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.

Chronic Kidney Disease and Complications

Ten board-style, single-best-answer questions covering diagnosis, interpretation, acute and chronic management, complications and clinical reasoning in advanced chronic kidney disease (CKD).

1 / 10

A 63-year-old man has an estimated GFR of 42 mL/min/1.73 m2 and a urine albumin:creatinine ratio of 35 mg/mmol. According to KDIGO classification, which description best categorises his CKD?

CKD G3a A2

CKD G4 A1

CKD G3b A3

CKD G2 A3

CKD G5 A2

CKD staging uses eGFR G-categories and albuminuria A-categories; eGFR 30–44 is G3b and uACR >30 mg/mmol is A3.

G categories are based on eGFR: G3a is 45–59, G3b is 30–44, G4 is 15–29, G5 is <15 mL/min/1.73 m2. The patient's eGFR of 42 places him in G3b. Albuminuria categories (using common UK units) are A1 <3 mg/mmol, A2 3–30 mg/mmol, A3 >30 mg/mmol. His uACR of 35 mg/mmol is A3. Therefore the correct KDIGO descriptor is G3b A3. Other options are incorrect because they misclassify either the G or A category.

2 / 10

A 70-year-old woman with CKD stage 4 presents with generalised weakness. ECG shows peaked T waves and QRS widening. Serum potassium is 7.2 mmol/L. Which immediate intervention is most appropriate to reduce the risk of life‑threatening arrhythmia?

Intravenous calcium gluconate

Enteral sodium polystyrene sulfonate (sodium exchange resin)

Start haemodialysis immediately

Intravenous sodium bicarbonate as first-line stabilisation

Oral patiromer

In hyperkalaemia with ECG changes, give IV calcium promptly to stabilise the heart, then employ measures to shift or remove potassium.

When hyperkalaemia produces ECG changes (peaked T waves, QRS widening), the immediate priority is to stabilise the cardiac membrane with intravenous calcium (usually calcium gluconate or calcium chloride). This does not reduce serum potassium but reduces arrhythmic risk. Measures to lower potassium (insulin with glucose, nebulised salbutamol, bicarbonate if acidotic, or dialysis) follow or are given concurrently as appropriate. Enteral sodium polystyrene sulfonate and oral patiromer act slowly and are not suitable for immediate stabilisation. Haemodialysis is definitive in refractory or severe cases but is not the first immediate action to protect the myocardium.

3 / 10

A 58-year-old man with CKD stage 4 has a persistent serum bicarbonate of 18 mmol/L on two separate measurements and progressive muscle wasting. Which is the most appropriate next step to manage his metabolic disturbance?

Start acetazolamide to increase renal bicarbonate excretion

Begin oral sodium bicarbonate therapy

Urgent initiation of haemodialysis solely for correction of bicarbonate

Institute a low-potassium, low-sodium diet only

Administer intravenous 0.9% saline bolus

In CKD with persistent metabolic acidosis (HCO3 <22 mmol/L), oral bicarbonate supplementation is indicated to correct acidosis and improve outcomes.

Chronic metabolic acidosis in CKD (serum bicarbonate persistently <22 mmol/L) is commonly treated with oral sodium bicarbonate to correct acidosis, improve nutrition and slow progression of muscle wasting. Acetazolamide causes bicarbonate wasting and would worsen metabolic acidosis. Urgent haemodialysis is not indicated solely for mild–moderate chronic metabolic acidosis unless there are other indications for dialysis. Dietary measures alone are insufficient to correct serum bicarbonate.

4 / 10

A 66-year-old man with CKD stage 3b is found to have haemoglobin 8.8 g/dL. Ferritin is 40 µg/L and transferrin saturation is 12%. Blood pressure is well controlled. Which of the following is the most appropriate initial management step?

Start an erythropoiesis-stimulating agent immediately

Begin a trial of oral iron supplementation

Arrange urgent referral for bone marrow biopsy

Offer red cell transfusion as first-line therapy

Start intravenous iron without attempting oral therapy

Correct iron deficiency before initiating ESAs in non-dialysis CKD; start with oral iron unless there are reasons to use IV iron.

In CKD-related anaemia, iron deficiency should be corrected before starting erythropoiesis-stimulating agents (ESAs). Ferritin 40 µg/L and transferrin saturation 12% indicate iron deficiency. In non-dialysis CKD, a trial of oral iron is generally appropriate as the initial step unless there is intolerance, poor absorption, or need for rapid repletion—then intravenous iron is used. ESAs are generally considered after iron repletion if Hb remains low (typically when Hb persistently <10 g/dL and other causes excluded). Bone marrow biopsy is not first-line for suspected iron-deficiency anaemia in CKD, and transfusion is reserved for symptomatic anaemia or acute needs.

5 / 10

A 55-year-old woman with CKD stage 4 has persistently elevated parathyroid hormone (PTH) but serum calcium and phosphate are within reference ranges. Her 25-hydroxyvitamin D is low. Which is the best next step in management of her CKD–MBD (mineral and bone disorder)?

Start a calcium-containing phosphate binder

Immediate referral for parathyroidectomy

Begin oral cholecalciferol (nutritional vitamin D) repletion

Start oral cinacalcet (calcimimetic) now

Institute a long-term low-calcium, low-phosphate diet only

In secondary hyperparathyroidism with low 25(OH)D, correct nutritional vitamin D deficiency before escalating to calcimimetics or surgery.

When PTH is elevated and 25-hydroxyvitamin D is low in CKD, the initial step is to correct vitamin D deficiency with nutritional vitamin D such as cholecalciferol or ergocalciferol. Calcium-containing phosphate binders are used for selected hyperphosphataemia, not isolated PTH elevation with normal phosphate. Oral cinacalcet and parathyroidectomy are generally reserved for severe or refractory secondary hyperparathyroidism after appropriate medical management; cinacalcet is not an intravenous drug. Diet alone will not correct vitamin D deficiency.

6 / 10

A 62-year-old man with CKD stage 4 (eGFR 24 mL/min/1.73 m2) and no history of atherosclerotic cardiovascular disease asks whether he should be prescribed a statin. Which is the best evidence-based recommendation?

Offer a statin (or statin/ezetimibe) for primary prevention

Do not prescribe a statin; wait until dialysis is started

Statins are contra‑indicated in CKD stage 4

Start aspirin instead of a statin for primary prevention of vascular events

Only prescribe a statin if LDL cholesterol is >5.0 mmol/L

In adults with CKD not on dialysis, statin therapy for primary prevention is generally recommended, especially in older adults.

Guideline recommendations support offering a statin (with or without ezetimibe) for adults with CKD not on dialysis who are of typical age for primary prevention (KDIGO suggests most adults ≥50 years). Statins reduce atherosclerotic events in non-dialysis CKD. Starting dialysis alters indications and does not necessarily mean starting a statin de novo. Statins are not contraindicated in CKD stage 4. Aspirin is not an alternative to statins for primary prevention in this context and decisions should be individualised. LDL thresholds alone are not the sole determinant for statin use in CKD as guidelines recommend considering CKD itself as a risk marker.

7 / 10

A 58-year-old woman with type 2 diabetes has eGFR 32 mL/min/1.73 m2 and has been taking metformin 1 g twice daily. According to standard guidance, what is the most appropriate immediate action regarding her metformin therapy?

Continue metformin at the same dose without change

Stop metformin permanently because any CKD precludes its use

Reduce the dose and monitor renal function regularly

Switch to sulfonylurea immediately

Administer intravenous fluids to allow continued high-dose metformin

For eGFR 30–45, reduce metformin dose and monitor renal function; stop metformin if eGFR falls <30 or during acute intercurrent illness.

NICE and other guidance advise that metformin can be continued with caution when eGFR is 30–45 mL/min/1.73 m2 with dose reduction and close monitoring; it should be stopped when eGFR is <30 or if there is intercurrent illness with AKI risk. Therefore the appropriate action is to reduce the dose and monitor renal function regularly. Permanently stopping metformin is unnecessary at this eGFR. Switching agents or giving IV fluids are not the standard immediate actions; IV fluids are only relevant if there is volume depletion/AKI.

8 / 10

A 59-year-old man with progressive CKD has an eGFR that has fallen from 22 to 12 mL/min/1.73 m2 over 6 months. He is likely to need haemodialysis within a few months. What is the most appropriate action regarding vascular access planning?

Defer any referral until dialysis is actually required

Plan for a central venous dialysis catheter as the preferred long-term access

Arrange timely referral for creation of an arteriovenous fistula (AVF)

Schedule peritoneal dialysis catheter insertion immediately instead of considering AVF

Start erythropoiesis-stimulating agents to delay need for access

Refer for AV fistula formation in advance when dialysis is likely within months; early planning reduces catheter-dependence.

For patients likely to start haemodialysis within months, timely referral for creation of a native arteriovenous fistula (AVF) is recommended because AVFs have superior long-term outcomes compared with central venous catheters. Delaying referral risks starting dialysis with a catheter. Choice of modality (haemodialysis versus peritoneal dialysis) is individualised, but planning for AVF when haemodialysis is anticipated is appropriate. ESAs do not meaningfully delay the need for dialysis in this context. A central venous catheter is not preferred as long-term access due to higher complication rates.

9 / 10

A 48-year-old man with longstanding CKD presents with chest discomfort. Echocardiography shows a pericardial effusion without haemodynamic compromise. He is dyspnoeic and has a history of missed dialysis sessions. Which is the most appropriate next step in management?

Start high-dose nonsteroidal anti-inflammatory drug therapy

Intensify or urgently resume dialysis (dialysis prescription review/increase frequency)

Immediate pericardiocentesis in all cases of uraemic pericardial effusion

Administer systemic corticosteroids

Conservative management with observation only

Uraemic pericarditis is treated primarily by intensifying dialysis; invasive drainage is for tamponade or refractory effusions.

Uraemic pericarditis/pericardial effusion in patients with inadequate dialysis is best managed by intensifying or urgently resuming dialysis to remove uraemic toxins; this often leads to resolution. NSAIDs are generally avoided because of nephrotoxicity and bleeding risk. Pericardiocentesis is reserved for cardiac tamponade or large symptomatic effusions not responsive to dialysis. Corticosteroids are not standard therapy for uraemic pericarditis. Observation alone is inappropriate in a symptomatic patient with missed dialysis sessions.

10 / 10

A 67-year-old woman with CKD stage 4 has recurrent hyperkalaemia (K+ ~5.8–6.2 mmol/L) that repeatedly necessitates dose reduction or stopping of her renin–angiotensin–aldosterone system inhibitor, which she derives clear renal and cardiac benefit from. Which approach is most appropriate to enable continuation of RAAS blockade?

Permanently discontinue the RAAS inhibitor and accept loss of benefit

Reduce dietary potassium only and continue same RAAS inhibitor dose

Introduce a novel potassium binder (e.g., patiromer or sodium zirconium cyclosilicate) to control potassium and continue RAAS therapy

Switch to an alternative antihypertensive with similar RAAS activity but lower hyperkalaemia risk

Prescribe long-term oral sodium polystyrene sulfonate as first-line

Novel potassium binders can permit continuation of RAAS inhibitors in CKD patients with recurrent hyperkalaemia when other measures are inadequate.

Newer potassium binders such as patiromer and sodium zirconium cyclosilicate can effectively control chronic hyperkalaemia and are used to enable continued RAAS inhibitor therapy in patients who benefit from these drugs. Permanently stopping RAAS blockade forfeits proven renal/cardiovascular benefits. Dietary measures may help but are often insufficient alone. Old exchange resins (sodium polystyrene sulfonate) have limited evidence for long-term use and safety concerns; they are not the preferred long-term strategy. Switching to another agent with similar RAAS effects is unlikely to avoid hyperkalaemia; there are no direct alternatives that preserve the same benefits without hyperkalaemia risk.

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Board-level postgraduate nephrology self-assessment.

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

Acute Kidney Injury

Ten advanced, board-style single-best-answer MCQs covering diagnosis, interpretation, acute and ongoing management, complications and follow-up of acute kidney injury (AKI).

1 / 10

A 78-year-old man with heart failure on long-term loop diuretic therapy is admitted with a 48-hour rise in serum creatinine. He is oliguric. Bedside observations show no hypotension. There is peripheral oedema. You want to distinguish pre-renal (functional) AKI from intrinsic tubular injury. Which test is most useful in this context?

Fractional excretion of sodium (FENa)

Fractional excretion of urea (FEUrea)

Urine eosinophil microscopy

Immediate renal ultrasound

Urine osmolality

In patients on diuretics, use FEUrea rather than FENa to help distinguish pre-renal from intrinsic AKI.

FEUrea is the preferred fractional excretion index when patients are taking diuretics. Loop diuretics increase urinary sodium excretion and thus can make FENa falsely high, reducing its reliability to detect pre-renal (functional) AKI. FEUrea is less affected by diuretics and better differentiates pre-renal azotaemia (low FEUrea, indicating avid urea reabsorption) from intrinsic tubular injury (higher FEUrea). Urine eosinophils are neither sensitive nor specific for intrinsic renal disease and are not recommended for routine use. Renal ultrasound is appropriate when obstruction is suspected but does not differentiate pre-renal from intrinsic tubular injury. Urine osmolality may be influenced by diuretics and is less reliable in this setting.

2 / 10

A 58-year-old woman develops rapidly progressive renal impairment over 5 days with haemoptysis and a urinary sediment showing numerous red cell casts. Blood pressure is 150/90 mmHg. Which immediate investigation would best guide early disease-specific therapy?

Start high-dose intravenous methylprednisolone now without further testing

Commence empirical plasma exchange immediately

Arrange urgent percutaneous renal biopsy today

Send urgent anti-GBM and ANCA serology

Treat as acute tubular necrosis and provide supportive care

In suspected pulmonary–renal syndromes, obtain urgent ANCA and anti-GBM serology promptly to guide disease-specific therapies.

The presentation is highly suggestive of a pulmonary–renal syndrome such as anti-GBM disease or ANCA-associated vasculitis. Urgent serology for anti-GBM antibodies and ANCA will rapidly help distinguish causes and guide specific early treatments (e.g. plasma exchange for anti-GBM). While high clinical suspicion may require early treatment, starting high-dose steroids or plasma exchange empirically without serology may be appropriate in some centres when delays are expected, but the best immediate diagnostic step to direct therapy is urgent serology. Renal biopsy is important for diagnosis and prognostication but may be deferred until initial serology and stabilisation; biopsy is invasive and may not be the initial immediate test in a patient with pulmonary haemorrhage. Treating as ATN would miss immune-mediated rapidly progressive glomerulonephritis and delay specific therapy.

3 / 10

Which of the following is generally regarded as an absolute indication for urgent initiation of renal replacement therapy (RRT) in a patient with AKI?

Uraemic pericarditis or encephalopathy

Serum creatinine above a specific numeric threshold

Oliguria lasting 6 hours

Mild metabolic acidosis responsive to intravenous bicarbonate

Chronic kidney disease stage 3 with new AKI but stable clinically

Initiate urgent RRT for life-threatening uraemic complications (pericarditis, encephalopathy) or other refractory metabolic disturbances, not based on a fixed creatinine number.

Uraemic complications such as pericarditis or encephalopathy indicate severe toxin accumulation and are widely regarded as urgent indications for dialysis irrespective of serum creatinine level. Absolute indications for RRT commonly include life-threatening electrolyte disturbances refractory to medical therapy, severe metabolic acidosis not responding to treatment, refractory pulmonary oedema, and uraemic complications (pericarditis/encephalopathy). A specific numeric creatinine threshold is not used because clinical context varies. Oliguria by itself (e.g. 6 hours) is not an absolute indication; duration, trends and associated derangements matter. Mild acidosis responsive to bicarbonate does not necessitate immediate RRT. CKD stage 3 with a stable clinical state does not by itself mandate urgent dialysis.

4 / 10

A 66-year-old patient in septic shock is developing worsening AKI in the ICU. Regarding choice of resuscitation fluid to minimise worsening kidney injury, which is the best option?

Hydroxyethyl starch (colloid)

Hypertonic saline (3%)

High-dose albumin infusion as first-line

No fluid; rely on vasopressors alone

Balanced crystalloid solution (e.g. plasmalyte/Ringer's lactate)

Use balanced crystalloids rather than chloride-rich colloids or high-volume 0.9% saline in septic patients at risk of AKI.

In patients with sepsis and risk of AKI, balanced crystalloids are generally preferred over 0.9% saline because large volumes of chloride-rich saline may be associated with hyperchloraemic metabolic acidosis and worse renal outcomes in some studies. Hydroxyethyl starch solutions are associated with increased risk of AKI and should be avoided. Hypertonic saline is not appropriate for routine sepsis resuscitation. Albumin may have a role in some patients (e.g. hypoalbuminaemia) but is not first-line for initial resuscitation to protect the kidney. Withholding fluids in a fluid-responsive, hypotensive septic patient is inappropriate; vasopressors are used once adequate intravascular volume is restored.

5 / 10

A 70-year-old woman with eGFR 28 mL/min/1.73m2 requires contrast-enhanced CT angiography. Which strategy is most evidence-based to reduce the risk of contrast-associated AKI?

Give oral N-acetylcysteine before and after the procedure

Withhold all antihypertensive medications on the day of the scan

Administer isotonic intravenous crystalloid hydration before and after contrast exposure

Use high-dose diuretics during contrast administration to maintain urine flow

Administer routine intravenous sodium bicarbonate for all patients

Peri-procedural isotonic crystalloid hydration is the cornerstone of prevention for contrast-associated AKI in at-risk patients.

The most evidence-based preventive measure for contrast-associated AKI in patients with reduced eGFR is adequate intravascular volume expansion with isotonic crystalloid (e.g. 0.9% saline or balanced crystalloids) before and after contrast exposure, unless contraindicated by fluid overload. Routine use of N-acetylcysteine has not been consistently shown to prevent contrast nephropathy and is not universally recommended. Withholding antihypertensives may be appropriate in selected patients (e.g. renin–angiotensin system blockers in volume-depleted patients) but is not a primary prevention strategy for contrast AKI. Diuretics during contrast administration are not recommended and can worsen renal perfusion. Routine sodium bicarbonate infusion has not demonstrated consistent benefit over saline and is not standard for all patients.

6 / 10

A patient with severe fluid overload and AKI is oliguric despite multiple boluses of loop diuretic. Which of the following statements best reflects the role of loop diuretics in AKI?

Loop diuretics are indicated to manage volume overload and may improve urine output but do not reduce the need for RRT or improve mortality

High-dose loop diuretics reduce mortality in AKI and should be used liberally

Thiazide diuretics are preferred over loop diuretics in oliguric AKI

Diuretics should be withheld entirely in AKI because they worsen renal perfusion

Continuous use of loop diuretics will prevent progression of AKI to CKD

Use loop diuretics to treat fluid overload in AKI, recognising they improve symptoms and urine output but have not been shown to change hard outcomes like need for RRT or survival.

Loop diuretics are useful to manage fluid overload and to attempt to convert oliguric to non-oliguric AKI, which may aid fluid management, but randomized data do not show that diuretics reduce progression to RRT or improve survival. They should be used judiciously; high-dose diuretics are not proven to reduce mortality. Thiazides are not preferred in oliguric AKI because they are weaker and less effective when urine output is low. Diuretics, when indicated, do not intrinsically worsen renal perfusion if used appropriately; withholding them entirely may leave volume overload untreated. Continuous loop infusion or combination therapy may be used for diuretic resistance, but they do not prevent AKI progression to CKD.

7 / 10

A 63-year-old man has a sudden rise in creatinine and inability to pass urine after radical pelvic surgery. He has suprapubic pain and a palpable bladder. What is the most appropriate immediate action?

Arrange urgent CT urogram to look for ureteric obstruction

Insert urinary (urethral) catheter for bladder decompression

Proceed directly to antegrade nephrostomy

Start empirical broad-spectrum antibiotics and observe

Schedule elective urology review next week

In suspected post-renal AKI from urinary retention, immediate bladder catheterisation is the first, often therapeutic, step.

The clinical features indicate acute lower urinary tract obstruction (acute urinary retention) causing post-renal AKI. Immediate bladder decompression with urethral catheterisation is the appropriate first step and is often rapidly diagnostic and therapeutic. CT urogram or imaging may be helpful if upper tract obstruction or ureteric injury is suspected after initial stabilisation, but they should not delay catheterisation. Antegrade nephrostomy is indicated for upper tract obstruction not relieved by lower tract catheterisation or when urethral access is not possible; it is not first-line for simple urinary retention. Starting antibiotics without addressing obstruction fails to relieve the cause and risks worsening renal injury. Elective review next week would be inappropriate given acute retention and rising creatinine.

8 / 10

A 61-year-old patient with AKI has serum potassium 6.9 mmol/L and ECG changes with peaked T waves and widening QRS. Which is the most urgent immediate treatment to reduce the risk of cardiac arrhythmia?

Intravenous insulin and glucose to shift potassium intracellularly

Nebulised salbutamol to promote cellular potassium uptake

Oral potassium-binding resin only

Intravenous calcium gluconate to stabilise the cardiac membrane

Start haemodialysis immediately without prior measures

In hyperkalaemia with ECG changes, give intravenous calcium immediately to stabilise the myocardium, then proceed to measures that lower serum potassium and consider dialysis if needed.

When hyperkalaemia is accompanied by ECG changes (peaked T waves, widened QRS), the immediate priority is to stabilise the cardiac membrane with intravenous calcium (calcium gluconate or calcium chloride) to reduce the risk of malignant arrhythmia. This should be done before attempts to shift potassium intracellularly (insulin/dextrose, nebulised beta-agonist) or remove potassium. Insulin+dextrose and nebulised salbutamol are important next steps to lower serum potassium but do not immediately stabilise the myocardium. Oral potassium binders act slowly and are not appropriate as the sole immediate therapy in the presence of ECG changes. Urgent dialysis may be required to remove potassium definitively, but calcium should be given immediately to protect the heart while preparing for dialysis or other therapies.

9 / 10

Which of the following hospitalised patients recovering from AKI most clearly requires specialist nephrology follow-up after discharge (rather than routine primary care review)?

A 45-year-old with transient Stage 1 AKI after brief gastroenteritis whose creatinine returned to baseline prior to discharge

A 70-year-old with AKI stage 1 related to reversible dehydration and preserved baseline eGFR

A 58-year-old who had Stage 3 AKI requiring temporary dialysis during admission but is now dialysis-independent

A 30-year-old with mild AKI attributable to a short course of aminoglycoside with normal renal function at discharge

An 82-year-old with stable CKD stage 3 and a minor creatinine fluctuation during admission

Arrange nephrology follow-up for patients who had stage 2–3 AKI, especially those who required RRT, as they have increased risk of CKD and complications.

Patients who experienced severe AKI (e.g. stage 3) or required renal replacement therapy during admission should have timely nephrology follow-up after discharge because of high risk of incomplete recovery and progression to chronic kidney disease. Those with transient low-stage AKI that resolved and patients with minor fluctuations or reversible causes often do not require routine nephrology follow-up beyond primary care unless other risks exist. The 58-year-old who required temporary dialysis is high risk and needs specialist follow-up for monitoring, medication reconciliation and planning if CKD or dialysis dependence emerges.

10 / 10

A haemodynamically unstable ICU patient with septic shock and multi-organ failure has severe AKI and is oliguric despite optimisation. What renal replacement modality is most appropriate in the immediate period for haemodynamic stability?

Intermittent haemodialysis (IHD) three times weekly

Peritoneal dialysis in the ICU

Intermittent haemofiltration with very high flow rates

Sustained low-efficiency daily dialysis (SLEDD) on the ward

Continuous renal replacement therapy (CRRT) in the ICU

CRRT is the preferred modality for haemodynamically unstable ICU patients requiring RRT because it minimises rapid fluid and solute shifts.

In haemodynamically unstable ICU patients, continuous renal replacement therapy (CRRT) is commonly preferred because it provides gentle, continuous solute and fluid removal with less haemodynamic perturbation compared with conventional intermittent haemodialysis. Intermittent haemodialysis (IHD) may cause rapid fluid and osmotic shifts that worsen hypotension. Peritoneal dialysis is generally not practical for rapid clearance needs in unstable, ventilated ICU patients, and has limitations in sepsis and with intra-abdominal concerns. Intermittent haemofiltration with very high flow rates or SLEDD may be used in some centres, but CRRT is the standard for immediate haemodynamic stability in many ICUs.

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Board-level postgraduate nephrology self-assessment.

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

Renal Physiology and Clinical Approach

1 / 10

An 82-year-old woman with chronic heart failure on chronic loop diuretic therapy is admitted with oliguria and a rise in creatinine from baseline 90 to 240 µmol/L. Urine sodium is 80 mmol/L and fractional excretion of sodium (FENa) is 3.5%. Which urinary finding is the most specific indicator of intrinsic acute tubular necrosis in this patient receiving diuretics?

Fractional excretion of urea (FEUrea)

Urine osmolality

Presence of muddy brown granular casts on urine microscopy

Spot urine sodium concentration

Fractional excretion of sodium (FENa)

Muddy brown granular casts on urine microscopy are a specific indicator of acute tubular injury; FEUrea can be useful when diuretics confound FENa.

Muddy brown granular casts and renal tubular epithelial cell casts on urine microscopy are highly specific for acute tubular injury. Diuretics can raise urine sodium and FENa, making those indices unreliable for distinguishing pre-renal physiology from ATN. FEUrea may be useful when diuretics confound FENa, but the question asks for the most specific indicator of ATN. Urine osmolality and spot urine sodium are also affected by diuretic therapy.

2 / 10

A 58-year-old man presents with palpitations. Serum potassium is 6.8 mmol/L and his ECG shows peaked T waves and a widened QRS. Which immediate therapy should be given first?

Intravenous insulin with 50% dextrose

Nebulised salbutamol

Intravenous furosemide

Oral sodium polystyrene sulfonate

Intravenous calcium (eg, calcium gluconate)

In life-threatening hyperkalaemia with ECG changes, give IV calcium immediately to stabilise myocardium, then implement potassium-shifting and removal strategies.

Correct answer: Intravenous calcium (option E). The immediate priority in hyperkalaemia with ECG changes is to stabilise the myocardium with IV calcium (calcium gluconate or calcium chloride) to reduce the risk of malignant arrhythmia. This does not lower serum potassium but protects the heart while definitive potassium-lowering therapies are given. Insulin with glucose (option A) and nebulised salbutamol (option B) are rapid potassium-shifting therapies and should follow calcium for membrane stabilisation. IV furosemide (option C) can promote renal potassium excretion if effective urine output will occur but is not the initial life-saving intervention. Oral ion-exchange resins (option D) act slowly and are not appropriate as first-line acute therapy for ECG changes.

3 / 10

A frail 78-year-old woman with marked sarcopenia has a serum creatinine of 80 µmol/L; her clinician suspects reduced GFR despite this ‘normal’ creatinine. Which investigation most reliably provides a better estimation of GFR in this patient?

Cystatin C–based estimated GFR

24-hour urine creatinine clearance

Calculate Cockcroft–Gault creatinine clearance

Serum creatinine alone is sufficient

Measure urinary albumin:creatinine ratio (ACR)

Use cystatin C–based eGFR when creatinine is unreliable (eg, sarcopenia) to improve accuracy of GFR estimation.

Correct answer: Cystatin C–based estimated GFR (option A). Cystatin C is less dependent on muscle mass than creatinine and gives a more accurate estimate of GFR in patients with low muscle mass/sarcopenia. Measured GFR with exogenous filtration markers (eg, iohexol) is the gold standard but is not listed here. A 24-hour urine creatinine clearance (option B) is error-prone (collection inaccuracies) and overestimates GFR due to tubular secretion; it is also still creatinine-based and affected by low muscle mass. Cockcroft–Gault (option C) is an estimate of creatinine clearance using serum creatinine and body weight and is unreliable in extremes of muscle mass. Serum creatinine alone (option D) is inadequate in sarcopenia. Urinary ACR (option E) assesses albuminuria rather than GFR.

4 / 10

A patient has the following arterial blood gas and electrolytes: Na+ 140 mmol/L, Cl− 100 mmol/L, HCO3− 12 mmol/L. Calculate the anion gap and assess the acid–base disturbance. Which is the best interpretation?

Normal anion gap metabolic acidosis

Mixed high-anion-gap metabolic acidosis and normal anion gap metabolic acidosis

Respiratory acidosis with metabolic compensation

High-anion-gap metabolic acidosis without an additional metabolic disorder

Metabolic alkalosis with respiratory compensation

Use the delta/delta (ΔAG/ΔHCO3) ratio to detect mixed metabolic acid–base disorders; 1–2 suggests a pure high-anion-gap metabolic acidosis.

Correct answer: High-anion-gap metabolic acidosis without an additional metabolic disorder (option D). Anion gap = Na − (Cl + HCO3) = 140 − (100 + 12) = 28 mmol/L (elevated; normal ~12). Delta AG = 28 − 12 = 16; delta HCO3 = 24 − 12 = 12; the delta/delta ratio ≈ 1.33, which falls within the 1–2 range consistent with a pure high-anion-gap metabolic acidosis (no concurrent normal anion gap acidosis or metabolic alkalosis). Option A is incorrect because the anion gap is elevated (so it is not a normal AG acidosis). Option B (mixed high AG + normal AG) would be suggested by a delta/delta <1. Option C and E are incorrect because the primary disorder is a metabolic acidosis (not primary respiratory or alkalosis).

5 / 10

Which patient with nephrotic syndrome has the highest long-term risk of venous thromboembolism and therefore is most often considered for individualized thromboprophylaxis?

A patient with diabetic nephropathy and moderate proteinuria

A patient with biopsy-proven membranous nephropathy with severe hypoalbuminaemia

A patient with minimal change disease, preserved albumin, on high-dose steroids

A patient with focal segmental glomerulosclerosis and controlled oedema

A patient with immune complex GN and low cholesterol

Membranous nephropathy with severe hypoalbuminaemia carries the highest VTE risk among nephrotic syndromes; thromboprophylaxis decisions should be individualized.

Correct answer: Membranous nephropathy with severe hypoalbuminaemia (option B). Membranous nephropathy is associated with the highest risk of venous thromboembolism among nephrotic syndromes, particularly when serum albumin is markedly low; such patients are most commonly considered for individualized prophylactic anticoagulation after weighing bleeding risk. Diabetic nephropathy (option A) typically has lower thrombotic risk attributable to nephrosis per se. Minimal change disease (option C) can be associated with nephrotic-range proteinuria and thrombotic risk if albumin is severely low, but membranous has the highest incidence. FSGS (option D) has increased risk but less than membranous on average. Immune complex GN with low cholesterol (option E) is not the typical high-thrombosis profile.

6 / 10

A 64-year-old man becomes oliguric after an episode of prolonged hypotension. Urine microscopy reveals numerous muddy brown granular casts. Which immediate management decision is the most appropriate?

Arrange urgent renal biopsy to establish diagnosis

Give high-dose loop diuretics to convert oliguria to non-oliguria

Administer intravenous albumin to restore renal perfusion

Initiate immediate chronic haemodialysis

Stop nephrotoxins and optimise haemodynamics (blood pressure/volume) as first-line supportive treatment

ATN management is supportive: correct haemodynamics and remove nephrotoxins; dialysis only for acute indications.

Correct answer: Stop nephrotoxins and optimise haemodynamics (option E). Muddy brown granular casts indicate acute tubular necrosis (ATN) due to ischaemic injury. Management is supportive: restore and maintain adequate renal perfusion, correct volume status, avoid or stop nephrotoxins, and treat the underlying cause. Renal biopsy (option A) is rarely required in typical ATN and is not first-line. High-dose loop diuretics (option B) do not improve renal recovery and are not recommended routinely to convert oliguria into non-oliguria. IV albumin (option C) may be used in specific circumstances (eg, hypoalbuminaemia with intravascular depletion) but is not universally indicated. Immediate initiation of chronic haemodialysis (option D) is unnecessary unless the patient has urgent indications for renal replacement therapy (refractory hyperkalaemia, severe acidaemia, volume overload or uraemia).

7 / 10

A patient with stage 4 CKD (eGFR ~22 mL/min/1.73 m2) develops recurrent hyperkalaemia (5.8–6.2 mmol/L) while on an ACE inhibitor that reduces proteinuria and blood pressure. The patient is otherwise stable. Which approach best aligns with guideline-based management to optimise kidney outcomes?

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

Reduce dietary potassium alone and continue the ACE inhibitor

Add an oral potassium-binding therapy to enable continuation of the ACE inhibitor

Start a thiazide diuretic to promote renal potassium excretion

Do nothing; accept the higher potassium as a consequence of renin–angiotensin blockade

When hyperkalaemia threatens RAS inhibitor therapy, consider potassium-lowering measures (eg, oral binders) to allow continuation of renoprotective drugs where appropriate.

Correct answer: Add an oral potassium-binding therapy (option C). Contemporary guidance supports using measures to control recurrent hyperkalaemia (including oral potassium binders) to enable continuation of renin–angiotensin system (RAS) inhibitors when these agents provide clear renal and cardiovascular benefit. Permanently stopping the ACE inhibitor (option A) may worsen long-term kidney and cardiovascular outcomes and should be a last resort after considering mitigation strategies. Diet alone (option B) may help but is often insufficient for recurrent hyperkalaemia. Thiazide diuretics (option D) have limited efficacy at low eGFR and may be ineffective; loop diuretics are favoured if diuretics are required. Doing nothing (option E) is inappropriate because recurrent hyperkalaemia risks arrhythmia and may require prompt management.

8 / 10

A 45-year-old woman with progressive dyspnoea has persistent severe metabolic acidaemia (arterial pH 7.09) despite optimisation of ventilation and fluids. Which of the following is the clearest indication to commence renal replacement therapy now?

Start urgent renal replacement therapy for refractory severe metabolic acidaemia

Delay RRT and give repeated boluses of sodium bicarbonate

Treat conservatively and aim to normalise pH with non-invasive ventilation

Administer intravenous albumin and observe

Arrange outpatient dialysis when available

Refractory severe metabolic acidaemia is an indication for urgent renal replacement therapy.

Correct answer: Start urgent renal replacement therapy for refractory severe metabolic acidaemia (option A). Severe refractory acidemia (eg, pH ≤7.1 that does not respond to supportive measures) is an established indication for urgent RRT because it can cause haemodynamic instability and reduced myocardial contractility. Repeated bicarbonate boluses (option B) are of limited benefit and can cause volume overload and sodium load; they may be used transiently but are not a substitute for RRT when acidaemia is refractory. Non-invasive ventilation (option C) is not a primary therapy for metabolic acidosis. IV albumin (option D) is not indicated to correct acid–base disturbance in this context. Arranging outpatient dialysis (option E) is inappropriate for an acute, life-threatening metabolic derangement.

9 / 10

A patient presents with a normal anion gap metabolic acidosis. Urine pH is 6.3 and the urine anion gap (Na + K − Cl) is positive. Which renal tubular disorder is most consistent with these findings?

Proximal (type 2) renal tubular acidosis

Distal (type 1) renal tubular acidosis

Hyperkalaemic (type 4) renal tubular acidosis

Metabolic acidosis due to loss of bicarbonate from the gastrointestinal tract

Respiratory acidosis with renal compensation

A high urine pH with a positive urine anion gap in normal AG metabolic acidosis points to distal RTA (impaired urinary acidification).

Correct answer: Distal (type 1) renal tubular acidosis (option B). In a normal anion gap metabolic acidosis, a urine pH >5.5 suggests impaired distal acidification consistent with distal RTA. A positive urine anion gap indicates low urinary ammonium excretion (low NH4+), supporting a renal cause for reduced acid excretion rather than gastrointestinal bicarbonate loss. Proximal RTA (option A) typically shows variable urine pH (can be <5.5 once plasma bicarbonate stabilises) and is associated with marked bicarbonaturia and other proximal tubular defects. Type 4 RTA (option C) is associated with hyperkalaemia and often a low urine pH may be seen; UAG findings vary. Gastrointestinal bicarbonate loss (option D) typically results in a negative UAG due to appropriate renal NH4+ excretion. Respiratory acidosis with renal compensation (option E) is not relevant to these urinary indices.

10 / 10

A patient has bilateral ureteric obstruction which is rapidly relieved. Over the next 24 hours urine output rises to 8 L with falling blood pressure and hypokalaemia. What is the best immediate management strategy?

Restrict fluids to limit further diuresis and allow repletion of intravascular volume later

Give a bolus of hypotonic (0.45%) saline to replace free water losses

Administer oral potassium supplements only and observe urine output

Replace urine losses with isotonic crystalloid guided by measured urine output and monitor electrolytes closely

Start continuous renal replacement therapy immediately to stop diuresis

After relief of obstruction, manage post-obstructive diuresis by replacing urine losses with isotonic fluid and correcting electrolytes while monitoring closely.

Correct answer: Replace urine losses with isotonic crystalloid guided by measured urine output and monitor electrolytes closely (option D). Post-obstructive diuresis can be physiologically appropriate and large, causing hypovolaemia and electrolyte losses (sodium, potassium). Management is to match losses with isotonic fluid (eg, 0.9% saline) guided by urine output, correct electrolyte deficits (eg, potassium), and monitor vitals and biochemistry frequently. Fluid restriction (option A) is inappropriate in the presence of ongoing large-volume losses and falling blood pressure. Hypotonic saline (option B) risks worsening hyponatraemia if sodium loss predominates; isotonic fluid is preferred for volume repletion. Oral potassium alone (option C) is insufficient when intravascular volume needs replacement and the patient may require IV supplementation. Immediate renal replacement therapy (option E) is not indicated to “stop” diuresis and would not address hypovolaemia.

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Postgraduate clinical case-vignette self-assessment. Complete all 10 questions to receive detailed explanations on the results page.

Hypophosphatemia and CKD-Mineral Bone Disorder Clinical Case Vignettes — Advanced

Advanced postgraduate clinical case-vignette assessment focused on Hypophosphatemia and CKD-Mineral Bone Disorder. Detailed explanations appear only after completion.

1 / 10

A patient with severe hypomagnesemia has a low PTH and hypocalcemia. Why may calcium replacement alone be ineffective?

Calcium replacement always worsens magnesium deficiency immediately

Calcium cannot be absorbed in any patient with CKD

Hypomagnesemia causes permanent calcitonin excess

PTH secretion and action remain impaired until magnesium is repleted

Magnesium is required for normal PTH secretion and peripheral PTH signaling. In severe deficiency, calcium may rise only transiently or remain low until magnesium repletion restores the hormonal response.

2 / 10

A patient with CKD G4 has persistent hyperphosphatemia and elevated PTH. Which first principle is most appropriate?

Stop monitoring phosphate because it is expected in CKD

Give routine phosphate supplementation

Suppress all PTH regardless of calcium and phosphate

Address dietary phosphate burden and evaluate phosphate-lowering therapy within CKD-MBD care

CKD-related phosphate retention contributes to secondary hyperparathyroidism and vascular or skeletal complications. Management uses dietary assessment, CKD-MBD monitoring, and individualized phosphate-lowering therapy rather than indiscriminate supplementation or complete PTH suppression.

3 / 10

A malnourished patient after refeeding develops profound hypophosphatemia, weakness, and respiratory failure. Which mechanism is most likely?

Primary hyperparathyroidism alone

Insulin-driven intracellular phosphate shift with increased cellular demand

Reduced intracellular phosphate uptake

Pseudohypophosphatemia from hyperalbuminemia

Refeeding increases insulin secretion and drives phosphate into cells for ATP and anabolic processes. In a patient with depleted total-body stores, serum phosphate can fall rapidly and cause respiratory muscle weakness, hemolysis, and cardiac dysfunction.

4 / 10

A patient with hypophosphatemia has glucosuria despite normal blood glucose, aminoaciduria, and bicarbonate wasting. Which process is most likely?

Proximal tubular dysfunction with renal phosphate wasting

Isolated distal sodium retention

Primary respiratory alkalosis

Pseudohypophosphatemia from hemolysis

Glucosuria with normal plasma glucose, aminoaciduria, bicarbonate wasting, and phosphate loss indicates proximal tubular dysfunction, as in Fanconi syndrome. The mechanism is impaired reabsorption of multiple filtered solutes in the proximal tubule.

5 / 10

A patient with severe hypophosphatemia develops muscle weakness and rhabdomyolysis. Which intervention is most important?

High-dose loop diuretic therapy

Immediate phosphate restriction

Careful phosphate replacement with monitoring for calcium-phosphate complications

Avoid measuring calcium

Severe symptomatic hypophosphatemia may require carefully dosed phosphate replacement, with attention to renal function and serial calcium, phosphate, and potassium values. Rapid or excessive replacement can cause hypocalcemia and calcium-phosphate precipitation.

6 / 10

A patient with CKD has high PTH, high alkaline phosphatase, low-normal calcium, and high phosphate. Which skeletal process is most consistent?

No bone effect from phosphate retention

Adynamic bone disease caused by excessive PTH activity

Osteomalacia from isolated hypercalcemia

High-turnover bone disease from secondary hyperparathyroidism

Elevated PTH and alkaline phosphatase with CKD and phosphate retention suggest increased bone turnover from secondary hyperparathyroidism. Adynamic bone disease is characterized by low turnover and often occurs when PTH is excessively suppressed.

7 / 10

A patient with hypophosphatemia has a high fractional excretion of phosphate and an elevated FGF23 level. Which mechanism is likely?

FGF23-mediated inhibition of proximal phosphate reabsorption and calcitriol production

PTH-independent increase in phosphate reabsorption

Increased intestinal phosphate absorption only

Laboratory artifact from low sodium

FGF23 lowers proximal tubular phosphate reabsorption and suppresses calcitriol synthesis, producing renal phosphate wasting and reduced intestinal phosphate absorption. Tumor-induced osteomalacia is a classic acquired setting, but inherited FGF23 disorders are also possible.

8 / 10

A dialysis patient has persistent hyperphosphatemia despite reported adherence to a phosphate binder. Which next step is most useful?

Automatically double the dose without review

Review timing with meals, binder type, dietary phosphate sources, and adherence

Stop all vitamin D analogues permanently

Recommend phosphate supplements

Phosphate binders work by binding dietary phosphate in the gastrointestinal tract, so timing with meals and the dietary source of phosphate are central. Assessment should also consider adherence, binder formulation, pill burden, and CKD-MBD treatment context before escalating therapy.

9 / 10

A patient with CKD has a very low PTH, normal calcium, and recurrent fractures while receiving intensive PTH-suppressive therapy. Which concern is greatest?

Acute phosphate depletion from diarrhea only

Uncontrolled secondary hyperparathyroidism

Adynamic bone disease with low bone turnover

Primary hyperaldosteronism

Very low PTH in CKD with fractures raises concern for adynamic bone disease, in which bone turnover and remodeling are suppressed. Excessive PTH suppression and calcium loading can contribute, so treatment should be reassessed rather than intensified reflexively.

10 / 10

A patient with hypophosphatemia from chronic antacid use has low urinary phosphate excretion. What does this indicate?

Distal renal tubular acidosis

Primary renal phosphate wasting

FGF23 excess is proven

Appropriate renal conservation consistent with reduced phosphate intake or absorption

Low urinary phosphate in hypophosphatemia indicates that the kidneys are conserving phosphate appropriately. Chronic antacid use can reduce gastrointestinal phosphate absorption, producing a low filtered phosphate load without primary renal wasting.

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Postgraduate clinical case-vignette self-assessment. Complete all 10 questions to receive detailed explanations on the results page.

Hypokalemia and Renal Potassium-Wasting Clinical Case Vignettes — Advanced

Advanced postgraduate clinical case-vignette assessment focused on Hypokalemia and renal potassium wasting. Detailed explanations appear only after completion.

1 / 10

A patient has potassium 2.6 mmol/L, hypertension, metabolic alkalosis, and suppressed renin. Which diagnosis is most likely?

Primary hyperaldosteronism

Renal tubular acidosis

Addison disease

Diarrhea-induced potassium loss

Hypertension with hypokalemic metabolic alkalosis and suppressed renin points toward mineralocorticoid activity, classically primary hyperaldosteronism. Gastrointestinal losses usually produce low blood pressure or volume depletion and do not cause persistent renal chloride wasting.

2 / 10

A patient with hypokalemia has a urine potassium-to-creatinine ratio that indicates ongoing renal potassium loss. Which additional finding supports vomiting rather than diuretic use?

Severe hyperphosphatemia

High urine chloride

Low urine chloride

Marked hypercalcemia

Vomiting causes chloride depletion and a low urine chloride concentration once the kidneys conserve chloride. Diuretics and some mineralocorticoid states usually maintain a higher urine chloride, although timing and recent treatment must be considered.

3 / 10

A patient with hypokalemia, normal blood pressure, metabolic alkalosis, and hypomagnesemia has recurrent episodes after starting a medication. Which drug class is most likely?

ACE inhibitor

Loop or thiazide diuretic

Potassium-sparing diuretic

Carbonic anhydrase inhibitor causing acidosis only

Loop and thiazide diuretics increase distal sodium delivery and activate mechanisms that promote renal potassium and magnesium wasting, often causing metabolic alkalosis. The clinical pattern is less consistent with ACE inhibition or potassium-sparing therapy.

4 / 10

A patient with hypokalemia and non-anion-gap metabolic acidosis has a positive urine anion gap. What does this suggest?

Appropriate ammonium excretion from diarrhea

Excessive bicarbonate ingestion without renal effects

Primary respiratory alkalosis

Impaired renal ammonium excretion

A positive urine anion gap is a surrogate for low urinary ammonium excretion, supporting a renal cause of non-anion-gap acidosis such as renal tubular acidosis. In diarrhea, ammonium excretion rises and the urine anion gap is typically negative.

5 / 10

A patient with severe hypokalemia has muscle weakness and ECG U waves. What is the most urgent management principle?

Prompt potassium replacement with cardiac monitoring and assessment of magnesium

Ignore the ECG because potassium is not cardiotoxic

Give sodium bicarbonate routinely

Restrict potassium until the ECG normalizes spontaneously

Severe hypokalemia can cause ventricular arrhythmias and neuromuscular weakness. Potassium should be replaced promptly with appropriate monitoring, and concomitant hypomagnesemia should be corrected because magnesium deficiency promotes persistent renal potassium wasting.

6 / 10

A patient with hypokalemia has hypertension, low renin, and low aldosterone. Which mechanism is most consistent?

Renal salt wasting

Primary adrenal insufficiency

ENaC activation or apparent mineralocorticoid excess

Proximal renal tubular acidosis

Low renin and low aldosterone with hypertension suggests a non-aldosterone mineralocorticoid effect, such as ENaC activation or apparent mineralocorticoid excess. These states increase sodium retention and distal potassium secretion without elevated aldosterone.

7 / 10

A patient with hypokalemia and metabolic alkalosis has a high urine chloride and a history of laxative use. Which interpretation is most appropriate?

Laxatives alone fully explain the urine chloride pattern

Urine chloride is never useful in metabolic alkalosis

The result proves primary hyperaldosteronism

Consider a concurrent renal chloride-wasting process or recent diuretic exposure

Laxative-associated diarrhea usually produces a low urine chloride due to extrarenal chloride loss. A persistently high urine chloride should prompt review for diuretics, vomiting with recent saline, mineralocorticoid states, or inherited salt-wasting disorders rather than attributing everything to laxatives.

8 / 10

A patient with hypokalemia and hypertension has an adrenal nodule and an elevated aldosterone-to-renin ratio. What is the next diagnostic principle?

Diagnose pheochromocytoma solely from the potassium level

Confirm autonomous aldosterone secretion before subtype evaluation

Start potassium restriction

Assume familial periodic paralysis

An elevated aldosterone-to-renin ratio is a screening result, not by itself definitive proof. Confirmatory testing for autonomous aldosterone secretion is generally considered before adrenal vein sampling or other subtype-directed evaluation, depending on the clinical context.

9 / 10

A patient with hypokalemia has a normal acid-base status and episodic weakness after carbohydrate-rich meals. Which process is most likely?

Transcellular potassium shift such as periodic paralysis

Chronic gastrointestinal potassium loss

Primary renal potassium wasting in every episode

Pseudohypokalemia from thrombocytosis

Episodic weakness after carbohydrate loading with otherwise limited evidence of total-body potassium depletion suggests a transcellular shift, as in periodic paralysis. The distinction matters because aggressive potassium replacement can cause rebound hyperkalemia when potassium shifts back extracellularly.

10 / 10

A patient on a loop diuretic remains hypokalemic despite replacement. Which concurrent abnormality commonly makes correction difficult?

Isolated hyperchloremia

Hypernatremia alone

Hypomagnesemia

High HDL cholesterol

Magnesium deficiency increases renal potassium secretion and impairs correction of hypokalemia. Repletion of potassium without addressing magnesium may produce a poor response, particularly in patients receiving ongoing diuretic therapy.

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Difficulty: Advanced postgraduate self-assessment focused on Thrombotic Microangiopathy Pathology Cases. Complete all 10 questions to view detailed clinical explanations on the results page.

Thrombotic Microangiopathy Pathology Cases — Advanced

Advanced postgraduate nephrology self-assessment focused on Thrombotic Microangiopathy Pathology Cases. Complete all 10 questions to view detailed clinical explanations on the results page.

1 / 10

Which renal biopsy lesion is most characteristic of acute thrombotic microangiopathy?

Fibrin thrombi with endothelial swelling and mesangiolysis

Subepithelial humps

Diffuse podocyte foot-process effacement only

Granular IgA in the mesangium only

Acute renal TMA reflects endothelial injury and can show fibrin or platelet thrombi, endothelial swelling, mesangiolysis, and arteriolar damage. The pathology should trigger assessment for thrombocytopenia, hemolysis, hypertension, pregnancy, drugs, complement, and systemic disease.

2 / 10

A patient has thrombocytopenia, schistocytes, neurologic symptoms, and AKI. Which urgent test is most relevant while treatment is considered?

Anti-PLA2R antibody only

ADAMTS13 activity and inhibitor testing

Urine eosinophils only

Serum IgA alone

The combination suggests a systemic TMA and raises concern for TTP, in which severe ADAMTS13 deficiency is typical. Testing should not delay urgent specialist-directed management when the clinical probability is high.

3 / 10

Which biopsy feature suggests chronic TMA rather than only acute endothelial injury?

Isolated interstitial edema

Only fresh luminal fibrin

Double-contour capillary walls and arteriolar intimal fibrosis

A single cellular crescent

Chronic TMA can produce duplicated or double-contoured GBM, mesangiolysis, arteriolar intimal fibrosis, and onion-skin changes. These lesions indicate repeated or persistent endothelial injury and may be accompanied by chronic ischemic scarring.

4 / 10

A pregnant patient develops hypertension, thrombocytopenia, hemolysis, and AKI. Which principle is most important?

Use kidney biopsy as the only initial test

Assume all cases are simple preeclampsia

Delay evaluation until delivery regardless of severity

Urgently distinguish pregnancy-related TMA from TTP, complement-mediated TMA, and other causes with multidisciplinary evaluation

Pregnancy-associated TMA has overlapping phenotypes and may reflect preeclampsia/HELLP, TTP, complement-mediated disease, or other secondary causes. Timing, ADAMTS13, complement evaluation, systemic findings, and response to delivery or treatment guide management.

5 / 10

Which medication is a recognized trigger of secondary TMA in susceptible patients?

Calcineurin inhibitors

Topical emollients

Oral iron in every patient

Saline infusion

Calcineurin inhibitors can cause endothelial injury and secondary TMA, as can several other drugs including certain antineoplastics and antiplatelet agents. Medication review is essential, but stopping or changing therapy must be coordinated with the treating specialty.

6 / 10

What does mesangiolysis represent in renal TMA?

A specific antibody deposit

Disruption and dissolution of the mesangial matrix from endothelial injury

A normal aging change

Pure podocyte apoptosis

Mesangiolysis is a morphologic consequence of severe endothelial and mesangial injury, producing loss or dissolution of mesangial architecture. It supports TMA in the right context but should be interpreted alongside other lesions and clinical data.

7 / 10

A patient has renal-limited TMA, normal ADAMTS13, and persistent disease without an obvious trigger. Which mechanism deserves consideration?

Primary membranous nephropathy

Isolated minimal change disease

Complement dysregulation causing complement-mediated TMA

Simple cystitis

Complement-mediated TMA can occur with genetic or acquired dysregulation of the alternative pathway, even when systemic hemolysis is modest. Complement studies, genetic testing, trigger assessment, and expert review may inform diagnosis and treatment.

8 / 10

Which laboratory combination supports microangiopathic hemolysis?

Low LDH and reticulocytopenia only

High haptoglobin with no schistocytes

Isolated elevated serum albumin

Elevated LDH, low haptoglobin, schistocytes, and an indirect bilirubin rise

Microangiopathic hemolysis is suggested by red-cell fragmentation, elevated LDH, reduced haptoglobin, and often indirect hyperbilirubinemia with reticulocytosis. The pattern should be interpreted with platelet count and organ injury.

9 / 10

Why can kidney biopsy fail to identify the cause of TMA by itself?

Many etiologies produce overlapping acute and chronic endothelial lesions

TMA never affects the kidney

Biopsy always identifies the mutation

Clinical data are unnecessary

Renal TMA is a pattern of injury rather than a single disease. Hypertension, pregnancy, drugs, infection, transplantation, autoimmune disease, TTP, and complement dysregulation can overlap histologically, so cause requires clinicopathologic integration.

10 / 10

Which finding would favor chronic ischemic injury accompanying TMA?

Only reversible endothelial swelling

Global glomerulosclerosis, interstitial fibrosis, tubular atrophy, and arterial intimal sclerosis

Pure neutrophilic interstitial inflammation

Subepithelial humps alone

Chronic ischemic lesions indicate cumulative vascular injury and reduced recovery potential. The activity-chronicity distinction helps determine whether removing a trigger or treating complement-mediated injury is likely to improve function.

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Difficulty: Advanced postgraduate self-assessment focused on Tubulointerstitial Nephritis Pathology Cases. Complete all 10 questions to view detailed clinical explanations on the results page.

Tubulointerstitial Nephritis Pathology Cases — Advanced

Advanced postgraduate nephrology self-assessment focused on Tubulointerstitial Nephritis Pathology Cases. Complete all 10 questions to view detailed clinical explanations on the results page.

1 / 10

A biopsy in acute interstitial nephritis most typically shows which combination?

Interstitial edema with inflammatory infiltrates and tubulitis

Diffuse subepithelial deposits with spikes

Linear GBM IgG staining

Mesangial IgA dominance

Acute interstitial nephritis is characterized by interstitial edema and inflammatory infiltrates, often with tubulitis. Eosinophils may be present but are neither required nor specific; the drug timeline and clinical context remain essential.

2 / 10

Which feature favors chronic tubulointerstitial nephritis over acute interstitial nephritis?

Only interstitial edema

Interstitial fibrosis, tubular atrophy, and chronic inflammatory infiltrates

A single day of pyuria

Transient glycosuria alone

Chronic tubulointerstitial injury produces fibrosis, tubular atrophy, and chronic inflammatory infiltrates, with progressive loss of concentrating ability and eGFR. These lesions indicate chronicity and are less likely to reverse after removing a trigger.

3 / 10

A biopsy shows intratubular crystals with acute tubular injury. Which clinical step is most important?

Start anticoagulation for every patient

Assume immune-complex GN

Identify the drug or metabolic exposure and correct volume and urine chemistry when appropriate

Ignore the crystals as an incidental finding

Crystal nephropathy requires identification of the responsible exposure or metabolic abnormality. Stopping the culprit, restoring appropriate hydration, correcting urine chemistry when evidence supports it, and monitoring obstruction or AKI can prevent further injury.

4 / 10

What is the principal pathology in analgesic nephropathy?

Isolated glomerular endotheliosis

Pure membranous nephropathy

Diffuse crescentic GN in all cases

Chronic tubulointerstitial injury with papillary necrosis in an appropriate exposure context

Chronic analgesic exposure can cause papillary necrosis and chronic tubulointerstitial nephritis. The diagnosis requires exposure history and clinicopathologic correlation; hematuria, concentrating defects, sterile pyuria, or progressive CKD may occur.

5 / 10

Which biopsy pattern is compatible with sarcoid-associated interstitial nephritis?

Noncaseating granulomatous interstitial inflammation after excluding infection and other causes

Linear IgG along the GBM

Subepithelial humps only

Pure podocyte effacement

Granulomatous interstitial nephritis can occur with sarcoidosis, drugs, infections, and other systemic conditions. Granulomas are not specific, so stains, cultures, exposure history, imaging, and systemic evaluation are required before attributing them to sarcoidosis.

6 / 10

A patient with Sjögren syndrome has hypokalemic hyperchloremic metabolic acidosis and biopsy-proven interstitial nephritis. Which tubular defect is likely?

Isolated proximal glucose wasting only

Distal renal tubular acidosis from impaired acid secretion

Nephrogenic diabetes insipidus alone

A primary glomerular filtration defect

Autoimmune tubulointerstitial disease, especially with Sjögren syndrome, can impair distal acid secretion and cause hypokalemic normal-anion-gap metabolic acidosis. Urine pH, potassium, bicarbonate, and other tubular findings help characterize the defect.

7 / 10

Which finding supports acute pyelonephritis rather than sterile drug-associated interstitial nephritis?

Smooth linear GBM staining

Only eosinophils in blood

Neutrophilic tubulointerstitial inflammation with compatible infection evidence

Diffuse foot-process effacement

Acute pyelonephritis produces neutrophilic interstitial inflammation and tubulitis, often with clinical or microbiologic evidence of infection. Drug-associated AIN may have pyuria but usually requires a different exposure and exclusion of infection.

8 / 10

A biopsy shows tubular injury and numerous light-chain casts. Which process should be considered urgently?

Simple dehydration only

Primary minimal change disease

Isolated anti-GBM disease

Monoclonal immunoglobulin-related cast nephropathy

Light-chain cast nephropathy results from filtered monoclonal free light chains interacting with tubular proteins and obstructing or injuring distal nephron segments. Serum and urine monoclonal studies and rapid hematologic evaluation are important.

9 / 10

Which laboratory pattern is typical of proximal tubular dysfunction?

Phosphate wasting, normoglycemic glycosuria, aminoaciduria, and bicarbonate loss

Persistent high urine pH with no bicarbonate loss

Only heavy albuminuria

Linear complement staining

Proximal tubule injury can cause Fanconi-type losses of phosphate, glucose despite normal serum glucose, amino acids, bicarbonate, urate, and low-molecular-weight proteins. The pattern helps distinguish tubular from primarily glomerular disease.

10 / 10

When should kidney biopsy be considered in suspected AIN?

Only after five years of CKD

When diagnostic uncertainty or the treatment decision is substantial after initial evaluation

Never, because urine tests are definitive

Only when proteinuria is absent

Biopsy is useful when the diagnosis is uncertain, kidney function is worsening, an essential medication cannot be stopped, or corticosteroid treatment carries meaningful risk. It can separate active AIN from infection, tubular injury, obstruction, or chronic scarring.

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Difficulty: Advanced postgraduate self-assessment focused on Immunosuppressant Pharmacology in Kidney Transplantation. Complete all 10 questions to view detailed clinical explanations on the results page.

Immunosuppressant Pharmacology in Kidney Transplantation — Advanced

Advanced postgraduate nephrology self-assessment focused on Immunosuppressant Pharmacology in Kidney Transplantation. Complete all 10 questions to view detailed clinical explanations on the results page.

1 / 10

Tacrolimus nephrotoxicity is most commonly related to which mechanism?

Calcineurin-mediated renal vasoconstriction and chronic arteriolar injury

Selective destruction of podocytes by anti-GBM antibodies

Ureteric stone formation in every patient

Complement deficiency

Tacrolimus can cause dose-related afferent arteriolar vasoconstriction and, with chronic exposure, arteriolar hyalinosis and interstitial fibrosis. Trough levels, drug interactions, blood pressure, magnesium, and biopsy findings may be needed to distinguish toxicity from rejection.

2 / 10

Which interaction can substantially increase tacrolimus exposure?

A nonabsorbed antacid only

A strong CYP3A inhibitor such as clarithromycin

Topical emollient

Normal dietary sodium

Tacrolimus is metabolized through CYP3A pathways and is a substrate for P-glycoprotein. Macrolides, azole antifungals, some calcium-channel blockers, and grapefruit can increase exposure, so levels and toxicity risk require prompt reassessment.

3 / 10

Mycophenolate mofetil primarily inhibits which pathway?

Calcineurin phosphatase directly

Cyclooxygenase-2 irreversibly

Inosine monophosphate dehydrogenase and de novo guanine synthesis

mTOR exclusively

Mycophenolate inhibits inosine monophosphate dehydrogenase, limiting de novo guanine synthesis in lymphocytes. Dose-limiting effects include gastrointestinal toxicity, leukopenia, infection risk, and teratogenicity, with monitoring tailored to the clinical situation.

4 / 10

Which adverse effect is particularly associated with mTOR inhibitors such as sirolimus?

Permanent suppression of erythropoietin

Immediate anti-GBM antibody formation

Universal severe hypocalcemia

Proteinuria, dyslipidemia, impaired wound healing, and mouth ulcers

mTOR inhibitors can cause dyslipidemia, oral ulcers, impaired wound healing, cytopenias, pneumonitis, and proteinuria. They may be useful in selected patients but require assessment of graft function, proteinuria, wound status, and drug levels.

5 / 10

A transplant recipient has rising creatinine and a low tacrolimus trough. What is the most important next principle?

Assess adherence, interactions, timing of the level, obstruction, infection, and rejection rather than assuming one cause

Double tacrolimus without evaluation

Stop all immunosuppression

Diagnose chronic rejection from one laboratory value

A low trough may reflect nonadherence, drug interaction, malabsorption, incorrect timing, or intentional dose reduction. Graft dysfunction also requires assessment for obstruction, infection, rejection, and other injury; treatment should not be based on the level alone.

6 / 10

Why is therapeutic drug monitoring useful for tacrolimus?

Tacrolimus has no clinically meaningful interactions

Exposure varies between patients and over time, while toxicity and rejection risks are concentration-sensitive

Trough levels predict every biopsy diagnosis

Monitoring replaces clinical examination

Tacrolimus pharmacokinetics vary with genetics, interacting drugs, diarrhea, liver function, adherence, and time after transplant. Levels help guide exposure but must be interpreted with graft function, symptoms, blood pressure, electrolytes, and biopsy when indicated.

7 / 10

Which counseling point is most important for a patient taking mycophenolate?

Ignore diarrhea because it cannot affect exposure

Stop contraception because mycophenolate improves fertility

Discuss contraception, pregnancy avoidance, infection risk, and blood-count monitoring

Avoid all vaccines permanently

Mycophenolate is teratogenic and can cause cytopenias and infection. Counseling should cover reproductive planning, reliable contraception when appropriate, laboratory monitoring, infection precautions, and the need to report severe gastrointestinal symptoms or bleeding.

8 / 10

A transplant recipient develops tremor, hypertension, hyperglycemia, and hypomagnesemia. Which drug effect is most likely?

Steroid withdrawal

Isolated mycophenolate malabsorption

C3 glomerulopathy

Calcineurin-inhibitor toxicity

Tremor, hypertension, hyperglycemia, and renal magnesium wasting are characteristic calcineurin-inhibitor toxicities. The clinician should review level timing and interacting agents and evaluate graft function before adjusting therapy.

9 / 10

Which statement about switching immunosuppression is safest?

A planned change requires transplant-team oversight, therapeutic monitoring, and reassessment of rejection and toxicity risk

Any patient can switch abruptly without monitoring

Stopping the antimetabolite always prevents rejection

Drug levels are irrelevant after conversion

Immunosuppressant conversion changes exposure and the balance between rejection and toxicity. It should be coordinated by the transplant team with overlap or taper plans, drug-level monitoring when applicable, laboratory follow-up, and assessment of infection, malignancy, and reproductive risks.

10 / 10

A patient on tacrolimus develops severe diarrhea. Why may the tacrolimus level rise unexpectedly?

Diarrhea always lowers tacrolimus exposure

Intestinal inflammation and altered metabolism can increase bioavailability

Tacrolimus is destroyed in the colon

Diarrhea has no pharmacokinetic effect

Diarrhea can increase tacrolimus exposure through altered intestinal CYP3A and transporter activity, while dehydration can worsen nephrotoxicity. Prompt level and kidney-function monitoring is appropriate rather than assuming underexposure.

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Difficulty: Advanced postgraduate self-assessment focused on Nephrotoxic Drug Syndromes. Complete all 10 questions to view detailed clinical explanations on the results page.

Nephrotoxic Drug Syndromes — Advanced

Advanced postgraduate nephrology self-assessment focused on Nephrotoxic Drug Syndromes. Complete all 10 questions to view detailed clinical explanations on the results page.

1 / 10

A patient develops AKI, rash, fever, and pyuria two weeks after starting a proton-pump inhibitor. Which renal syndrome is most likely?

Acute interstitial nephritis

Pure postrenal obstruction

Isolated renal-vein thrombosis

Chronic diabetic nephropathy

Drug-associated acute interstitial nephritis may present with AKI, pyuria, hematuria, rash, or fever, although the classic triad is often incomplete. A careful drug timeline and evaluation for competing causes are essential; biopsy may be needed when the diagnosis or treatment decision is uncertain.

2 / 10

Which biopsy finding most strongly supports acute tubular injury from an ischemic or nephrotoxic insult?

Diffuse subepithelial immune deposits

Tubular epithelial flattening, loss of brush border, and luminal debris

Linear IgG along the GBM

Mesangial IgA-dominant staining

Acute tubular injury is characterized by epithelial simplification, brush-border loss, dilation, detachment, and granular casts. These findings differ from immune-complex glomerular disease and should be interpreted with clinical timing and urine findings.

3 / 10

Aminoglycoside nephrotoxicity is most closely related to which pattern?

Exclusive ureteric obstruction

Direct podocyte antibody formation

Proximal tubular accumulation and injury

Mesangial proliferation only

Aminoglycosides accumulate in proximal tubular cells and can cause dose- and duration-related tubular injury. Risk increases with repeated exposure, high concentrations, concomitant nephrotoxins, and reduced renal reserve, so monitoring and de-escalation are important.

4 / 10

A patient develops AKI and eosinophilia after an antibiotic, with sterile pyuria. What is the most appropriate immediate medication action when clinically feasible?

Wait for creatinine to normalize before reviewing medications

Increase the suspected drug dose

Add a second nephrotoxin

Stop the suspected offending drug and substitute an appropriate alternative

Prompt withdrawal of a suspected culprit is a central intervention in drug-associated AIN, provided an appropriate alternative is available. The broader evaluation should exclude infection, obstruction, and other causes, with biopsy or corticosteroids considered in selected cases.

5 / 10

Which drug class can cause hemodynamic AKI by reducing afferent arteriolar vasodilation?

NSAIDs

Loop diuretics only

Proton-pump inhibitors only

Erythropoiesis-stimulating agents

NSAIDs inhibit renal prostaglandin synthesis, reducing afferent arteriolar vasodilation, especially during volume depletion or reduced effective arterial volume. The risk is amplified when combined with diuretics and renin-angiotensin system blockade.

6 / 10

A patient taking tenofovir develops phosphate wasting, glycosuria with normal serum glucose, and tubular proteinuria. Which lesion is most likely?

Primary membranous nephropathy

Proximal tubular dysfunction

Renal-limited anti-GBM disease

Collecting-duct obstruction

Proximal tubular dysfunction can cause phosphate wasting, normoglycemic glycosuria, bicarbonate loss, aminoaciduria, and tubular proteinuria. The pattern supports a proximal tubulopathy and should prompt review of exposure, duration, alternative agents, and kidney function.

7 / 10

Which finding favors pigment nephropathy rather than immune-complex GN?

Linear GBM staining

Low complement with dysmorphic RBCs and RBC casts

Positive urine blood with few or no red blood cells and a compatible exposure

Subepithelial humps

Myoglobin or hemoglobin can produce a heme-positive dipstick with few red cells. Clinical context such as rhabdomyolysis or hemolysis, creatine kinase, plasma free hemoglobin, and sediment findings help distinguish pigment injury from glomerular inflammation.

8 / 10

A patient with AKI has recent high-dose acyclovir exposure and crystalline material in the urine. Which mechanism is most plausible?

Renal cortical necrosis from hypertension

Anti-PLA2R antibody production

Complement-only glomerulopathy

Intrarenal crystal precipitation causing tubular obstruction and injury

Some drugs and metabolites precipitate in tubular fluid, particularly with high doses, low urine volume, or pre-existing impairment. Management includes stopping or changing the drug when possible, correcting volume status, and avoiding further nephrotoxic exposure.

9 / 10

Which approach best distinguishes drug-associated AIN from acute tubular injury when the diagnosis remains uncertain?

Integrate timeline, urinalysis, systemic findings, imaging, and sometimes kidney biopsy

Use eosinophiluria as a definitive test

Assume every AKI after medication is AIN

Rely only on a single fractional excretion value

No single urine biomarker reliably establishes AIN. Diagnostic reasoning integrates exposure timing, pyuria or WBC casts, rash or fever, hemodynamics, ultrasound, competing diagnoses, and, when management depends on certainty, biopsy.

10 / 10

Why should recurrent exposure to a drug that previously caused AIN generally be avoided?

Tolerance is guaranteed after the first episode

Re-exposure may trigger recurrent and potentially more severe interstitial inflammation

AIN only occurs once

Re-exposure improves renal recovery

A prior episode strongly raises concern for recurrence with re-exposure. The culprit should be documented clearly, alternatives selected, and future clinicians informed because recurrent interstitial inflammation can accelerate chronic scarring and reduce recovery.

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Postgraduate self-assessment focused on C3 Glomerulopathy. Complete all 10 questions to view detailed clinical explanations on the results page.

C3 Glomerulopathy — Advanced

Advanced postgraduate nephrology self-assessment on C3 Glomerulopathy. Difficulty: Advanced. Explanations are shown after quiz completion.

1 / 10

C3 glomerulopathy is primarily caused by dysregulation of:

The alternative complement pathway

The coagulation cascade only

The classical pathway exclusively

Renin secretion

Review the glomerular disease principles in this topic.

Correct: The alternative complement pathway.

C3 glomerulopathy reflects abnormal alternative-pathway activation and regulation.

2 / 10

The characteristic immunofluorescence finding is dominant deposition of:

Linear IgG only

C3 with absent or limited immunoglobulin

IgA alone in every case

C1q only

Review the glomerular disease principles in this topic.

Correct: C3 with absent or limited immunoglobulin.

Dominant C3 staining with little immunoglobulin supports C3 glomerulopathy.

3 / 10

Which serum complement result is common in active C3 glomerulopathy?

Always low C4 with normal C3

High C3 in every patient

Low C3

Absent serum albumin by definition

Review the glomerular disease principles in this topic.

Correct: Low C3.

C3 is often reduced because of alternative-pathway consumption, although normal levels do not exclude disease.

4 / 10

A useful evaluation in C3 glomerulopathy includes:

Only serum sodium

Only anti-PLA2R antibody

No evaluation for monoclonal gammopathy

Complement studies, nephritic-factor testing, and assessment for genetic or secondary drivers

Review the glomerular disease principles in this topic.

Correct: Complement studies, nephritic-factor testing, and assessment for genetic or secondary drivers.

The evaluation seeks acquired and genetic complement abnormalities and secondary conditions such as monoclonal gammopathy.

5 / 10

Dense deposit disease is distinguished ultrastructurally by:

Highly electron-dense intramembranous deposits within the GBM

Subepithelial humps only

Linear IgG deposits only

Amyloid fibrils

Review the glomerular disease principles in this topic.

Correct: Highly electron-dense intramembranous deposits within the GBM.

Dense deposit disease is the intramembranous ultrastructural form within the C3G spectrum.

6 / 10

C3 glomerulopathy may clinically present with:

Only isolated edema with no urinary abnormalities

Hematuria, proteinuria, hypertension, and progressive kidney dysfunction

Only hypernatremia

Exclusive pulmonary hemorrhage

Review the glomerular disease principles in this topic.

Correct: Hematuria, proteinuria, hypertension, and progressive kidney dysfunction.

Clinical expression ranges from hematuria and proteinuria to nephritic or nephrotic syndrome and CKD progression.

7 / 10

A monoclonal gammopathy in an adult with C3 glomerulopathy is important because it may:

Exclude kidney disease

Guarantee spontaneous remission

Drive complement dysregulation and require clone-directed evaluation

Only cause respiratory alkalosis

Review the glomerular disease principles in this topic.

Correct: Drive complement dysregulation and require clone-directed evaluation.

Monoclonal proteins can activate or dysregulate complement and may alter treatment strategy.

8 / 10

Kidney biopsy is important in suspected C3 glomerulopathy because it:

Replaces all complement testing

Is unnecessary when C3 is low

Diagnoses every genetic mutation

Establishes the pattern of complement-dominant glomerular injury and chronicity

Review the glomerular disease principles in this topic.

Correct: Establishes the pattern of complement-dominant glomerular injury and chronicity.

Biopsy defines the renal lesion and its chronicity, while complement testing addresses mechanism.

9 / 10

Treatment of C3 glomerulopathy should first address:

Supportive kidney care and any identifiable secondary driver

Routine high-dose immunosuppression for every patient

Avoidance of blood-pressure control

No assessment of proteinuria

Review the glomerular disease principles in this topic.

Correct: Supportive kidney care and any identifiable secondary driver.

Supportive care and treatment of secondary causes are central; immunomodulatory therapy is individualized.

10 / 10

A major prognostic marker in C3 glomerulopathy is:

A single normal C3 measurement

Persistent proteinuria and declining eGFR

Hair loss

Serum chloride alone

Review the glomerular disease principles in this topic.

Correct: Persistent proteinuria and declining eGFR.

Ongoing proteinuria and loss of filtration are clinically meaningful markers of progression.

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