematuria with sensorineural hearing loss) strongly suggests Alport syndrome, which is most efficiently confirmed by genetic testing for mutations in type IV collagen genes (COL4A5, COL4A3, COL4A4). Genetic testing is preferred as first‑line because it is non‑invasive and defines inheritance, prognosis and informs family counselling. Urine culture is irrelevant if haematuria is not suspected to be infectious. Doppler ultrasound will not diagnose Alport syndrome. Complement levels are used for suspected complement-mediated glomerulonephritis, not Alport. Renal biopsy with electron microscopy can show characteristic basement membrane changes and may be used when genetic testing is inconclusive, but it is not the first‑line test if genetic testing is available.

6 / 10

A 10-year-old with newly identified stage 2 hypertension (BP consistently >95th percentile for age/height) is slim, with no family history of essential hypertension, and has a past history of urinary tract infections. Which initial investigation is most appropriate in assessing a secondary renal cause?

Urinalysis (dipstick for blood/protein) and urine albumin:creatinine ratio

Ambulatory blood pressure monitoring only

Commence an ACE inhibitor immediately without investigations

Renal biopsy

Plasma aldosterone/renin ratio

Children with hypertension are more likely to have secondary causes than adults, the commonest being renal parenchymal disease. Initial evaluation should include urinalysis (dipstick for haematuria/protein) and urine albumin:creatinine ratio to look for renal parenchymal disease, along with renal ultrasound and basic blood tests. Ambulatory BP monitoring can help confirm hypertension but does not evaluate underlying secondary causes. Starting ACE inhibitor therapy without basic investigations and baseline renal function/urinalysis is not appropriate. Renal biopsy is not a first‑line test unless urinalysis, imaging and bloods point to intrinsic glomerular disease requiring histology. Plasma aldosterone/renin testing is reserved for suspected primary hyperaldosteronism or renovascular hypertension and is not the initial screen in a child with suspected renal parenchymal disease.

7 / 10

Urinalysis (dipstick for blood/protein) and urine albumin:creatinine ratio

Ambulatory blood pressure monitoring only

Commence an ACE inhibitor immediately without investigations

Renal biopsy

Plasma aldosterone/renin ratio

8 / 10

A 4-year-old presents with sudden anuria, palpable distended bladder and bilateral flank pain. Bladder catheterisation yields 250 mL urine and the anuria resolves. What was the most important immediate management action?

Immediate peritoneal dialysis

Urgent decompression of the urinary bladder with catheterisation

Start IV broad-spectrum antibiotics immediately

Administer furosemide to force diuresis

Obtain a renal biopsy

The child has acute urinary retention causing post‑renal obstructive AKI. The most important immediate step is prompt decompression of the urinary tract by bladder catheterisation to relieve obstruction and restore urine flow. Peritoneal dialysis may be required later if obstruction causes sustained renal failure or complications, but immediate decompression takes priority. Broad-spectrum antibiotics are indicated if there is evidence of infection but are not the immediate manoeuvre to relieve obstruction. Furosemide is not appropriate in the presence of mechanical obstruction and will not relieve retention. Renal biopsy is irrelevant for acute obstructive presentation.

9 / 10

A 7-year-old boy develops periorbital oedema and cola-coloured urine 2 weeks after a sore throat. Which laboratory test will most strongly support a diagnosis of post-infectious (post‑streptococcal) glomerulonephritis?

Elevated serum C‑reactive protein (CRP)

Depressed serum complement C3 level

Positive anti‑nuclear antibody (ANA)

Low serum immunoglobulin G (IgG)

Positive urine culture

Post‑streptococcal glomerulonephritis typically presents 1–3 weeks after a streptococcal pharyngitis or skin infection with nephritic features and is commonly associated with low serum complement C3 levels (which usually recover over 6–8 weeks). Elevated CRP is non‑specific and not diagnostic. A positive ANA suggests autoimmune disease such as lupus, not classical post‑streptococcal GN. Low IgG would suggest hypogammaglobulinaemia and is unrelated. A positive urine culture indicates urinary infection rather than post‑streptococcal GN; it would not support that diagnosis.

10 / 10

A 15-year-old with nephrotic syndrome is admitted with sudden onset unilateral calf pain and swelling. Which factor most strongly increases the risk of venous thromboembolism in children with nephrotic syndrome?

Use of oral corticosteroids

History of recurrent urinary tract infections

Presence of a central venous catheter

Age under 2 years

Concurrent ACE inhibitor therapy

Children with nephrotic syndrome have an increased thrombotic risk due to hypercoagulability, but the presence of a central venous catheter is a particularly strong, modifiable risk factor for venous thrombosis. Corticosteroid therapy is commonly used but is not the dominant determinant of thrombotic risk. Recurrent UTIs are not a major thrombotic risk factor. Younger age (under 2 years) tends to be associated with lower thrombotic risk compared with adolescents; older children and adolescents have higher thrombotic risk. ACE inhibitor therapy is not associated with increased thrombotic risk.

Your score is

The average score is 0%

By Wordpress Quiz plugin

Board-level postgraduate nephrology self-assessment.

Complete all 10 single-best-answer questions to receive detailed clinical explanations on the results page.

Critical Care Nephrology and Kidney Support

High-yield, board-style questions on AKI recognition, indications and modalities for renal replacement therapy (RRT), anticoagulation strategies for extracorporeal circuits, fluid choice, catheter complications and transitions of care in critically ill patients requiring kidney support.

1 / 10

A child is found to have a congenital solitary kidney discovered incidentally. For long-term renal preservation which follow-up strategy is most appropriate?

No follow-up required if initial function is normal

Annual blood pressure measurement and urine protein testing with avoidance of nephrotoxins

Immediate referral for pre-emptive renal transplant listing

Restrict physical activity and sports participation permanently

Start ACE inhibitor prophylactically regardless of proteinuria

A child with a congenital solitary kidney requires long-term surveillance for hyperfiltration injury. Annual blood pressure measurement and urine protein assessment, together with avoidance of nephrotoxins and escalation if hypertension, proteinuria, or reduced kidney function develops, is appropriate. Routine permanent restriction of physical activity, prophylactic ACE inhibition without hypertension or proteinuria, or transplant listing with normal kidney function is not indicated.

2 / 10

A 72-year-old man in the ICU with congestive heart failure is on intravenous loop diuretics. Over 24 hours his serum creatinine rises from 120 to 210 μmol/L and urine output falls to 0.3 mL/kg/h. A single spot urine sodium is 80 mmol/L. Which is the most useful next test to determine whether his acute kidney injury is predominantly pre-renal (functional) versus intrinsic renal?

Repeat the urine sodium measurement after withholding diuretics for 24 hours

Calculate the fractional excretion of sodium (FENa)

Calculate the fractional excretion of urea (FEUrea)

Order a renal ultrasound with Doppler

Obtain serum BNP to assess cardiac filling status

In patients receiving diuretics, urine sodium and FENa are unreliable because diuretics increase natriuresis and raise urine sodium irrespective of intravascular volume status. FEUrea is less affected by diuretics and a low FEUrea (classically <35%) suggests a pre-renal (functional) aetiology. Renal ultrasound is useful to exclude obstruction but does not reliably distinguish pre-renal from intrinsic renal causes. Serum BNP provides information about cardiac strain but is not specific enough to determine the mechanism of AKI in this setting.

3 / 10

A 60-year-old woman with oliguric acute kidney injury and serum potassium 7.1 mmol/L has ECG changes (peaked T waves and widening QRS). She has already received IV calcium, insulin with glucose, and nebulised salbutamol but remains hyperkalaemic with ongoing ECG abnormalities. What is the most appropriate next step?

Repeat insulin/glucose infusion at a higher dose

Proceed to urgent renal replacement therapy (haemodialysis)

Give oral potassium-binding resin (sodium polystyrene sulfonate)

Administer intravenous sodium bicarbonate and observe

Start a continuous infusion of low-dose insulin without glucose bolus

Persistent hyperkalaemia with ECG changes despite temporising measures is an indication for urgent removal of potassium by renal replacement therapy (usually haemodialysis if available rapidly). Repeating temporising therapies may delay definitive treatment when ECG abnormalities persist. Oral/resin binders act slowly and are unsuitable as sole therapy in this emergency. Sodium bicarbonate may help if there is severe acidosis, but if ECG changes persist it is insufficient alone. An insulin infusion strategy is not a standard immediate substitute for dialysis when temporising measures have failed.

4 / 10

A 58-year-old man with septic shock (on norepinephrine 0.2 μg/kg/min), invasive ventilation and oliguric AKI needs renal support. He is haemodynamically unstable with frequent vasopressor requirement. Which RRT modality is most appropriate initially?

Intermittent haemodialysis (IHD) three times per week

Short daily haemodialysis (4–6 days per week)

Peritoneal dialysis

Continuous renal replacement therapy (CRRT)

Sustained low-efficiency dialysis (SLED) without anticoagulation

In haemodynamically unstable critically ill patients requiring ongoing vasopressor support, continuous renal replacement therapy (CRRT) is generally preferred because it provides slower, continuous solute and fluid removal with better haemodynamic tolerance. Intermittent haemodialysis may precipitate hypotension in unstable patients. Short daily IHD is used chronically but is not appropriate acutely in severe shock. Peritoneal dialysis is rarely used in high-acuity septic shock in modern ICUs and provides limited ultrafiltration in the presence of intra-abdominal processes. SLED can be considered where CRRT is unavailable, but CRRT remains the standard for persistent severe haemodynamic instability.

5 / 10

A 65-year-old patient with acute liver failure (INR elevated, bilirubin 350 μmol/L) requires CRRT for AKI but also has a high bleeding risk. Which anticoagulation strategy for the extracorporeal circuit is most appropriate?

Avoid citrate anticoagulation; use no anticoagulation and maximise circuit care with saline flushes

Use regional citrate anticoagulation (RCA) as first-line because bleeding risk is high

Administer a continuous low-dose heparin infusion systemically

Use low-molecular-weight heparin into the circuit

Add oral warfarin to achieve INR 2–3 for circuit protection

Regional citrate anticoagulation is generally preferred for CRRT in patients without contraindications, especially when bleeding risk is high, because it limits systemic anticoagulation. However, severe liver failure (or severe shock with impaired citrate metabolism) is a relative contraindication to citrate due to risk of citrate accumulation and metabolic complications. In this context, avoiding citrate and running CRRT without anticoagulation (with higher blood flow rates, regular saline flushes and maximised circuit care) is appropriate. Systemic unfractionated heparin increases bleeding risk and is undesirable in severe hepatic failure with coagulopathy. LMWH is contraindicated if bleeding risk is high and is poorly controllable. Warfarin is inappropriate for extracorporeal circuit protection.

6 / 10

A 70-kg ICU patient is prescribed CRRT. According to contemporary guideline recommendations, what delivered effluent dose should be targeted to provide adequate solute clearance?

10 mL/kg/h delivered

15 mL/kg/h delivered

30–35 mL/kg/h delivered

40–50 mL/kg/h delivered

20–25 mL/kg/h delivered

KDIGO guidelines recommend prescribing an effluent volume that achieves an average delivered dose of approximately 20–25 mL/kg/h for CRRT. Higher doses (e.g., 35–50 mL/kg/h) have not shown outcome benefit in randomised trials and increase costs/complications. Lower doses (<20 mL/kg/h) risk inadequate solute control. The figure refers to delivered (not simply prescribed) dose; attention should be paid to interruptions and clotting which reduce delivered therapy.

7 / 10

A 59-year-old man with oliguric AKI is acidotic with arterial pH 7.05 despite IV bicarbonate therapy and is becoming progressively drowsy. Which statement best reflects current guidance about initiating dialysis for acid–base control?

Dialysis is not indicated solely for acidosis; manage medically unless pH <6.9

Start RRT because severe metabolic acidosis refractory to medical therapy is an indication for dialysis

Delay dialysis until serum bicarbonate <8 mmol/L is sustained for 12 hours

Initiate haemodialysis only if hyperkalaemia coexists

Switch from CRRT to intermittent haemodialysis to correct the acidosis more rapidly

Severe metabolic acidosis that is refractory to appropriate medical therapy and associated with clinical consequences (hemodynamic instability, progressive encephalopathy) is an accepted indication for initiating renal replacement therapy. There is no fixed rule requiring pH <6.9 before dialysis; waiting that low would be unsafe. The presence of hyperkalaemia is not required to start dialysis for acidosis. Choice of modality (CRRT versus intermittent haemodialysis) depends on haemodynamic stability; switching to intermittent haemodialysis just to correct acidosis is not appropriate if the patient is unstable.

8 / 10

A 45-year-old woman in the ICU has confirmed heparin-induced thrombocytopenia and requires CRRT. Citrate anticoagulation is contraindicated and monitoring for an alternative direct thrombin inhibitor is available. Which systemic anticoagulant is the preferred option for the extracorporeal circuit?

Continue unfractionated heparin but at a lower dose

Use a direct thrombin inhibitor such as argatroban

Start low molecular weight heparin (enoxaparin)

Use regional citrate anticoagulation despite HIT diagnosis

Administer fondaparinux as standard circuit anticoagulation

In confirmed HIT, all heparin products should be stopped. When citrate is contraindicated and systemic monitoring is available, a direct thrombin inhibitor such as argatroban is an appropriate preferred systemic anticoagulant for the extracorporeal circuit. Regional citrate is an alternative only when not contraindicated; LMWH and unfractionated heparin should not be used.

9 / 10

In patients with sepsis and AKI requiring large-volume fluid resuscitation, which intravenous crystalloid is currently favoured to reduce the risk of worsening kidney function?

5% dextrose

Half-normal saline (0.45% NaCl)

Hypertonic saline (3% NaCl)

Balanced crystalloids (e.g., Plasma-Lyte, Hartmann's solution)

0.9% sodium chloride (saline) as first-line for all septic patients

Recent evidence and guideline interpretations favour the use of balanced crystalloids over 0.9% saline in patients with sepsis to reduce the risk of kidney injury and need for RRT. Balanced solutions have lower chloride content and more physiologic strong ion difference, which may reduce hyperchloraemic metabolic acidosis and adverse renal effects. 0.9% saline is still used but is not preferred in this context. Dextrose-containing fluids and hypotonic or hypertonic saline are not appropriate for routine large-volume resuscitation in sepsis.

10 / 10

A patient on acute intermittent haemodialysis through a non-tunnelled jugular dialysis catheter develops Staphylococcus aureus bacteraemia confirmed on blood cultures. According to accepted nephrology practice, what is the best management of the catheter?

Remove the dialysis catheter promptly and place a new access at a different site

Leave the catheter in place and treat with 7 days of IV antibiotics only

Exchange the catheter over a guidewire and continue antibiotics

Administer oral antibiotics and observe; remove only if recurrent positive cultures

Attempt antibiotic lock therapy without systemic antibiotics

S. aureus bacteraemia in a patient with a vascular access device is a high-risk situation associated with metastatic infection; guidance supports prompt removal of the implicated catheter and systemic antibiotic therapy. Exchanging the catheter over a guidewire risks ongoing seeding. Short IV antibiotics alone without catheter removal are insufficient. Antibiotic lock therapy is adjunctive and never a sole therapy for S. aureus bacteraemia.

Your score is

The average score is 75%

By Wordpress Quiz plugin

Board-level postgraduate nephrology self-assessment.

Complete all 10 single-best-answer questions to receive detailed clinical explanations on the results page.

Pregnancy and Kidney Disease

Board-style MCQs covering diagnosis, interpretation, acute and chronic management, complications and transplant considerations in pregnancy with kidney disease.

1 / 10

A 34-year-old woman with stage 3b chronic kidney disease (eGFR 38 mL/min/1.73 m2), chronic hypertension and baseline proteinuria of 1.5 g/24h asks about pregnancy. Which preconception factor most strongly predicts adverse maternal and fetal outcomes in women with CKD?

Duration of hypertension (years since diagnosis)

Type of antihypertensive used preconception

Baseline maternal renal function (level of eGFR)

Maternal age over 35 years

Presence of low-dose aspirin prophylaxis planned

Baseline eGFR is the major determinant of pregnancy risk in CKD; counsel and optimise renal function before conception.

Correct answer: Baseline maternal renal function (level of eGFR).

Rationale: The degree of maternal renal impairment is the strongest predictor of both maternal and fetal complications in pregnancy. Lower baseline eGFR (more advanced CKD) is associated with higher risks of pre-eclampsia, pregnancy loss, preterm birth and decline in maternal renal function. While duration of hypertension, choice of antihypertensive and maternal age influence risk, they are less predictive than the baseline level of kidney function. Low-dose aspirin reduces risk of pre-eclampsia in high-risk women but is preventive rather than a primary determinant of baseline risk.

Why the others are less appropriate:
- Duration of hypertension: Longer duration increases risk but is secondary to the presence and severity of end-organ damage (e.g. impaired renal function).
- Type of antihypertensive: Some drugs (ACE inhibitors/ARBs) must be stopped before conception, but drug class is not the dominant predictor of overall pregnancy outcome.
- Maternal age >35: Advanced maternal age increases obstetric risk but does not outweigh the impact of impaired renal function.
- Planned aspirin prophylaxis: Aspirin can reduce pre-eclampsia risk but does not change the baseline prognostic importance of maternal renal function.

2 / 10

A pregnant patient at 30 weeks with CKD presents with severe hypertension (BP 170/115 mmHg). Which antihypertensive is the most appropriate initial agent for acute blood-pressure control in severe pregnancy hypertension?

Intravenous labetalol

Oral ramipril

Oral atenolol

Oral spironolactone

Intravenous enalaprilat

For acute severe hypertension in pregnancy use pregnancy-safe agents such as IV labetalol, IV hydralazine or oral immediate-release nifedipine; avoid ACEi/ARBs and other contraindicated drugs.

Correct answer: Intravenous labetalol.

Rationale: For severe hypertension in pregnancy (commonly defined as systolic ≥160 mmHg or diastolic ≥110 mmHg), immediate BP lowering is recommended using agents with established safety and efficacy in pregnancy. Intravenous labetalol is a first-line option for acute control, along with intravenous hydralazine or oral immediate-release nifedipine depending on local availability and clinical context. ACE inhibitors (e.g. ramipril, enalaprilat), ARBs, atenolol and spironolactone are contraindicated or not recommended in pregnancy because of fetal toxicity or lack of evidence of safety.

Why the others are less appropriate:
- Oral ramipril and IV enalaprilat (ACE inhibitors): Contraindicated in pregnancy due to fetopathy (renal dysplasia, oligohydramnios, skull hypoplasia).
- Oral atenolol (beta-blocker): Some beta-blockers are used in pregnancy (e.g. labetalol), but atenolol is associated with fetal growth restriction and is not a first-line choice for acute severe hypertension.
- Oral spironolactone: Anti-androgenic effects and lack of safety data make it inappropriate in pregnancy.

3 / 10

A 28-year-old woman with known stage 2 CKD (baseline creatinine 90 μmol/L) at 34 weeks' gestation develops new-onset hypertension and an increase in proteinuria from 0.4 g/24h to 3.0 g/24h. Which investigation provides the best additional information to distinguish superimposed pre-eclampsia from progression of chronic kidney disease?

Repeat 24-hour urine collection for protein quantification

Serum uric acid level

Percutaneous renal biopsy at 34 weeks

Empiric escalation of antihypertensive therapy and observe response

Measurement of maternal angiogenic markers (sFlt-1/PlGF ratio)

Angiogenic biomarkers (sFlt‑1/PlGF) are useful adjuncts to differentiate pre-eclampsia from CKD progression when baseline proteinuria exists.

Correct answer: Measurement of maternal angiogenic markers (sFlt-1/PlGF ratio).

Rationale: In late pregnancy, distinguishing superimposed pre-eclampsia from chronic kidney disease progression is challenging. Angiogenic biomarkers (sFlt‑1 and PlGF) and their ratio are useful adjuncts: an elevated sFlt‑1/PlGF ratio supports a diagnosis of pre-eclampsia, whereas a low ratio makes it unlikely. This has particular value when baseline proteinuria is present. Repeat urine protein quantification documents the degree of proteinuria but cannot reliably distinguish the aetiology. Serum uric acid is nonspecific. Renal biopsy in late third trimester carries increased maternal/fetal risk and is rarely the first-line diagnostic step. Empiric escalation of antihypertensives may be necessary for BP control but does not clarify the diagnosis.

Why the others are less appropriate:
- Repeat 24-hour urine: Confirms proteinuria magnitude but not the cause (CKD progression vs pre-eclampsia).
- Serum uric acid: Elevated in pre-eclampsia but lacks specificity and sensitivity in CKD.
- Percutaneous renal biopsy at 34 weeks: Higher procedural risk in third trimester and usually deferred unless results would change management and safer timing cannot be found.
- Empiric antihypertensive escalation: Important for maternal safety but not diagnostic; cannot reliably differentiate pre-eclampsia from CKD progression.

4 / 10

A 30-year-old woman has a severe postpartum haemorrhage with 2.5 L estimated blood loss during delivery. In the first 24 hours she required vasopressors; urine output fell and creatinine rose from 70 to 230 μmol/L. What is the most likely diagnosis causing her acute kidney injury?

Obstructive uropathy from ureteric injury during delivery

Ischaemic acute tubular necrosis (ATN) secondary to hypovolaemic/ischaemic injury

Rapidly progressive glomerulonephritis triggered by pregnancy

Acute interstitial nephritis from peri-partum antibiotics

Atypical haemolytic uraemic syndrome initiated by delivery

Severe hypovolaemia from postpartum haemorrhage commonly causes ischaemic ATN; consider other causes (TMA, AIN, obstruction) if additional features suggest them.

Correct answer: Ischaemic acute tubular necrosis (ATN) secondary to hypovolaemic/ischaemic injury.

Rationale: A large postpartum haemorrhage with hypotension and vasopressor requirement is a classic setting for ischaemic ATN due to renal hypoperfusion. Presentation over hours to days with oliguria and rising creatinine is typical. Obstructive uropathy from ureteric injury is uncommon and would usually present with pain and hydronephrosis; it does not explain hypotension and shock. Rapidly progressive glomerulonephritis is less likely to present acutely in the immediate post-PPH period without prior urinary abnormalities. Acute interstitial nephritis from antibiotics is possible but usually presents with eosinophilia, rash, and a less immediate severe creatinine rise. Atypical HUS can present postpartum with thrombocytopenia and microangiopathic haemolysis plus AKI, but the vignette lacks haemolysis/low platelets; ATN is the most likely immediate cause.

Why the others are less appropriate:
- Obstructive uropathy: Unlikely in the context of profound haemodynamic instability and immediate AKI.
- RPGN: Would usually have haematuria, RBC casts and subacute progression, not solely following hypotension.
- AIN: Typically drug-related with systemic features and not so immediate after hypovolaemia.
- aHUS: Consider if thrombocytopenia and MAHA are present; requires specific testing and therapies but is less likely here without those features.

5 / 10

A 25-year-old woman at 18 weeks' gestation presents with new nephrotic-range proteinuria, oedema and declining renal function. The team is considering renal biopsy. Which statement best describes the accepted approach to renal biopsy in pregnancy?

Renal biopsy should be deferred until after delivery in all pregnant women.

Perform percutaneous renal biopsy in the first trimester for best diagnostic yield.

Percutaneous renal biopsy is most safely performed in the second trimester when results will alter management.

Transjugular renal biopsy is contraindicated in pregnancy.

Empiric immunosuppression should always be started without biopsy in pregnancy.

If biopsy will change management, the second trimester is generally the safest time to perform a percutaneous renal biopsy in pregnancy.

Correct answer: Percutaneous renal biopsy is most safely performed in the second trimester when results will alter management.

Rationale: If the diagnostic result will change management, a percutaneous renal biopsy is generally safest in the second trimester (commonly quoted as 14–28 weeks) when the risks to mother and fetus are lower than in the first trimester and the technical difficulties/risks of third trimester (enlarged uterus, vascularity) are greater. Biopsy should not be deferred automatically if the diagnosis will influence therapy. First-trimester biopsy carries higher relative risk to the fetus; transjugular biopsy can be considered in selected high-bleeding-risk patients and is not universally contraindicated. Empiric immunosuppression without tissue diagnosis may be appropriate in selected severe cases but is not ‘always’ indicated.

Why the others are less appropriate:
- Deferring until after delivery: May delay necessary treatment and worsen maternal/fetal outcomes when biopsy would alter management.
- First trimester biopsy: Higher miscarriage risk and often avoided unless absolutely necessary.
- Transjugular biopsy contraindicated: Incorrect—transjugular approach can be used when percutaneous biopsy is high risk (e.g. coagulopathy), though it carries its own risks.
- Empiric immunosuppression always: Inappropriate—decision should be individualised and informed by the likelihood of specific diagnoses and risks of therapy.

6 / 10

A woman on chronic haemodialysis becomes pregnant. Which dialysis strategy is associated with the best fetal outcomes and is therefore recommended when feasible?

Maintain conventional thrice-weekly dialysis without change

Increase dialysis intensity and frequency (e.g. daily or extended sessions)

Switch from haemodialysis to peritoneal dialysis during pregnancy

Reduce ultrafiltration volumes to avoid intradialytic hypotension even if uraemia increases

Cease dialysis temporarily during first trimester to avoid fetal exposure

Pregnancy in dialysis patients usually requires intensifying dialysis frequency/duration to improve fetal outcomes and optimise maternal fluid/metabolic control.

Correct answer: Increase dialysis intensity and frequency (e.g. daily or extended sessions).

Rationale: Pregnant women on dialysis have better fetal outcomes when dialysis is intensified—more frequent and/or longer sessions to lower predialysis blood urea, optimise volume status and reduce uraemia-related fetal risks. Many centres aim for increased weekly dialysis dose and more frequent sessions. Maintaining conventional thrice-weekly dialysis is generally associated with worse outcomes (higher rates of polyhydramnios, preterm birth). Switching to peritoneal dialysis is an option in some patients but is not universally superior and may be complicated by increased intra-abdominal pressure and infections. Reducing ultrafiltration to avoid hypotension is sensible, but not at the cost of inadequate solute clearance; careful fluid and dialysis prescription adjustments are needed. Ceasing dialysis is unsafe.

Why the others are less appropriate:
- Conventional thrice-weekly: Often insufficient to optimise metabolic milieu for pregnancy.
- Switch to peritoneal dialysis: Not routinely recommended solely for pregnancy; selection depends on patient factors.
- Reduce ultrafiltration at expense of uraemic control: Avoid intradialytic hypotension but maintain adequate dialysis dose; balance is needed.
- Cease dialysis: Dangerous for mother and fetus.

7 / 10

Which immunosuppressive drug should be stopped and substituted before conception because of a well-established risk of teratogenicity and pregnancy loss in women with kidney disease or transplant?

Mycophenolate mofetil (MMF)

Azathioprine

Prednisolone

Tacrolimus

Cyclosporine

Stop mycophenolate before conception and substitute with pregnancy-compatible immunosuppression (e.g. azathioprine) under specialist supervision.

Correct answer: Mycophenolate mofetil (MMF).

Rationale: Mycophenolate is teratogenic and associated with pregnancy loss and congenital malformations. Women of reproductive potential should be switched to alternative agents (commonly azathioprine) prior to conception and must use effective contraception until an appropriate washout period and substitution are completed. Azathioprine, prednisolone and calcineurin inhibitors (tacrolimus, cyclosporine) are generally considered compatible with pregnancy when clinically indicated, with careful monitoring.

Why the others are less appropriate:
- Azathioprine: Considered acceptable in pregnancy and often used as a safer alternative to MMF.
- Prednisolone: Used in pregnancy when needed; crosses placenta in limited amounts relative to maternal dose.
- Tacrolimus and cyclosporine: Calcineurin inhibitors can be used in pregnancy with monitoring; they are not teratogenic like MMF.

8 / 10

A woman develops severe hypertension at 36 weeks with thrombocytopenia and microangiopathic haemolysis (schistocytes), and rapidly progressive AKI requiring RRT. Delivery has taken place but renal function continues to deteriorate and platelet count does not recover. Which diagnosis becomes most likely in this postpartum deteriorating picture?

Classic HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets)

Thrombotic thrombocytopenic purpura (TTP) with severe ADAMTS13 deficiency

Atypical haemolytic uraemic syndrome (aHUS) with complement-mediated thrombotic microangiopathy

Acute fatty liver of pregnancy

Disseminated intravascular coagulation from retained products

If microangiopathic haemolysis and thrombocytopenia with progressive AKI persist or worsen after delivery, aHUS should be strongly considered and urgent nephrology/haematology input sought.

Correct answer: Atypical haemolytic uraemic syndrome (aHUS) with complement-mediated thrombotic microangiopathy.

Rationale: While HELLP and TTP commonly present in late pregnancy, a hallmark that points towards complement-mediated aHUS is persistence or worsening of microangiopathic haemolysis, thrombocytopenia and particularly renal failure after delivery. HELLP typically improves after delivery. TTP is characterised by severe ADAMTS13 deficiency (<10%) and often responds to plasma exchange. Atypical HUS often presents or worsens postpartum and is associated with predominant and progressive renal injury; it may require complement inhibition (eculizumab) when diagnosed. Acute fatty liver of pregnancy has prominent liver dysfunction and hypoglycaemia and usually improves after delivery. DIC would usually have broader coagulation abnormalities and a clear trigger. Why the others are less appropriate: - HELLP: Usually improves within days after delivery; persistence of worsening renal failure argues against isolated HELLP. - TTP: ADAMTS13 testing is required; severe deficiency supports TTP, but normal/near-normal ADAMTS13 plus persistent renal failure favours aHUS. - Acute fatty liver: Distinguished by profound liver failure and metabolic derangements rather than isolated renal deterioration. - DIC from retained products: Usually associated with consumptive coagulopathy and clinical signs of bleeding; does not classically cause isolated progressive renal failure.

9 / 10

A 35-year-old woman wishes to conceive after a successful kidney transplant. Which of the following is the most widely recommended advice regarding timing of conception post-transplant?

Attempt pregnancy as soon as graft function is adequate, with no minimum interval

Wait at least 12 months after transplant with stable graft function and no recent rejection episodes

Do not attempt pregnancy if on any calcineurin inhibitor

Delay pregnancy for 5 years to avoid long-term graft damage

Switch immunosuppression to mycophenolate immediately before conception

Aim for conception after at least 12 months of stable graft function and no recent rejection; review and adjust immunosuppression preconception.

Correct answer: Wait at least 12 months after transplant with stable graft function and no recent rejection episodes.

Rationale: The usual recommendation is to delay conception until graft function is stable and there have been no recent rejection episodes—commonly for at least 12 months post-transplant. This allows optimisation of immunosuppression, stabilisation of graft function and minimises maternal and fetal risk. Calcineurin inhibitors are not absolute contraindications to pregnancy. Delaying 5 years is unnecessarily long for most patients. Mycophenolate is contraindicated in pregnancy and should be stopped well before conception and switched to a pregnancy-compatible agent; it should not be started immediately before conception.

Why the others are less appropriate:
- No minimum interval: Early pregnancy risks are higher and a period of stability is generally advised.
- Avoid calcineurin inhibitors: These are used in pregnancy with monitoring if needed; they are not absolute contraindications.
- Delay 5 years: Unnecessary except in exceptional clinical scenarios.
- Switch to mycophenolate immediately before conception: MMF is teratogenic and should be stopped well before conception, not started.

10 / 10

Which statement about aspirin prophylaxis to reduce the risk of pre-eclampsia is correct for women with chronic kidney disease planning pregnancy?

Low-dose aspirin is contraindicated in CKD because of bleeding risk

Low-dose aspirin should be started in early pregnancy (around 12 weeks) for women with CKD and continued until birth

Aspirin should only be given if proteinuria exceeds nephrotic range

Aspirin is only beneficial if given after 28 weeks' gestation

High-dose aspirin (≥300 mg daily) is recommended for pre-eclampsia prevention in CKD

Offer low-dose aspirin from approximately 12 weeks until birth to pregnant women with CKD who are at increased risk of pre-eclampsia, unless contraindicated.

Women with CKD are at increased risk of pre-eclampsia and are generally offered low-dose aspirin prophylaxis from around 12 weeks of pregnancy until birth, unless contraindicated, according to guideline-based practice. Low-dose aspirin is not contraindicated solely because of CKD. It is not restricted to women with nephrotic-range proteinuria, starting after 28 weeks is too late for optimal prophylaxis, and high-dose aspirin is not recommended for this purpose.

Your score is

The average score is 0%

By Wordpress Quiz plugin

Board-level postgraduate nephrology self-assessment.

Complete all 10 single-best-answer questions to receive detailed clinical explanations on the results page.

Hypertension and Secondary Hypertension

Ten board-level single-best-answer clinical vignettes on diagnosis, investigation, acute and chronic management, complications and targeted therapy for secondary causes of hypertension.

1 / 10

A 54-year-old man attends clinic with clinic blood pressures of 160–170/95–105 mmHg on three separate visits despite being prescribed an ACE inhibitor, a calcium-channel blocker and a thiazide-like diuretic at maximal tolerated doses. He reports occasional missed doses. Which of the following is the most appropriate next step to confirm whether this is resistant hypertension before further investigation for secondary causes?

Add spironolactone and reassess in 4 weeks

Proceed to plasma renin and aldosterone measurement

Arrange an urgent CT renal angiography for renal artery stenosis

Obtain ambulatory blood pressure monitoring (24-hour ABPM) and assess adherence

Start clonidine and evaluate response

Confirm true resistant hypertension with out-of-office BP measurement (ABPM) and assess adherence before further investigation or intensification.

Correct answer: Obtain ambulatory blood pressure monitoring (24-hour ABPM) and assess adherence. True resistant hypertension should be confirmed by demonstrating persistently elevated out-of-office blood pressure and ensuring adequate adherence and dosing. White-coat effect and non-adherence are common causes of apparent resistant hypertension. ABPM (or home BP monitoring) provides objective measurement outside the clinic; concurrently adherence should be optimised (pill counts, pharmacy records, direct questioning).

Why the others are less appropriate:
- Adding spironolactone (A) before confirming true resistance risks unnecessary drug exposure and side effects; spironolactone is often effective for true resistant hypertension but should be used after confirming resistance and evaluating secondary causes.
- Proceeding immediately to renin/aldosterone testing (B) or CT angiography (C) assumes a secondary cause without first confirming persistent out-of-office hypertension and adherence; this leads to unnecessary investigations and misinterpretation (medications can confound tests).
- Starting clonidine (E) is not appropriate to diagnose resistant hypertension and has adverse effects; it is not recommended as a next diagnostic or first-line intervention in this context.

In summary, before embarking on further investigations or adding fourth-line agents, confirm uncontrolled hypertension with ABPM and assess adherence.

2 / 10

A 48-year-old woman with hypertension is referred for evaluation of primary aldosteronism. Her current medications are ramipril, bendroflumethiazide and spironolactone. Her clinician asks whether a plasma aldosterone–renin ratio (ARR) can be reliably measured while she remains on these drugs. What is the most appropriate immediate action?

Stop spironolactone for at least 4–6 weeks and switch to antihypertensives that have minimal effect on the ARR before testing

Measure ARR now; spironolactone does not affect the ratio significantly

Proceed directly to adrenal CT to look for an adenoma without biochemical testing

Replace spironolactone with high-dose amlodipine and measure ARR the next day

Start adrenal vein sampling immediately

Confirmatory ARR testing requires withdrawal of mineralocorticoid receptor antagonists (washout weeks) and substitution with agents that minimally affect renin/aldosterone.

Correct answer: Stop spironolactone for at least 4–6 weeks and switch to antihypertensives that have minimal effect on the ARR before testing. Mineralocorticoid receptor antagonists (spironolactone, eplerenone) markedly alter aldosterone and renin levels, rendering the ARR unreliable; they should be withdrawn for several weeks before ARR screening. If blood pressure needs treatment during washout, use agents that minimally affect ARR (e.g., verapamil, hydralazine, doxazosin, amlodipine), with close monitoring.

Why the others are less appropriate:
- Measuring ARR now (B) risks false-negative or false-positive results due to drug interference and is not reliable.
- Proceeding directly to CT (C) without biochemical confirmation is inappropriate because adrenal imaging alone cannot distinguish unilateral from bilateral disease and adenomas/incidentalomas are common; biochemical confirmation is required before imaging.
- Replacing spironolactone with high-dose amlodipine and measuring ARR the next day (D) is inadequate: the washout period for spironolactone is several weeks because of lasting effects on the aldosterone pathway.
- Adrenal vein sampling (E) is an invasive procedure used to lateralise disease after biochemical confirmation; it is not appropriate without prior reliable biochemical screening.

Thus the first step is cessation of interfering drugs with safe alternative antihypertensives and then ARR testing.

3 / 10

A 62-year-old man with poorly controlled hypertension and a unilateral 2.5 cm atrophic right kidney on ultrasound is suspected to have atherosclerotic renal-artery stenosis. His eGFR is 55 mL/min/1.73 m2 and serum creatinine is 125 µmol/L. He is claustrophobic but willing to have contrast studies. Which non-invasive imaging modality is the most appropriate next test to establish the diagnosis?

Ultrasound renal artery Doppler study

Contrast-enhanced MR angiography (Gadolinium-enhanced MRA)

Renal radionuclide scan (ACE inhibitor renography)

Computed tomography renal angiography (CTRA) with iodinated contrast

Immediate invasive digital subtraction angiography without prior non-invasive imaging

Use non-invasive imaging such as CT renal angiography to evaluate suspected renovascular disease; reserve invasive angiography for planned intervention or inconclusive non-invasive studies.

CT renal angiography is an appropriate non-invasive next test in a patient with a high pre-test probability of atherosclerotic renal-artery stenosis, reasonable kidney function, and difficulty tolerating MRI. Duplex ultrasound is a reasonable alternative where expertise is available. Invasive digital subtraction angiography is generally reserved for situations in which revascularisation is planned or non-invasive imaging is inconclusive, because it carries procedural and contrast risks.

4 / 10

A 39-year-old woman presents with episodic headaches, palpitations and sweating; clinic blood pressure is 180/110 mmHg. An abdominal CT shows a 3 cm left adrenal mass. Which of the following is the most appropriate initial biochemical test to confirm a suspected pheochromocytoma?

Plasma aldosterone and renin activity

Plasma-free metanephrines (or urinary fractionated metanephrines)

Serum cortisol measured at 0900 h

Plasma free normetanephrine only (not metanephrine)

Immediate adrenal biopsy to obtain histology

Use plasma free metanephrines (or urinary fractionated metanephrines) to biochemically confirm pheochromocytoma before any invasive procedures or surgery.

Correct answer: Plasma-free metanephrines (or urinary fractionated metanephrines). Biochemical confirmation of pheochromocytoma is best achieved by measurement of plasma free metanephrines or 24-hour urinary fractionated metanephrines; these tests have high sensitivity. If results are equivocal, clonidine suppression or repeat testing may be used. Appropriate biochemical confirmation is required before any intervention.

Why the others are less appropriate:
- Plasma aldosterone and renin (A) assess mineralocorticoid excess, not catecholamine-secreting tumours.
- Serum cortisol at 0900 h (C) screens for Cushing's syndrome, not pheochromocytoma.
- Measuring plasma free normetanephrine only (D) is incomplete—both metanephrine and normetanephrine should be measured because tumours can produce one or both metabolites.
- Adrenal biopsy (E) is contraindicated prior to biochemical confirmation because biopsy can precipitate a hypertensive crisis and is not useful to diagnose functional adrenal tumours; biopsy of an adrenal mass is only considered in selected cases when metastasis is suspected and biochemical causes have been excluded.

After biochemical confirmation, localisation imaging and perioperative alpha- then beta-blockade are required for safe management.

5 / 10

A 46-year-old man presents with sudden visual disturbance and severe headache. Examination shows papilloedema and BP 240/140 mmHg. Blood tests reveal microangiopathic haemolytic anaemia (schistocytes, elevated LDH) and rising creatinine. Which of the following is the most appropriate immediate management step?

Start plasma exchange for presumed thrombotic thrombocytopenic purpura (TTP)

Give rapid oral nifedipine 10 mg to quickly lower BP

Begin controlled intravenous BP reduction with a titratable agent (e.g., IV labetalol or nitroprusside)

Administer high-dose corticosteroids and refer for renal biopsy

Immediate initiation of haemodialysis without addressing BP

In hypertensive emergencies with malignant features and TMA, controlled parenteral BP lowering with titratable agents is the priority; treat underlying cause after stabilisation.

Correct answer: Begin controlled intravenous BP reduction with a titratable agent (e.g., IV labetalol or nitroprusside). This presentation is consistent with malignant hypertensive emergency with microangiopathic haemolysis (hypertensive thrombotic microangiopathy). The priority is controlled reduction of mean arterial pressure using intravenous, titratable antihypertensives to limit further end-organ damage. Rapid but controlled lowering (not precipitous) is essential.

Why the others are less appropriate:
- Plasma exchange (A) is the treatment for TTP; although the lab picture can be similar, in hypertensive emergency the first step is BP control. TTP should be considered if features persist despite BP control or ADAMTS13 testing supports it.
- Rapid oral nifedipine (B) is not recommended—immediate large drops in BP with sublingual or rapid oral agents can cause ischaemia; IV titratable agents are preferred in hypertensive emergencies.
- High-dose corticosteroids and renal biopsy (D) are not initial steps and carry risk; biopsy is contraindicated acutely until BP is controlled and the diagnosis is clearer.
- Immediate haemodialysis (E) without addressing severe hypertension is inappropriate unless there is refractory uraemia or hyperkalaemia; BP control is the immediate priority.

After stabilisation, evaluate for secondary causes and manage complications; specialist input from nephrology and ophthalmology is required.

6 / 10

A 71-year-old woman with long-standing hypertension and bilateral atherosclerotic disease is started on an ACE inhibitor. Her baseline creatinine was 120 µmol/L; after one week it has risen to 175 µmol/L (≈46% increase) and she has oliguria. Which is the most appropriate immediate action?

Stop the ACE inhibitor and arrange urgent renal imaging to assess for bilateral renal-artery stenosis

Continue the ACE inhibitor as renal-function rise <50% is acceptable and monitor

Add a loop diuretic to enhance renal perfusion and continue ACE inhibitor

Increase the ACE inhibitor dose to overcome pharmacodynamic tolerance

Arrange urgent dialysis and keep ACE inhibitor unchanged

A significant rise in creatinine after ACE inhibitor initiation (commonly >30%) warrants stopping the drug and investigating for renal-artery stenosis before rechallenge.

Correct answer: Stop the ACE inhibitor and arrange urgent renal imaging to assess for bilateral renal-artery stenosis. An acute rise in creatinine ≥30% after starting an ACE inhibitor suggests haemodynamically significant renal-artery stenosis (especially if bilateral or single functioning kidney) and ACEi should be stopped. Bilateral RAS can precipitate acute kidney injury due to dependence on angiotensin II–mediated efferent arteriolar constriction; cessation may permit recovery and further imaging/investigation is indicated.

Why the others are less appropriate:
- Continuing the ACE inhibitor (B) risks progression to severe AKI; the threshold for stopping is typically a creatinine rise >30% (some clinicians use >30–50%).
- Adding a loop diuretic (C) is unlikely to correct the cause and may worsen renal perfusion/hypovolaemia.
- Increasing ACE inhibitor dose (D) is contraindicated in the context of creatinine rise and oliguria.
- Arranging dialysis (E) may become necessary if uraemia, fluid overload or severe electrolyte disturbance occurs, but immediate management is to stop the offending agent and investigate reversible causes; dialysis is not the first reflex.

After stopping the ACE inhibitor, reassess renal function and consider imaging for RAS if creatinine remains abnormal or hypertension is resistant; multidisciplinary discussion is required for revascularisation decisions.

7 / 10

A 29-year-old man is evaluated for longstanding hypertension. On examination he has a blood pressure of 160/90 mmHg in the right arm and 120/70 mmHg in the left arm, a weak femoral pulse and delayed femoral-to-radial pulse transmission. Which of the following is the most likely diagnosis and the best next diagnostic test?

Takayasu arteritis; schedule an FDG-PET scan to assess large-vessel inflammation

Aortic coarctation; perform CT aortography to define the anatomy for possible repair

Subclavian steal syndrome; do a duplex ultrasound of vertebral arteries

Horner's syndrome due to sympathetic chain lesion; arrange MRI of the cervical spine

Pulmonary hypertension causing differential arm pressures; perform echocardiography

In adults with brachial–femoral delay and upper limb hypertension, suspect aortic coarctation and define anatomy with CT aortography for planning repair.

Correct answer: Aortic coarctation; perform CT aortography to define the anatomy for possible repair. The clinical triad of upper limb hypertension, brachial–femoral delay and differential blood pressures with weak femoral pulses is classical for coarctation of the aorta. In adults, CT aortography (or MR angiography if renal function permits) gives high-resolution anatomy to plan surgical or endovascular repair (stenting) and assess collateral circulation.

Why the others are less appropriate:
- Takayasu arteritis (A) can cause limb blood-pressure differences but typically affects young women and is an inflammatory large-vessel vasculitis; investigations may include imaging for vessel inflammation, but the described classical coarctation features (femoral delay) point to congenital coarctation.
- Subclavian steal (C) causes arm claudication and vertebrobasilar symptoms with reversal of vertebral flow, usually produces arm BP asymmetry but not the brachial–femoral delay or weak femoral pulses characteristic of coarctation.
- Horner's syndrome (D) causes ptosis, miosis and anhidrosis, unrelated to limb BP differences.
- Pulmonary hypertension (E) would not cause the peripheral findings described.

Appropriate referral to cardiothoracic/vascular services is required after imaging for definitive management.

8 / 10

A 45-year-old woman with features of Cushing's syndrome (central obesity, proximal myopathy, easy bruising) is hypertensive. Which initial screening test is most appropriate to detect endogenous cortisol excess as the cause of her hypertension?

Random plasma cortisol measured at midday

Plasma ACTH alone

1 mg overnight dexamethasone suppression test (overnight DST) or late-night salivary cortisol

Serum aldosterone and renin ratio

Plasma free metanephrines

Screen suspected Cushing's syndrome with overnight dexamethasone suppression or late-night salivary cortisol before further endocrine localisation.

Correct answer: 1 mg overnight dexamethasone suppression test (overnight DST) or late-night salivary cortisol. The recommended first-line screening tests for Cushing's syndrome are either late-night salivary cortisol (sensitive for loss of diurnal variation) or the 1 mg overnight dexamethasone suppression test; both are validated screening tools for endogenous hypercortisolism. Choice depends on clinical context and local availability.

Why the others are less appropriate:
- Random midday cortisol (A) is not reliable for screening because cortisol has diurnal variation.
- Plasma ACTH alone (B) is used after biochemical confirmation of hypercortisolism to distinguish ACTH-dependent from ACTH-independent causes; it is not a screening test.
- Serum aldosterone and renin (D) screen for primary aldosteronism, not Cushing's.
- Plasma free metanephrines (E) screen for pheochromocytoma, not cortisol excess.

Once hypercortisolism is biochemically confirmed, further testing (e.g., 24-hour urinary free cortisol, low-dose dexamethasone suppression, imaging, and ACTH measurement) is required to subtype and plan management.

9 / 10

A 22-year-old man has severe hypertension with hypokalaemia. Biochemistry shows suppressed plasma renin activity and low aldosterone. Family history reveals hypertension in his father since young adulthood. Which of the following therapeutic choices is the most appropriate initial targeted treatment?

Spironolactone (mineralocorticoid receptor antagonist)

Start an ACE inhibitor (e.g., ramipril)

Begin amiloride (an ENaC blocker)

High-dose thiazide diuretic

Replace with fludrocortisone

Suspect Liddle's syndrome when hypertension with hypokalaemia has low renin and low aldosterone; treat specifically with amiloride or triamterene.

Correct answer: Begin amiloride (an ENaC blocker). The clinical picture (early-onset hypertension, hypokalaemia, low renin and low aldosterone) strongly suggests Liddle's syndrome, an activating mutation of the epithelial sodium channel (ENaC). The appropriate specific therapy is an ENaC blocker such as amiloride (or triamterene). These agents directly inhibit the mutated channel and correct sodium retention and hypokalaemia.

Why the others are less appropriate:
- Spironolactone (A) acts at the mineralocorticoid receptor and is ineffective in Liddle's syndrome because aldosterone levels are low and the defect is downstream at the channel.
- ACE inhibitors (B) reduce angiotensin II and aldosterone but are inadequate as targeted therapy for genetic ENaC activation; they may reduce BP modestly but do not correct the channel defect.
- High-dose thiazide diuretics (D) may worsen hypokalaemia and are not specific treatment.
- Fludrocortisone (E) is a mineralocorticoid agonist and would worsen hypertension and hypokalaemia.

Genetic testing and family screening should be considered once clinical suspicion is high; ENaC blockade is the specific treatment.

10 / 10

A 31-year-old pregnant woman at 28 weeks gestation is diagnosed with chronic hypertension on treatment with lisinopril preconception. Which of the following statements about antihypertensive therapy in pregnancy is most appropriate?

Continue lisinopril throughout pregnancy as ACE inhibitors are safe in pregnancy

Switch lisinopril to labetalol or nifedipine, as ACE inhibitors are contraindicated in pregnancy

Replace lisinopril with an angiotensin II receptor blocker (ARB), which is safer in pregnancy

Start spironolactone as first-line in pregnancy for resistant hypertension

Use atenolol as the drug of choice in pregnancy because it reduces maternal heart rate

ACE inhibitors and ARBs are contraindicated in pregnancy; switch to agents with established safety such as labetalol or nifedipine.

Correct answer: Switch lisinopril to labetalol or nifedipine, as ACE inhibitors are contraindicated in pregnancy. ACE inhibitors (and ARBs) are teratogenic and associated with foetal renal dysplasia and oligohydramnios; they should be stopped preconception or as soon as pregnancy is recognised. First-line antihypertensives in pregnancy include labetalol, nifedipine (modified-release), and methyldopa depending on the clinical situation and local guidance.

Why the others are less appropriate:
- Continuing lisinopril (A) risks serious foetal adverse effects and is contraindicated.
- Replacing with an ARB (C) is also contraindicated—ARBs have similar teratogenic risks.
- Spironolactone (D) is generally avoided in pregnancy due to anti-androgenic effects and lack of safety data; it is not first-line for resistant hypertension in pregnancy.
- Atenolol (E) is associated with fetal growth restriction when used in pregnancy and is not the preferred agent; labetalol and nifedipine are preferred.

Management should involve obstetric and hypertension specialists, with drug changes ideally made before conception when possible.

Your score is

The average score is 0%

By Wordpress Quiz plugin

Board-level postgraduate nephrology self-assessment.

Complete all 10 single-best-answer questions to receive detailed clinical explanations on the results page.

Acid-Base Disorders

Ten board-style single-best-answer questions testing advanced interpretation, diagnosis and management of acid–base disturbances across a range of clinical scenarios relevant to nephrology and acute medicine.

1 / 10

An ICU patient has arterial blood gas: pH 7.20, PaCO2 40 mmHg, HCO3- 12 mmol/L. Which is the most appropriate interpretation?

Acute metabolic acidosis with appropriate respiratory compensation

Primary metabolic acidosis with superimposed acute respiratory acidosis (mixed disorder)

Pure respiratory acidosis (acute) with metabolic compensation

Metabolic alkalosis with hypoventilatory compensation

Normal acid–base status for the measured PaCO2 and HCO3-

Use Winter's formula (expected PaCO2 ≈ 1.5×HCO3- + 8 ±2) to detect a mixed respiratory disorder superimposed on metabolic acidosis.

This ABG shows primary metabolic acidosis (low HCO3- and acid pH). Expected respiratory compensation for metabolic acidosis can be estimated by Winter's formula: expected PaCO2 ≈ 1.5 × [HCO3-] + 8 ± 2. For HCO3- = 12 mmol/L, expected PaCO2 ≈ 1.5×12 + 8 = 26 ± 2 mmHg. The measured PaCO2 is 40 mmHg, markedly higher than expected, indicating inadequate respiratory compensation consistent with a superimposed respiratory acidosis (i.e. mixed metabolic and respiratory acidosis). Option A is incorrect because the PaCO2 is not adequately reduced. Option C is wrong since primary respiratory acidosis would have elevated PaCO2 as the primary disturbance and compensatory HCO3- rise; here HCO3- is low. Option D is incorrect because the HCO3- is low (acidosis), not high. Option E is false because the measured PaCO2 is far from the expected compensatory value.

2 / 10

A patient has serum Na+ 140 mmol/L, Cl- 80 mmol/L, HCO3- 10 mmol/L. Calculate the anion gap and interpret the delta ratio. Which is the best conclusion?

Normal anion gap metabolic acidosis alone

High anion gap metabolic acidosis with an additional normal anion gap metabolic acidosis

High anion gap metabolic acidosis without additional disorders (pure high AG metabolic acidosis)

High anion gap metabolic acidosis with a coexisting metabolic alkalosis or pre-existing elevated bicarbonate

Primary respiratory alkalosis with compensatory metabolic acidosis

Use the delta ratio (ΔAG/ΔHCO3-) to detect mixed metabolic acid–base disorders: >2 suggests additional metabolic alkalosis or pre-existing raised bicarbonate.

Anion gap (AG) = Na+ − (Cl- + HCO3-) = 140 − (80 + 10) = 50 mmol/L → markedly raised (normal ~8–14 depending on lab). Delta AG = AG − normal AG (use ~12) ≈ 50 − 12 = 38. Delta HCO3- = normal HCO3- (24) − measured HCO3- (10) = 14. Delta ratio = 38 / 14 ≈ 2.7. A delta ratio >2 suggests that the increase in AG is disproportionately large relative to the fall in HCO3-, implying a concurrent metabolic alkalosis or a pre-existing elevated bicarbonate state (e.g. chronic metabolic alkalosis) that blunts the fall in HCO3-. Option A is wrong (AG is high). Option B (combined high AG + normal AG acidosis) corresponds to delta ratio ~0.8–1, not >2. Option C would have delta ratio ~1–2. Option E is unrelated. Therefore the best conclusion is a high AG metabolic acidosis with coexisting metabolic alkalosis or pre-existing raised bicarbonate.

3 / 10

A long-standing COPD patient has an arterial blood gas while clinically stable: pH 7.36, PaCO2 68 mmHg, HCO3- 38 mmol/L. What is the most accurate interpretation?

Chronic respiratory acidosis with metabolic compensation (compensated chronic respiratory acidosis)

Acute respiratory acidosis without compensation

Primary metabolic acidosis with respiratory compensation

Mixed metabolic alkalosis and respiratory acidosis

Primary respiratory alkalosis with metabolic compensation

In chronic respiratory acidosis (e.g. COPD), pH may be near normal due to renal bicarbonate retention; distinguish acute vs chronic by the degree of HCO3- rise relative to PaCO2.

The pH is near normal despite markedly elevated PaCO2 and elevated HCO3-, consistent with chronic respiratory acidosis with renal metabolic compensation. In chronic respiratory acidosis, renal retention of HCO3- increases (~3.5–4 mmol/L for each 10 mmHg increase in PaCO2 after chronicity) so a PaCO2 of 68 mmHg (≈28 mmHg above normal 40) would predict a substantial HCO3- rise, as seen. Option B is wrong because acute respiratory acidosis would have little HCO3- compensation and more pronounced acidemia. Option C is incorrect because HCO3- is elevated, not low. Option D is unlikely: metabolic alkalosis would cause elevated HCO3- but would not explain the very high PaCO2 unless hypoventilation coexisted; clinical context of stable COPD supports chronic compensation. Option E is the opposite direction.

4 / 10

A patient presents with fatigue and a non-anion gap metabolic acidosis. Labs: serum K+ 2.9 mmol/L, serum HCO3- 16 mmol/L, urine pH 6.0. Which diagnosis best fits these results?

Proximal (type 2) renal tubular acidosis

Hyperkalaemic (type 4) renal tubular acidosis

Organic acidosis from diabetic ketoacidosis

Metabolic acidosis due to diarrhoea

Distal (type 1) renal tubular acidosis (impaired urinary acidification)

A normal AG metabolic acidosis with hypokalaemia and urine pH >5.5 suggests distal (type 1) RTA due to impaired urinary acidification.

Features: normal anion gap metabolic acidosis with hypokalaemia and an inappropriately high urine pH (>5.5) despite systemic acidaemia suggests impaired distal urinary acidification — distal (type 1) RTA. Proximal RTA (type 2) typically presents with bicarbonate wasting, hypokalaemia, but once HCO3- is depleted the urine can be acidified (urine pH <5.5), so urine pH of 6.0 is less consistent with proximal RTA. Type 4 RTA is characterised by hyperkalaemia due to hypoaldosteronism; the patient is hypokalaemic, so option 2 is wrong. DKA (option 3) gives high anion gap metabolic acidosis and hyperglycaemia. Diarrhoea (option 4) causes normal AG metabolic acidosis with low urinary ammonium chloride excretion and typically low urine pH (acidic), and history would point to GI losses. Therefore distal (type 1) RTA is the best fit.

5 / 10

After a large-volume infusion of 0.9% saline during surgery the patient develops metabolic acidosis with low bicarbonate and normal anion gap; chloride is increased. Which management step is most appropriate?

Administer intravenous sodium bicarbonate immediately

Start a loop diuretic to increase bicarbonate reabsorption

Stop further 0.9% saline; change to a balanced crystalloid and reassess

Give 100% oxygen and hyperventilate to reduce PaCO2

Begin high-dose mineralocorticoid therapy

Hyperchloraemic (normal AG) metabolic acidosis after saline infusion is managed by stopping chloride-rich fluid and using balanced crystalloids; bicarbonate therapy is reserved for severe/acutely dangerous acidosis.

Large-volume 0.9% saline can cause a dilutional (hyperchloraemic) normal anion gap metabolic acidosis by increasing serum chloride and reducing strong ion difference. The first-line response is to stop the offending chloride-rich fluid and, if ongoing fluid resuscitation is needed, switch to a balanced crystalloid (e.g. Plasma-Lyte or similar) which has lower chloride and is less acidifying; reassess acid–base. Routine immediate intravenous sodium bicarbonate is usually unnecessary for moderate hyperchloraemic acidosis and may cause volume/Na overload and overshoot alkalosis. Loop diuretics (option B) are not an appropriate immediate treatment in a volume-resuscitated postoperative patient and may worsen electrolyte derangements. Hyperventilation (option D) treats respiratory alkalosis, not a metabolic acidosis cause. Mineralocorticoid therapy (option E) is not indicated.

6 / 10

A patient with recurrent vomiting has pH 7.60, HCO3- 44 mmol/L, PaCO2 50 mmHg and is symptomatic with light-headedness but stable circulation. Which is the most appropriate immediate management?

Administer intravenous 8.4% sodium bicarbonate to correct alkalosis

Give isotonic (0.9%) saline with potassium repletion

Start acetazolamide without addressing volume status

Intubate and hyperventilate to reduce PaCO2

Administer intravenous calcium gluconate to stabilise membranes

For vomiting-induced metabolic alkalosis the initial treatment is volume repletion with isotonic saline and potassium replacement; acetazolamide or acid infusion is reserved for refractory or severe cases after addressing volume and K+.

This is metabolic alkalosis due to vomiting with contraction alkalosis and hypokalaemia likely. First-line management is to correct the precipitant: restore intravascular volume with isotonic saline and replace potassium (as K+ repletion helps correct alkalosis by allowing renal H+ secretion). Option A (giving bicarbonate) would worsen the alkalosis. Option C (acetazolamide) can be useful for chloride-resistant metabolic alkalosis (often with fluid overload), but it is not appropriate before volume and potassium are corrected and is contraindicated if intravascular depletion exists. Option D (intubation/hyperventilation) would worsen alkalosis by reducing PaCO2 (this patient already has elevated PaCO2 as compensation). Option E (IV calcium) is for severe hypocalcaemic signs, not a routine treatment for metabolic alkalosis per se.

7 / 10

A dialysis patient treated with a high-bicarbonate dialysate develops perioral twitching and carpopedal spasm shortly after dialysis. Which is the most likely immediate cause and best immediate treatment?

Hypocalcaemia due to chelation by citrate in the dialysate — give IV calcium gluconate

Severe hypokalaemia from intracellular shift — give IV potassium chloride immediately

Metabolic alkalosis causing decreased ionised calcium — give IV calcium gluconate

Uraemic tetany unrelated to electrolyte shifts — escalate dialysis

Hypernatremia-induced neuromuscular irritability — give hypotonic fluid

Rapid reversal of acidosis during dialysis can cause metabolic alkalosis and decreased ionised calcium; treat symptomatic hypocalcaemia with IV calcium immediately.

Rapid correction of acidosis during haemodialysis using high-bicarbonate dialysate can cause alkalosis and increase protein binding of calcium, lowering ionised (active) calcium and precipitating signs of hypocalcaemia (tetany, twitching). The immediate treatment is IV calcium (e.g. calcium gluconate) to relieve symptoms and stabilise neuromuscular excitability. Option A incorrectly attributes citrate chelation—citrate is used in regional anticoagulation, not typical dialysate; immediate management in either case would still be IV calcium, but the scenario describes post-dialysis alkalosis rather than citrate toxicity. Option B (hypokalaemia) can occur but neuromuscular irritability with tetany is more typical of low ionised calcium; empiric IV K+ without checking could be harmful. Option D is incorrect—uriaemic tetany is less likely immediately post-dialysis and would not be managed by escalating dialysis. Option E is not relevant.

8 / 10

A patient presents with diabetic ketoacidosis (DKA). Initial labs: pH 7.12, HCO3- 8 mmol/L, serum K+ 5.6 mmol/L. According to standard acute management principles, what is the best next step regarding insulin and potassium?

Start intravenous insulin infusion now and monitor serum potassium closely

Hold insulin and administer large-volume potassium replacement until K+ <4.0 mmol/L

Start insulin with concurrent aggressive potassium replacement irrespective of level

Administer insulin bolus only (no infusion) to avoid rapid potassium shifts

Give oral potassium supplements and delay insulin therapy

In DKA start insulin promptly if serum K+ is adequate, and monitor/replace potassium as needed; if K+ is very low (e.g. <3.3 mmol/L) potassium should be corrected before starting insulin.

In DKA total body potassium is depleted despite normal or high serum K+. With a serum K+ of 5.6 mmol/L, it is appropriate to start insulin to treat the ketoacidosis while monitoring potassium closely; insulin will drive potassium intracellularly and serum K+ will fall, necessitating replacement as it declines. Holding insulin until potassium is much lower (option B) is only required when serum K+ is already low (commonly cited threshold is <3.3 mmol/L) because treating with insulin would provoke severe hypokalaemia; that threshold-based management is reflected in guidelines. Routine aggressive potassium replacement irrespective of level (option C) risks hyperkalaemia. Insulin bolus only (option D) is not standard; continuous insulin infusion is preferred. Oral potassium (option E) is inadequate in the acute setting. Hence option A is correct.

9 / 10

A patient has measured anion gap 12 mmol/L and serum albumin 20 g/L (normal ~40 g/L). You suspect occult high anion gap metabolic acidosis. How do you correct the anion gap for hypoalbuminaemia and which statement is true?

No correction is necessary; albumin does not affect the anion gap

Subtract 2.5 mmol/L from the measured AG for every 10 g/L fall in albumin

Add approximately 5 mmol/L to the measured AG because albumin is low (AG corrected ≈ 17 mmol/L) which supports a hidden high anion gap acidosis

Multiply the measured AG by (40/albumin) to correct for albumin

Corrected AG cannot be estimated and is clinically useless

Correct the anion gap for hypoalbuminaemia (add ≈2.5 mmol/L per 10 g/L drop in albumin) because low albumin can mask a high anion gap metabolic acidosis.

Albumin is a major unmeasured anion; hypoalbuminaemia lowers the measured anion gap and may mask a high anion gap metabolic acidosis. A commonly used correction is to add about 2.5 mmol/L to the AG for every 10 g/L decrease in albumin from normal (~40 g/L). Here albumin is 20 g/L (a fall of 20 g/L), so add ≈2.5×2 = 5 mmol/L: corrected AG = 12 + 5 = 17 mmol/L, which suggests a high anion gap metabolic acidosis. Option A is false because albumin affects AG. Option B has the direction reversed (it says subtract). Option D is not the standard correction method. Option E is incorrect—corrected AG is clinically useful to unmask hidden high AG acidosis.

10 / 10

Using the Stewart (strong ion) approach, which single change best explains a normal anion gap hyperchloraemic metabolic acidosis after large-volume 0.9% saline infusion?

An increase in arterial PaCO2 leading to respiratory acidosis

A significant decrease in serum albumin reducing weak acid concentration

An increase in unmeasured anions (e.g. lactate) increasing the anion gap

A rise in serum sodium with proportionate bicarbonate increase

A fall in the strong ion difference (SID) due to increased serum chloride

In the Stewart framework hyperchloraemic (normal AG) metabolic acidosis after saline is due to a reduced strong ion difference from increased serum chloride.

The Stewart approach emphasises that plasma pH is determined by three independent variables: PaCO2, strong ion difference (SID) and total weak acid concentration (predominantly albumin). Infusion of large volumes of 0.9% saline increases serum chloride disproportionately relative to sodium, reducing SID (Na+ − Cl-), which drives metabolic acidosis without increasing the anion gap (i.e. normal AG hyperchloraemic acidosis). Option E correctly identifies the mechanism. Option A describes respiratory rather than metabolic disturbance. Option B (decreased albumin) would cause an alkalinising effect by reducing weak acids. Option C increases the anion gap (high AG acidosis), not the normal AG hyperchloraemic acidosis. Option D is incorrect physiologically.

Your score is

The average score is 0%

By Wordpress Quiz plugin

Board-level postgraduate nephrology self-assessment.

Complete all 10 single-best-answer questions to receive detailed clinical explanations on the results page.

Calcium, Phosphate, PTH, and Kidney Bone Disease

Board-level MCQs covering diagnosis, interpretation, acute and chronic management, complications and investigations in disorders of mineral metabolism and renal bone disease (CKD-MBD).

1 / 10

A 62-year-old man with end-stage kidney disease (on haemodialysis) attends the emergency unit with confusion, polyuria earlier in the day, constipation and a measured total serum calcium 3.6 mmol/L. He is oliguric, blood pressure 95/60 mmHg and has acute on chronic kidney failure with eGFR estimated at 8 ml/min. Which is the most appropriate immediate management?

Urgent haemodialysis using a low-calcium dialysate (with supportive measures)

Aggressive IV 0.9% saline hydration followed by IV furosemide

IV zoledronic acid (single dose)

IV hydrocortisone and oral calcitriol

Subcutaneous calcitonin alone

In severe symptomatic hypercalcaemia with inadequate renal function or oligo/anuria, urgent haemodialysis with a low-calcium dialysate is the preferred immediate intervention; other measures (hydration, bisphosphonates, calcitonin) are adjuncts or for different clinical contexts.

Urgent haemodialysis with a low-calcium dialysate is the most appropriate immediate therapy in a patient with severe, symptomatic hypercalcaemia who is oliguric with very poor kidney function. Dialysis rapidly lowers serum calcium and is indicated when conventional measures are likely to be ineffective or unsafe (for example volume loading in oliguric/volume-overloaded patients, or when renal clearance of drugs is inadequate).

Why the others are less appropriate:
- IV saline + furosemide is a first-line approach in many severe hypercalcaemia cases with preserved urine output, but the patient is oliguric and hypotensive so aggressive volume loading may be ineffective or harmful.
- IV zoledronic acid is effective for lowering calcium in the following days but is renally excreted and may be contraindicated or require dose adjustment in severe renal impairment; it is not an immediate rescue therapy.
- IV hydrocortisone is useful in vitamin D–mediated hypercalcaemia (e.g. granulomatous disease) but is not first-line for severe, uraemic hypercalcaemia.
- Calcitonin has a rapid but modest and transient effect and should be used as an adjunct for short-term reduction; it is inadequate as sole therapy in severe symptomatic cases with renal failure.

2 / 10

A 54-year-old man on maintenance haemodialysis has an iPTH of 720 pg/mL (local assay upper limit of normal 65 pg/mL), corrected calcium 2.18 mmol/L and phosphate 2.1 mmol/L. He reports pruritus and bone aches. What is the most appropriate next step in management?

Schedule urgent parathyroidectomy

Intensify phosphate control and review dialysis adequacy before specific PTH-lowering therapy

Start immediate high-dose oral active vitamin D (calcitriol)

Begin bisphosphonate therapy to reduce bone turnover

Ignore biochemical abnormality and repeat PTH in 6 months

In CKD with markedly elevated PTH, correct reversible factors (phosphate control, dialysis adequacy, calcium and vitamin D status) before proceeding to parathyroidectomy or other definitive therapies.

The first step in managing very high PTH in CKD is to identify and correct reversible contributors: hyperphosphataemia, hypocalcaemia, vitamin D deficiency, inadequate dialysis or medication non-adherence. In this patient phosphate is elevated and contributes to secondary hyperparathyroidism; intensifying phosphate control (dietary measures, phosphate binders, dialysis prescription) and ensuring dialysis adequacy are appropriate initial strategies. Parathyroidectomy is reserved for refractory severe hyperparathyroidism despite medical therapy, or for significant symptoms/complications unresponsive to medical measures.

Why the others are less appropriate:
- Urgent parathyroidectomy is premature without optimising modifiable factors and attempting medical therapy.
- Immediate high-dose calcitriol risks hypercalcaemia and should be considered only after assessing and addressing phosphate and calcium and with monitoring; also many centres prefer selective vitamin D receptor activators.
- Bisphosphonates are not indicated for high-turnover secondary hyperparathyroidism and are potentially harmful in severe CKD unless specific indications exist for osteoporosis, with caution.
- Repeating PTH in 6 months without intervening on correctable drivers is inappropriate given the marked elevation and symptoms.

3 / 10

A 58-year-old woman with end-stage renal disease on haemodialysis presents with extremely painful purpuric plaques that evolve to retiform necrosis on her thighs. She is on long-term warfarin and has hyperphosphataemia and a corrected calcium of 2.7 mmol/L. Skin biopsy confirms calcific small-vessel thrombosis. Which of the following interventions is most appropriate as part of initial management?

Increase dose of calcium-containing phosphate binders to lower phosphate

Urgent systemic corticosteroids and broad-spectrum antibiotics

Discontinue warfarin, optimise phosphate/calcium control and consider intravenous sodium thiosulfate with wound care

Immediate high-dose intravenous bisphosphonate therapy

Start low-molecular-weight heparin and continue warfarin until surgical debridement

Calciphylaxis requires urgent multidisciplinary care: stop vitamin K antagonists, correct phosphate/calcium balance (avoid calcium load), provide wound care and consider sodium thiosulfate as an adjunct.

This presentation is typical of calciphylaxis (calcific uremic arteriolopathy). Initial management should be multidisciplinary: discontinue vitamin K antagonists (e.g. warfarin) because they are associated with increased risk, optimise mineral metabolism (reduce phosphate and avoid calcium loading), aggressive wound care, pain control and consider sodium thiosulfate as an adjunctive therapy. Prompt correction of modifiable risk factors is essential.

Why the others are less appropriate:
- Increasing calcium-containing binders will increase calcium load and may worsen vascular calcification—contraindicated.
- Systemic corticosteroids are not standard therapy for calciphylaxis; antibiotics only if there is infection, but steroids are not first-line.
- Bisphosphonates are not established as initial therapy for calciphylaxis and may not be appropriate in advanced CKD.
- Continuing warfarin is harmful; switching anticoagulation should be individualised, but immediate continuation until surgery is not advised; low-molecular-weight heparin may also carry risk and dosing is complex in ESRD.

4 / 10

A 46-year-old man undergoes subtotal parathyroidectomy for severe secondary hyperparathyroidism. On the first postoperative night he becomes peripherally paraesthetic and tetanic. Serum ionised calcium is low. What is the most appropriate immediate treatment?

Oral calcium carbonate 1.25 g and outpatient follow-up

IV calcium gluconate bolus followed by a continuous IV calcium infusion with concomitant high-dose oral calcium and initiation of active vitamin D (calcitriol)

Single intramuscular injection of bisphosphonate to stabilise bone skeleton

IV magnesium sulphate and no calcium replacement

High-dose oral phosphate to redistribute calcium into bone

Post-parathyroidectomy hungry bone syndrome causes severe symptomatic hypocalcaemia that requires rapid IV calcium replacement, ongoing infusion as needed, and concurrent oral calcium with active vitamin D.

Hungry bone syndrome after parathyroidectomy results from rapid influx of calcium into bone and presents with symptomatic hypocalcaemia. Immediate management is intravenous calcium replacement: an initial bolus of IV calcium gluconate followed by a continuous infusion often required, together with high-dose oral elemental calcium and active vitamin D (calcitriol) to facilitate calcium absorption and reduce ongoing bone uptake. Monitoring and adjustment are essential.

Why the others are less appropriate:
- Oral calcium alone is too slow and insufficient for symptomatic postoperative hypocalcaemia with neuromuscular signs.
- Bisphosphonates are contraindicated in acute hypocalcaemia as they further suppress bone resorption and will worsen hypocalcaemia.
- IV magnesium is used if hypomagnesaemia contributes but is not the primary therapy for hypocalcaemic tetany unless magnesium is low.
- High-dose oral phosphate would lower calcium further by precipitating calcium-phosphate; it is dangerous and not indicated.

5 / 10

A 39-year-old woman with a functioning renal transplant 18 months ago has persistent hypercalcaemia (corrected calcium 2.75 mmol/L) with elevated PTH (intact PTH 180 pg/mL). She has recurrent nephrolithiasis and reduced bone mineral density. Which is the most appropriate definitive management?

Conservative management and repeat assessment in 12 months

Begin high-dose oral phosphate supplements to lower serum calcium

Parathyroidectomy (surgical removal of hyperfunctioning parathyroid tissue)

Start long-term high-dose calcitriol to suppress PTH

Start monthly IV zoledronic acid to treat hypercalcaemia

In persistent symptomatic or complication-causing tertiary hyperparathyroidism after renal transplantation, parathyroidectomy is the definitive therapy to correct autonomous hypersecretion.

This patient likely has tertiary hyperparathyroidism after transplantation characterised by autonomous parathyroid hypersecretion with hypercalcaemia and end-organ complications (stones, bone loss). Definitive therapy for symptomatic or complication-associated persistent tertiary hyperparathyroidism is usually parathyroidectomy. Surgical removal of hyperfunctioning tissue has the highest chance of cure.

Why the others are less appropriate:
- Conservative observation is inappropriate with complications (stones, low BMD) and persistent hypercalcaemia.
- Oral phosphate is not a recommended long-term strategy for tertiary hyperparathyroidism and can cause GI side effects and soft-tissue calcification.
- High-dose calcitriol may worsen hypercalcaemia and is not appropriate where hypercalcaemia is established from autonomous parathyroid secretion.
- IV bisphosphonates treat hypercalcaemia temporarily and address bone resorption, but they are not a definitive therapy for autonomous parathyroid tissue; they also carry caution in renal impairment and transplant patients.

6 / 10

A laboratory reports total serum calcium 2.20 mmol/L and serum albumin 20 g/L in an outpatient with CKD stage 3. Using the usual albumin-correction rule of thumb, what is the best estimate of the albumin-corrected total calcium (mmol/L)?

2.60 mmol/L

2.00 mmol/L

3.00 mmol/L

1.80 mmol/L

Cannot be estimated without ionised calcium measurement

In routine practice an approximate correction adds 0.02 mmol/L to total calcium for each 1 g/L albumin below 40 g/L; ionised calcium is definitive when accuracy is required.

A commonly used albumin-correction approximation in SI units is to add 0.02 mmol/L to the total calcium for each 1 g/L decrease in albumin below 40 g/L. Here albumin is 20 g/L (20 g/L below 40), so correction = 0.02 × 20 = 0.40 mmol/L. Corrected calcium = 2.20 + 0.40 = 2.60 mmol/L.

Why the others are less appropriate:
- 2.00 and 1.80 mmol/L would represent lower corrected calcium and imply no correction or incorrect direction of correction.
- 3.00 mmol/L is an overestimate given the formula above.
- While ionised calcium is the definitive measure of biologically active calcium and should be used when available or in critical situations, the albumin correction provides a pragmatic estimate and is commonly used in outpatient practice.

Note: albumin-correction formulas are approximations and less reliable in acutely ill patients or with abnormal protein states; ionised calcium measurement is preferable if clinical suspicion is high.

7 / 10

A 68-year-old male with long-standing diabetes and 6 years on haemodialysis has low PTH levels (intact PTH 12 pg/mL), persistently normal serum calcium and phosphate, and evidence of extensive vascular calcification on imaging. He is asymptomatic with low bone pain. Which management approach is most appropriate?

Increase active vitamin D therapy to raise PTH and improve bone turnover

Avoid calcium loading (stop calcium-based phosphate binders and consider lowering dialysate calcium), and reduce oversuppression of PTH

Empirically start bisphosphonates to improve bone density

Aggressively lower serum phosphate with high-dose aluminium-containing binders

Immediate parathyroidectomy to correct low PTH state

In adynamic bone disease avoid calcium loading and oversuppression of PTH (stop calcium-based binders, review vitamin D dosing and dialysate calcium).

This clinical picture is most consistent with adynamic bone disease: low PTH, low bone turnover and a propensity for vascular calcification. Management aims to avoid further suppression of bone turnover and reduce calcium loading. Practical steps include stopping calcium-containing phosphate binders, avoiding high-dose active vitamin D and considering a lower-dialysate calcium to minimise calcium exposure.

Why the others are less appropriate:
- Increasing active vitamin D will further suppress PTH and may worsen adynamic bone disease and vascular calcification.
- Bisphosphonates are generally avoided in adynamic bone disease because they may further suppress bone turnover.
- Aluminium binders are not recommended due to aluminium toxicity and are inappropriate.
- Parathyroidectomy is indicated for refractory high PTH, not for low PTH states.

8 / 10

A 57-year-old dialysis patient with persistently high PTH despite phosphate control is being considered for cinacalcet. Which of the following scenarios is a contraindication or strong reason to avoid initiating cinacalcet?

Intact PTH of 800 pg/mL with corrected calcium 2.40 mmol/L

Moderate hyperphosphataemia despite binders

Corrected serum calcium 1.95 mmol/L with symptoms of hypocalcaemia

High alkaline phosphatase with bone pain

History of mild peptic ulcer disease

Do not start cinacalcet in patients with symptomatic or marked hypocalcaemia; correct calcium first and monitor levels closely after initiation.

Cinacalcet is a calcimimetic that lowers PTH by increasing the sensitivity of the calcium-sensing receptor; it commonly causes or aggravates hypocalcaemia. A baseline corrected calcium of 1.95 mmol/L with symptoms of hypocalcaemia is a contraindication or strong reason to avoid starting cinacalcet until hypocalcaemia is corrected. Patients must have adequate baseline calcium and be monitored closely.

Why the others are less appropriate:
- Very high PTH with borderline calcium is a common indication for cinacalcet (after addressing reversible factors).
- Hyperphosphataemia is not a contraindication; phosphate control should be optimised but does not preclude cinacalcet.
- High alkaline phosphatase may reflect high bone turnover and does not contraindicate cinacalcet.
- Mild peptic ulcer disease is not an absolute contraindication; dose adjustments and monitoring for GI side effects may be required.

9 / 10

A 72-year-old woman with stage 4 CKD (eGFR 24 ml/min) and progressive coronary artery calcification has persistent hyperphosphataemia despite dietary measures. Which phosphate-binding strategy is preferred to reduce calcium load and potential progression of vascular calcification?

Start calcium acetate as first-line binders and increase dose as needed

Use aluminium hydroxide binders intermittently to lower phosphate rapidly

Initiate a non-calcium-containing binder such as sevelamer or lanthanum

No binders—treat hyperphosphataemia only when eGFR <15 ml/min

Start high-dose oral vitamin D to reduce PTH and thereby phosphate

In CKD with vascular calcification, prefer non-calcium phosphate binders (sevelamer, lanthanum) to minimise calcium exposure and potential progression of calcification.

In patients with advanced CKD and evidence of vascular calcification, non-calcium-containing phosphate binders (sevelamer, lanthanum) are preferred to avoid further calcium loading that could exacerbate vascular calcification. KDIGO guidance suggests limiting calcium-based binders in those at risk of vascular calcification.

Why the others are less appropriate:
- Calcium-containing binders increase total calcium load and may worsen vascular calcification.
- Aluminium binders are discouraged because of risk of aluminium accumulation and toxicity, especially with long-term use.
- Delaying binder therapy until eGFR <15 ml/min ignores progressive hyperphosphataemia which should be addressed earlier when appropriate. - High-dose oral vitamin D will not lower phosphate and may increase calcium; it is not a strategy to reduce phosphate burden.

10 / 10

Immunoassays for parathyroid hormone (PTH) differ in their measurement of PTH fragments. Which statement about third-generation (so-called 'whole' or 'bio-intact') PTH assays is most accurate?

They measure total PTH including large proportions of PTH fragments and therefore overestimate biologically active hormone

They are identical to second-generation 'intact' assays in cross-reactivity with N-terminal PTH fragments

They selectively measure only full-length 1-84 PTH, reducing cross-reactivity with large C-terminal fragments and may better reflect biologically active PTH

They are unaffected by renal failure because PTH fragments do not accumulate in CKD

They eliminate the need for clinical correlation and imaging in hyperparathyroidism

Third-generation PTH assays are more specific for full-length 1-84 PTH and reduce cross-reactivity with C-terminal fragments, but interpretation still requires clinical correlation in CKD patients.

Third-generation PTH assays are designed to measure predominantly full-length 1-84 PTH and reduce cross-reactivity with large C-terminal fragments that accumulate in renal failure. This can yield values that more closely reflect biologically active hormone. However, while third-generation assays reduce fragment interference, they do not remove the need for clinical correlation and additional investigations (imaging, assessment of mineral metabolism) when managing hyperparathyroidism.

Why the others are less appropriate:
- Statement that they measure total PTH including many fragments is incorrect; that describes older assays' limitations.
- They are not identical to second-generation assays; second-generation 'intact' assays detect some fragments (e.g. 7-84) leading to potential differences in CKD.
- It is incorrect to state they are unaffected by renal failure—CKD still affects PTH physiology and fragments to some extent; assay performance improves specificity but clinical interpretation remains necessary.
- They do not eliminate the need for clinical correlation and imaging; biochemical assays are one component of assessment.

Your score is

The average score is 0%

By Wordpress Quiz plugin

Board-level postgraduate nephrology self-assessment.

Complete all 10 single-best-answer questions to receive detailed clinical explanations on the results page.

Potassium and Other Electrolyte Disorders

Ten advanced MRCP-style single-best-answer questions covering diagnosis, interpretation, acute and chronic management, complications and clinical reasoning in potassium and related electrolyte disorders.

1 / 10

A 67-year-old man with chronic kidney disease (eGFR 22 mL/min/1.73 m2) is brought to the emergency department after collapse at home. He is drowsy. ECG shows widened QRS and absent P waves. Serum potassium from a stat laboratory result is 7.4 mmol/L. Which immediate action should be taken first?

Give intravenous calcium gluconate (or calcium chloride) to stabilise the cardiac membrane

Give intravenous insulin with 50 mL 50% dextrose to drive potassium intracellularly

Start nebulised salbutamol to shift potassium into cells

Give intravenous sodium bicarbonate to correct acidosis and lower potassium

Arrange urgent haemodialysis as the first step

In hyperkalaemia with ECG changes, give IV calcium immediately to stabilise the heart, then use potassium-shifting measures and arrange definitive removal.

Correct answer: Give intravenous calcium to stabilise the myocardium. In life‑threatening hyperkalaemia with ECG evidence of cardiac membrane instability (widened QRS, absent P waves, severe bradyarrhythmia), the immediate priority is membrane stabilisation with IV calcium (calcium gluconate or calcium chloride) because it reduces the risk of ventricular arrhythmia within minutes. After stabilisation, potassium shifting therapies (insulin + dextrose, nebulised β2 agonist) and measures to remove potassium (diuretics if effective, binders for non-urgent situations, or urgent dialysis if refractory or with renal failure) should follow. Sodium bicarbonate is only helpful when hyperkalaemia is accompanied by significant metabolic acidosis and its potassium-lowering effect is unpredictable; it is not first-line for membrane stabilisation. Urgent haemodialysis is definitive in severe or refractory hyperkalaemia, especially in advanced CKD, but it is not the immediate first action when there is ECG change — you must stabilise the myocardium first while organising dialysis.

2 / 10

A 55-year-old woman has an incidental serum potassium of 6.1 mmol/L on routine blood tests. She is asymptomatic; ECG is normal. Review of laboratory information shows a platelet count of 900 x10^9/L and the sample was a serum tube. What is the most appropriate next step?

Commence insulin and dextrose to lower potassium immediately

Repeat potassium measurement using a plasma (heparinised) sample or a non-haemolysed specimen

Start oral sodium polystyrene sulfonate (resin) to treat hyperkalaemia

Arrange urgent nephrology review for emergent dialysis

Administer intravenous calcium to stabilise the myocardium

Consider pseudohyperkalaemia (haemolysis, thrombocytosis) and confirm with a plasma or repeat non‑haemolysed sample before treatment when clinical picture and ECG are not supportive.

Correct answer: Repeat the potassium using a plasma (heparinised) or otherwise non‑haemolysed specimen. Marked thrombocytosis or in vitro haemolysis can cause pseudohyperkalaemia when serum (clotted) samples are used because platelets release potassium during clotting. In an asymptomatic patient with a normal ECG and no other reason for hyperkalaemia, the appropriate immediate step is to verify the result with a properly collected plasma sample (or a fresh venous gas) before instituting potentially harmful therapies. Commencing insulin/dextrose, resins, or arranging dialysis is inappropriate without confirming true hyperkalaemia. IV calcium is only indicated when there are ECG changes or clinical instability.

3 / 10

A 29-year-old man presents with acute profound flaccid paralysis of all four limbs over several hours. He is known to take intermittent laxatives. Serum potassium is 1.9 mmol/L and ECG shows U waves and flattened T waves. Which of the following is the most appropriate immediate management?

Oral potassium chloride tablets at frequent intervals

Start intravenous potassium bicarbonate to correct underlying acidosis

Begin slow intravenous potassium chloride replacement via a central line with continuous cardiac monitoring

Administer intravenous insulin and glucose to raise intracellular potassium

Start spironolactone to reduce renal potassium wasting

Severe hypokalaemia with neuromuscular and ECG manifestations requires prompt IV potassium chloride replacement with appropriate monitoring.

Correct answer: Begin slow IV potassium chloride via a central line with cardiac monitoring. Severe hypokalaemia (<2.5 mmol/L) with neuromuscular weakness and ECG changes is a medical emergency; prompt potassium repletion is required, usually with intravenous potassium chloride. Because large amounts are often necessary and intravenous potassium can cause local irritation and arrhythmia, central access and continuous ECG monitoring are recommended for higher rates/concentrations. Oral therapy is too slow and may be impractical in profound paralysis. Potassium bicarbonate is not indicated unless there is concurrent metabolic acidosis and the potassium formulation should be KCl unless there is a specific reason to choose another salt. Insulin would shift potassium intracellularly and worsen hypokalaemia. Spironolactone is not an acute rescue therapy and would act too slowly.

4 / 10

A 68-year-old man with stage 3b CKD is repeatedly developing hyperkalaemia (5.8–6.2 mmol/L) after initiation of an ACE inhibitor for albuminuric CKD. He tolerated ACE inhibition previously but potassium rises limit therapy. According to contemporary guidance, the best next step to allow continuation of renin–angiotensin–aldosterone system (RAAS) blockade is:

Stop the ACE inhibitor permanently and switch to a calcium channel blocker

Reduce salt intake only and recheck potassium in 6 months

Start an oral sodium bicarbonate tablet and stop ACE inhibitor

Commence a potassium-binding agent (e.g. patiromer or sodium zirconium cyclosilicate) and reintroduce/continue RAAS inhibitor with monitoring

Begin long-term oral loop diuretic without other changes

Use potassium-binding agents to treat chronic hyperkalaemia and allow continuation or reintroduction of RAAS inhibitors when indicated, with close monitoring.

Correct answer: Commence a potassium-binding agent and reintroduce/continue RAAS inhibitor with monitoring. Contemporary guidelines and expert opinion support using potassium binders (patiromer or sodium zirconium cyclosilicate) to control chronic hyperkalaemia so patients can continue guideline-directed RAAS blockade when clinically indicated, with regular monitoring. Permanently stopping an ACE inhibitor may deprive the patient of renal and cardiovascular benefit. Reducing dietary salt alone is insufficient and delaying reassessment is inappropriate. Oral sodium bicarbonate may help when chronic metabolic acidosis is present but is not the standard approach solely to control RAAS inhibitor–associated hyperkalaemia. Adding a diuretic can lower potassium in some patients, but its effectiveness depends on renal function and volume status and it may cause other problems; a potassium binder is the preferred step to enable continuation of RAASi when available and appropriate.

5 / 10

A 21-year-old woman presents with diabetic ketoacidosis (DKA). Her serum potassium on arrival is 5.6 mmol/L. Which statement regarding potassium in DKA is most accurate?

Her total body potassium is likely increased due to extracellular shift

Serum potassium reliably reflects total body potassium stores in DKA

You should withhold potassium replacement because serum potassium is high and no deficit exists

Despite hyperkalaemia at presentation, total body potassium is usually depleted and potassium replacement is generally required once insulin therapy commences

Metabolic alkalosis in DKA causes potassium to shift into cells lowering serum potassium

In DKA, serum hyperkalaemia commonly masks total body potassium depletion; expect to replace potassium once insulin therapy starts.

Correct answer: Despite hyperkalaemia at presentation, total body potassium is usually depleted and potassium replacement is generally required once insulin therapy commences. In DKA, insulin deficiency and acidosis cause potassium to shift out of cells, raising serum potassium despite total body potassium depletion due to osmotic diuresis and urinary losses. When insulin is given and acidosis corrected, potassium moves intracellularly and serum potassium falls, so potassium replacement is commonly necessary to avoid dangerous hypokalaemia. Serum potassium does not reliably reflect total body stores in this context. The other statements are incorrect: total body potassium is typically low, you should not withhold replacement solely because serum potassium is initially high, and DKA is associated with acidosis (not alkalosis) that shifts potassium out of cells.

6 / 10

A patient with high‑grade non-Hodgkin lymphoma is started on cytotoxic chemotherapy. Baseline uric acid is elevated and there is a high tumour burden. Which prophylactic measure most effectively reduces the risk of tumour lysis syndrome (TLS) and hyperkalaemia in this high-risk patient?

Administer rasburicase and aggressive intravenous hydration prior to and during chemotherapy

Start oral allopurinol alone immediately before chemotherapy

Give a single dose of intravenous calcium to prevent hyperkalaemia

Begin oral sodium polystyrene sulfonate prophylactically

Withhold chemotherapy until potassium falls spontaneously

High‑risk tumour lysis syndrome is best prevented with rasburicase and vigorous hydration plus close monitoring to avoid hyperkalaemia and renal injury.

Correct answer: Administer rasburicase and aggressive IV hydration. In patients at high risk for TLS (high tumour burden, high uric acid), rasburicase rapidly lowers uric acid by converting it to allantoin and, together with aggressive hydration and monitoring, reduces the risk of uric acid nephropathy and associated electrolyte derangements including hyperkalaemia. Allopurinol prevents formation of new uric acid but does not reduce existing uric acid rapidly and is less effective in high-risk TLS. A single dose of IV calcium does not prevent hyperkalaemia and may be harmful if potassium subsequently changes. Sodium polystyrene sulfonate has slow and variable onset and is not a prophylactic substitute for definitive TLS prevention. Withholding chemotherapy is not an appropriate prophylactic strategy; rather TLS risk should be mitigated to enable safe treatment.

7 / 10

A 45-year-old woman on long-term thiazide diuretics presents with recurrent hypokalaemia refractory to oral potassium supplements. Serum magnesium is 0.45 mmol/L (low). Which action is most likely to correct her hypokalaemia?

Increase oral potassium dose only and monitor

Replace magnesium (oral or IV as indicated) while continuing potassium replacement

Stop potassium supplementation and start spironolactone immediately

Administer IV calcium to correct the hypomagnesaemia effect

Switch from thiazide to loop diuretic to conserve potassium

Hypokalaemia refractory to potassium repletion commonly reflects coexisting hypomagnesaemia — correct magnesium to enable potassium correction.

Correct answer: Replace magnesium while continuing potassium. Hypomagnesaemia increases renal potassium loss by impairing the normal potassium‑conserving mechanisms; unless magnesium is corrected, hypokalaemia is often refractory to potassium repletion. Therefore magnesium replacement (oral or IV depending on severity) should be undertaken alongside potassium replacement. Increasing potassium alone without correcting magnesium frequently fails. Spironolactone can help potassium retention but is not the immediate primary step when hypomagnesaemia is present; also address the magnesium deficiency. IV calcium does not treat hypomagnesaemia. Switching diuretics may be considered in the long term but is not the immediate corrective measure for refractory hypokalaemia due to low magnesium.

8 / 10

A 28-year-old man presents with chronic hypokalaemia and metabolic alkalosis. He has normal blood pressure and reports muscle cramps. Investigations show hypomagnesaemia and low urinary calcium excretion. Which inherited tubulopathy is the most likely diagnosis?

Liddle syndrome

Primary hyperaldosteronism

Gitelman syndrome

Classic Bartter syndrome

Apparent mineralocorticoid excess

Gitelman syndrome causes hypokalaemia, metabolic alkalosis, hypomagnesaemia and low urinary calcium with normal/low blood pressure.

Correct answer: Gitelman syndrome. Gitelman syndrome typically presents in adolescence or adulthood with hypokalaemia, metabolic alkalosis, hypomagnesaemia and hypocalciuria (low urinary calcium). Blood pressure is usually normal or low. Bartter syndrome classically presents earlier, often with salt wasting and hypercalciuria. Liddle syndrome causes hypertension with suppressed renin and aldosterone and features potassium wasting but without hypomagnesaemia and with hypertension. Primary hyperaldosteronism causes hypertension with suppressed renin and metabolic alkalosis but usually without hypomagnesaemia and often with normal/high urinary calcium. Apparent mineralocorticoid excess also causes hypertension and hypokalaemia; the presence of normal blood pressure and hypomagnesaemia with low urinary calcium points to Gitelman.

9 / 10

A 72-year-old woman with CKD stage 4 on an ACE inhibitor is found to have potassium of 6.0 mmol/L on routine testing. She has no ECG changes and is clinically well. Which is the most appropriate next immediate step?

Immediately stop the ACE inhibitor and arrange urgent dialysis

Ignore the result; redo blood tests in 3 months

Review for reversible contributors (medications, acidosis, constipation) and arrange prompt repeat potassium with dietary advice and close monitoring

Start chronic oral sodium polystyrene sulfonate to normalise potassium permanently

Prescribe spironolactone to correct potassium

In stable patients with moderate hyperkalaemia, seek and correct reversible causes and recheck potassium before stopping RAAS blockade; consider potassium-lowering strategies if hyperkalaemia persists.

Correct answer: Review for reversible contributors and arrange prompt repeat potassium with close monitoring. In a clinically well patient with moderate hyperkalaemia and no ECG changes, immediate steps should focus on identifying and treating reversible causes (other medications such as NSAIDs, potassium supplements, trimethoprim; metabolic acidosis; constipation), dietary counselling, and repeating the potassium promptly to confirm persistence, while planning management (e.g. consider diuretics or potassium binders) rather than reflexively stopping RAAS inhibitors. Immediate dialysis is not indicated without ECG changes or refractory hyperkalaemia. Waiting months is unsafe. Chronic sodium polystyrene sulfonate is not recommended as the first-line long-term strategy because of tolerability and uncertainty about safety; newer binders are preferred. Spironolactone would increase potassium and worsen hyperkalaemia.

10 / 10

A 58-year-old man with end-stage kidney disease on haemodialysis presents with K+ 7.2 mmol/L, peaked T waves and episodes of ventricular ectopy. He has already received IV calcium and insulin/dextrose with temporary improvement but potassium rebounds to 7.0 mmol/L and ECG changes recur. What is the most appropriate next step?

Repeat IV calcium bolus and observe on the ward

Administer nebulised salbutamol and start oral bicarbonate

Perform urgent haemodialysis to rapidly remove potassium

Begin long-term treatment with oral patiromer and arrange outpatient follow-up

Start an infusion of intravenous magnesium to stabilise cardiac membranes

In dialysis patients with severe or refractory hyperkalaemia and ECG changes, urgent haemodialysis is the definitive therapy.

Correct answer: Perform urgent haemodialysis. In end-stage kidney disease with severe hyperkalaemia that is refractory or recurrent despite membrane stabilisation and potassium-shifting therapies, urgent haemodialysis is the definitive method to remove potassium quickly and is indicated, particularly when ECG changes persist or recur. Repeating calcium alone is only temporising. Nebulised salbutamol and bicarbonate can be adjuncts but are not definitive when hyperkalaemia rebounds in a dialysis patient. Oral patiromer is for chronic management and has slow onset; it is not appropriate for immediate control of life‑threatening hyperkalaemia. IV magnesium does not treat hyperkalaemia or stabilise the cardiac membrane in this context.

Your score is

The average score is 0%

By Wordpress Quiz plugin

Board-level postgraduate nephrology self-assessment.

Complete all 10 single-best-answer questions to receive detailed clinical explanations on the results page.

Hereditary and Cystic Kidney Disease

Board-style advanced single-best-answer MCQs covering genetics, diagnosis, acute and chronic management, complications and transplantation considerations in hereditary and cystic kidney disease.

1 / 10

A 28-year-old woman has recently been diagnosed with autosomal dominant polycystic kidney disease (ADPKD). She asks what risk her future child has of inheriting the condition. Which is the most accurate statement?

Her child has a 25% chance of inheriting ADPKD.

Each child has a 50% chance of inheriting ADPKD.

If she has only mild disease there is no risk to her children.

The child will definitely be affected because ADPKD is fully penetrant.

Risk depends on the age of the parent at diagnosis, so it cannot be estimated.

ADPKD is autosomal dominant: each child of an affected parent has a 50% risk of inheriting the mutation regardless of parental disease severity.

Correct: Autosomal dominant conditions such as ADPKD are transmitted in a vertical autosomal dominant pattern; each child of an affected parent has a 50% chance of inheriting the pathogenic allele, independent of the parent’s disease severity. Option A is incorrect because 25% is the risk for autosomal recessive inheritance with both parents carriers, not ADPKD. Option C is incorrect because disease severity in the parent does not change the probability of transmission; there is variable expressivity but not altered Mendelian transmission. Option D is incorrect because although penetrance is high for many ADPKD mutations, penetrance is not absolute in all cases and disease expression varies; the correct point is the 50% transmission risk rather than certainty. Option E is incorrect because parental age at diagnosis does not change the Mendelian 50% transmission risk.

2 / 10

You need to measure total kidney volume (TKV) accurately to risk-stratify a patient with ADPKD for disease progression. Which imaging modality is the most appropriate choice for reproducible TKV measurement?

Renal ultrasound (US)

Non-contrast CT KUB

Magnetic resonance imaging (MRI)

99mTc-MAG3 nuclear renography

Plain abdominal radiograph

MRI is the preferred modality for accurate, reproducible measurement of total kidney volume in ADPKD when serial volumetry is required.

Correct: MRI provides high-resolution, reproducible kidney and cyst volume measurements without ionising radiation and is the preferred modality for accurate serial measurement of total kidney volume in ADPKD. Ultrasound is useful for screening but is operator-dependent and not reliable for precise TKV quantification. Non-contrast CT gives good anatomical detail but involves ionising radiation and is less preferred for repeated measurements. Nuclear renography assesses split function rather than morphology or volume. Plain radiograph does not provide kidney volume information.

3 / 10

A 45-year-old man with ADPKD has clinic blood pressure 150/95 mmHg and urine protein excretion 1.0 g/24 h. Which antihypertensive strategy is the most appropriate initial choice?

Start an ACE inhibitor as first-line therapy

Start a beta-blocker as first-line therapy

Start a loop diuretic as first-line therapy

Start a calcium‑channel blocker as first-line therapy

No antihypertensive required; advise lifestyle measures only

ACE inhibitors (or ARBs) are first-line antihypertensive agents in ADPKD, especially in the presence of proteinuria.

Correct: Renin–angiotensin system blockade (ACE inhibitor or ARB) is first-line antihypertensive therapy for patients with ADPKD, particularly when there is proteinuria, because it both lowers blood pressure and reduces intraglomerular pressure/proteinuria. Beta-blockers and calcium-channel blockers may be used as add-on agents but are not preferred first-line when RAAS blockade is indicated. Loop diuretics are reserved for volume overload and are not standard initial therapy for hypertension alone. Lifestyle measures are important but insufficient here given persistent clinic hypertension and significant proteinuria.

4 / 10

Which of the following statements best describes tolvaptan therapy in ADPKD?

Tolvaptan is an mTOR inhibitor that reduces cyst epithelial proliferation and requires lipid monitoring.

Tolvaptan is an immunosuppressant used to slow cyst growth and needs infection surveillance.

Tolvaptan is a vasopressin V2 receptor antagonist that causes aquaresis and requires regular liver function monitoring.

Tolvaptan is an enzyme replacement therapy given to correct a metabolic defect in ADPKD.

Tolvaptan is a diuretic that works like furosemide and requires potassium monitoring.

Tolvaptan is a vasopressin V2 receptor antagonist used to slow progression in selected patients with ADPKD and requires monitoring of liver function because of hepatotoxicity risk.

Correct: Tolvaptan is a selective vasopressin V2 receptor antagonist that reduces cAMP-mediated cyst growth and causes aquaresis (increased free water clearance). A recognized safety concern is idiosyncratic liver injury, so regular liver function testing is required during treatment and treatment should be stopped if significant liver enzyme rises occur. Option A confuses tolvaptan with mTOR inhibitors (e.g., sirolimus), which have a different mechanism and adverse effect profile. Option B incorrectly labels it as an immunosuppressant. Option D is incorrect; ADPKD is not treated with enzyme replacement. Option E incorrectly equates tolvaptan with loop diuretics; its mechanism is via V2 antagonism and it causes aquaresis rather than natriuresis.

5 / 10

A 52-year-old patient with ADPKD presents with 5 days of fever, flank pain and raised inflammatory markers. You suspect an infected renal cyst. Which of the following is the most appropriate initial empiric antibiotic choice?

Oral amoxicillin

IV cefuroxime

IV gentamicin

Oral/IV ciprofloxacin (a fluoroquinolone)

Oral metronidazole

When treating suspected infected renal cysts in ADPKD, choose antibiotics with good cyst penetration (e.g., fluoroquinolones), and consider drainage for non-responding or large infected cysts.

Correct: Antibiotics that penetrate cyst fluid well, notably fluoroquinolones (e.g., ciprofloxacin) and trimethoprim-sulfamethoxazole, are preferred empiric choices for suspected infected cysts in ADPKD. Many beta-lactams and aminoglycosides penetrate cysts poorly, making them less suitable as sole empiric therapy. Metronidazole targets anaerobes and is not appropriate as monotherapy for renal cyst infection. Definitive therapy should be guided by cultures and clinical response, and large infected cysts may require percutaneous drainage.

6 / 10

A 60-year-old woman with massive symptomatic polycystic liver disease (PLD) has abdominal fullness and early satiety despite conservative measures. Which therapeutic option has evidence of reducing liver volume and is appropriate to consider in selected patients?

Immediate orthotopic liver transplantation as first-line therapy

Somatostatin analogue therapy (e.g., octreotide/lanreotide)

High-dose corticosteroids to reduce cyst inflammation

mTOR inhibitor therapy (e.g., sirolimus) routinely for all patients

Do nothing; there are no effective medical therapies for symptomatic PLD

Somatostatin analogues can reduce liver cyst volume and may be considered for symptomatic polycystic liver disease in selected patients; invasive intervention or transplant is reserved for refractory severe cases.

Correct: Somatostatin analogues have been shown to reduce liver cyst growth and liver volume in some patients with symptomatic polycystic liver disease and are an option in selected patients, particularly when conservative measures have failed and before considering major surgery. Option A (immediate liver transplant) is reserved for very severe refractory cases with liver failure or unacceptable quality-of-life impairment and is not first-line. Corticosteroids are not effective for cyst reduction. mTOR inhibitors have had mixed results and are not routinely used as standard therapy for PLD. Option E is incorrect because there are effective medical options for some patients (e.g., somatostatin analogues) and interventional/surgical options for others.

7 / 10

An infant born with oligohydramnios and enlarged echogenic kidneys is diagnosed with autosomal recessive polycystic kidney disease (ARPKD). The infant has respiratory distress from pulmonary hypoplasia. What is the immediate priority in early management?

Immediate bilateral native nephrectomy to improve abdominal domain

Urgent initiation of ACE inhibitor therapy for hypertension prevention

Optimise respiratory support and neonatal intensive care management

Begin chronic peritoneal dialysis immediately

Start high-dose diuretics to reduce kidney size

In neonates with ARPKD, respiratory failure from pulmonary hypoplasia is the leading early cause of morbidity and requires priority neonatal respiratory support.

Correct: ARPKD in the neonate commonly presents with pulmonary hypoplasia secondary to oligohydramnios; the immediate priority is respiratory stabilisation and supportive care in a neonatal intensive care setting. Nephrectomy is not an initial intervention and is rare acutely; ACE inhibitors are used later to manage hypertension but are not the immediate priority in a crashing neonate. Dialysis decisions are complex in the neonatal period and depend on overall prognosis and stability; immediate chronic peritoneal dialysis is not the first step in the acute respiratory-compromised infant. High-dose diuretics will not effectively reduce massively enlarged dysplastic kidneys and are not indicated acutely.

8 / 10

A potential living kidney donor is the 40-year-old sibling of a patient with ADPKD. The affected sibling has a known pathogenic PKD1 mutation. What is the most appropriate action regarding genetic testing of the potential donor?

Decline the sibling as a donor because family members cannot donate to ADPKD patients.

Proceed with donation without testing if the donor’s renal ultrasound is normal.

Offer targeted genetic testing for the known familial mutation to the potential donor.

Perform whole-exome sequencing (WES) on the donor as standard practice.

Accept the donor if they have normal blood pressure, regardless of genetic status.

If a pathogenic familial ADPKD mutation is known, offer targeted genetic testing to at-risk living donors to confirm absence of the mutation before proceeding.

Correct: When a pathogenic familial mutation is known, targeted genetic testing of at-risk potential living donors is appropriate and can definitively determine whether the donor carries the family mutation; a donor who is mutation-positive should not donate. Option A is incorrect because family members can donate if they are proven not to carry the pathogenic mutation. Option B is unsafe because ultrasound may be normal in younger mutation carriers and cannot exclude presymptomatic disease reliably for all ages. Option D is inappropriate because WES is not routine for donor assessment and may identify unrelated incidental findings; targeted testing is the recommended focused approach. Option E is unsafe because normal blood pressure does not exclude a pathogenic mutation and future risk for kidney disease.

9 / 10

A patient with ADPKD presents with sudden painless gross haematuria and is haemodynamically stable. There is no fever. Which of the following is the most appropriate initial management step?

Conservative management with bed rest, hydration and observation

Immediate renal angiography and embolisation

Urgent bilateral nephrectomy

Start full anticoagulation to treat presumed renal vein thrombosis

Immediate extracorporeal shock wave lithotripsy (ESWL)

Most episodes of gross haematuria in ADPKD are managed conservatively if the patient is haemodynamically stable; escalate to intervention only for ongoing or severe bleeding.

Correct: In haemodynamically stable patients with gross haematuria from ADPKD, initial management is usually conservative (rest, hydration, analgesia, and observation) because haematuria often results from cyst rupture and will settle. Intervention (angiographic embolisation, surgery or endoscopic procedures) is reserved for ongoing or severe bleeding, haemodynamic instability, or specific lesions identified on imaging. Immediate angiography or nephrectomy is not indicated if the patient is stable. Anticoagulation is contraindicated in active bleeding unless there is a compelling separate indication. ESWL is for renal stones and is not appropriate for presumed cyst-related haematuria without confirmation.

10 / 10

A 55-year-old man with end-stage kidney disease due to ADPKD is being counselled about renal replacement therapy options. Which statement best reflects the recommended optimal long-term strategy for suitable candidates?

Peritoneal dialysis is contraindicated in ADPKD and should not be offered.

Haemodialysis is the only acceptable long-term option for ADPKD patients.

Native nephrectomy is required before all transplants in ADPKD.

Pre-emptive kidney transplantation is preferred for suitable ADPKD patients.

Patients with ADPKD should not be listed for transplant because of high recurrence risk.

Pre-emptive kidney transplantation is the preferred RRT for suitable ADPKD patients; dialysis modality choice should be individualised and ADPKD alone is not a contraindication to transplant.

Correct: For suitable candidates, pre-emptive kidney transplantation is the preferred long-term renal replacement therapy because it provides best outcomes and quality of life. Peritoneal dialysis is not universally contraindicated in ADPKD though very large kidneys can limit intraperitoneal volume and require individual assessment; it remains a viable modality for many patients. Haemodialysis is an acceptable RRT but not the only option. Native nephrectomy is not routinely required prior to transplantation and is performed selectively for symptom control or technical reasons. Kidney disease does not recur in the graft from ADPKD; there is no reason to deny listing on the basis of ADPKD alone.

Your score is

The average score is 0%

By Wordpress Quiz plugin

Assignment Level: Advanced

Services

Follow Us