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.

Tubulointerstitial Disease and Nephrotoxicity

Ten board-style single-best-answer questions covering diagnosis, investigation, acute and chronic management, complications, and pathology of tubulointerstitial disorders and nephrotoxicity.

1 / 10

A 62-year-old man develops progressive rise in serum creatinine from baseline 110 to 420 µmol/L over 10 days. He has fever, a maculopapular rash and eosinophilia. He started a proton-pump inhibitor (PPI) 3 weeks ago. Urinalysis shows white cells and white-cell casts; urine eosinophils are present. Which is the most appropriate immediate management?

Continue the PPI and observe renal function for 1 week

Stop the PPI and start systemic corticosteroid therapy promptly

Immediate renal biopsy before any treatment

Start empirical broad‑spectrum antibiotics for presumed pyelonephritis

Start urgent haemodialysis and defer other measures

In suspected drug-induced AIN stop the offending drug; for severe or progressive AKI consider early corticosteroids after excluding other causes.

This presentation is classical for drug-induced acute interstitial nephritis (AIN): recent new drug exposure, fever, rash, eosinophilia, pyuria and white-cell casts with rapid rise in creatinine. The first and immediate step is to stop the offending drug. In cases with severe or rapidly progressive renal impairment (large creatinine rise over days, oligo/anuria or failure to improve after withdrawal) early systemic corticosteroids are indicated and are associated with improved renal recovery. Immediate renal biopsy is not required in every case if clinical picture is typical and there are no contraindications to empiric steroids; biopsy is reserved for atypical presentations, diagnostic uncertainty, or where steroid therapy is being considered but diagnosis is unclear. Empiric antibiotics without evidence of infection are inappropriate. Haemodialysis is only indicated for standard indications (refractory hyperkalaemia, severe acidosis, volume overload, uremic complications) and is not first‑line purely to treat AIN.

2 / 10

Which of the following best describes the principal pathophysiological mechanism of aminoglycoside nephrotoxicity?

Immune complex deposition in glomeruli causing nephritic syndrome

Allergic interstitial inflammation mediated by T‑cells

Intravascular haemolysis causing pigment nephropathy

Accumulation within proximal tubular cells causing mitochondrial injury and acute tubular necrosis

Pre‑renal vasoconstriction from systemic hypotension

Aminoglycosides cause nephrotoxicity via proximal tubular accumulation and direct tubular cell injury leading to ATN; dosing strategies and monitoring minimise risk.

Aminoglycosides are taken up by proximal tubular epithelial cells and accumulate in lysosomes and mitochondria, causing oxidative and mitochondrial injury that results in proximal tubular cell dysfunction and acute tubular necrosis (ATN). They are not primarily associated with immune complex glomerulonephritis, allergic interstitial nephritis, haemolysis-related pigment nephropathy, or systemic hypotension as the main mechanism. Clinical features include non-oliguric AKI, rising creatinine typically after several days of therapy, and granular casts on urine microscopy.

3 / 10

You are planning a CT angiogram in a 74-year-old woman with chronic stable angina. Her eGFR is 28 mL/min/1.73 m2. Which of the following is the most evidence‑based preventive measure to reduce risk of contrast-associated AKI?

Peri-procedural intravenous isotonic (normal) saline hydration

Routine high‑dose N‑acetylcysteine in all patients

Peri-procedural intravenous calcium channel blocker

No special measures are required beyond standard monitoring

Oral sodium bicarbonate is superior to saline and should be used instead

Adequate isotonic saline hydration around the time of contrast exposure is the primary preventive measure for patients at high risk of contrast-associated AKI.

For patients at increased risk of contrast‑associated AKI (eg markedly reduced eGFR), the most evidence-supported preventive strategy is adequate intravascular volume expansion with isotonic crystalloid (normal saline) commenced before and continued after contrast exposure. Routine use of N‑acetylcysteine has conflicting evidence and is no longer uniformly recommended as a sole preventive strategy. Calcium channel blockers are not indicated to prevent contrast nephropathy. Saying no measures are required is inappropriate in a high-risk patient. Oral bicarbonate has been evaluated in trials with inconsistent benefit compared with saline and is not established as uniformly superior.

4 / 10

A 58-year-old man with newly diagnosed multiple myeloma presents with rapidly progressive oliguric kidney injury. Serum free light chains are markedly elevated. What is the most appropriate immediate management step to improve renal outcome?

Immediate plasma exchange to remove circulating light chains

Start high‑dose loop diuretics to maintain urine flow

Perform renal replacement therapy and defer myeloma therapy

Urgent initiation of anti‑myeloma chemotherapy (eg bortezomib‑based regimen)

Empirical high‑dose corticosteroids alone without myeloma therapy

Rapid initiation of effective anti‑myeloma therapy is central to management of light‑chain cast nephropathy to reduce free light chains and improve chance of renal recovery.

In myeloma cast nephropathy the priority is rapid reduction of circulating free light chains by effective anti‑myeloma therapy (commonly a bortezomib‑based regimen) as the key intervention to improve renal recovery. Renal replacement therapy may be required for standard indications but does not treat the underlying pathology by itself. The role of plasma exchange is unproven and not routinely recommended; it may remove some light chains but trials have not shown consistent benefit. Diuretics do not address the cause and may worsen renal perfusion if overused. Corticosteroids alone are insufficient without definitive myeloma-directed therapy.

5 / 10

A 35‑year‑old woman presents with normal anion gap metabolic acidosis and hypokalaemia. She has recurrent kidney stones and nephrocalcinosis on imaging. Which laboratory finding is most consistent with distal (type 1) renal tubular acidosis (dRTA)?

Negative urine anion gap indicating high urinary ammonium excretion

Elevated urinary sodium fractional excretion >2%

Positive urine anion gap consistent with low urinary ammonium excretion

Marked albuminuria (>3.5 g/24 h)

Elevated urinary beta2‑microglobulin only

A positive (or less negative) urine anion gap in the context of metabolic acidosis suggests impaired urinary NH4+ excretion, supporting a diagnosis of RTA, including dRTA.

dRTA is due to impaired distal acidification leading to reduced urinary NH4+ excretion; the urine anion gap (Na+ + K+ − Cl−) is typically positive (or less negative) indicating low urinary ammonium, which supports RTA. A negative urine anion gap would indicate appropriate urinary ammonium excretion (eg diarrhoea). Albuminuria in the nephrotic range is not a feature of primary RTA. Fractional sodium excretion and urinary beta2‑microglobulin are not diagnostic for dRTA; beta2‑microglobulin may rise in proximal tubular disease, and fractional sodium excretion is a marker used in AKI assessment, not for diagnosing dRTA.

6 / 10

Which of the following clinical features most characterises chronic analgesic nephropathy?

Nephrotic‑range proteinuria with heavy oedema

Renal papillary necrosis with chronic interstitial fibrosis and variable tubular dysfunction

Rapidly progressive crescentic glomerulonephritis

Isolated haematuria without progressive loss of GFR

Acute tubular necrosis after a single large dose of paracetamol

Chronic analgesic nephropathy causes papillary necrosis and chronic tubulointerstitial damage leading to progressive CKD.

Chronic analgesic nephropathy (typically from long-term combined analgesic use, especially phenacetin historically and some NSAIDs) is characterised by papillary necrosis and chronic tubulointerstitial nephritis with interstitial fibrosis and progressive renal impairment; tubular dysfunction and chronic kidney disease are common. It does not typically present with nephrotic‑range proteinuria or crescentic GN. Isolated haematuria without progressive GFR loss is not typical; acute tubular necrosis after a single paracetamol dose is not the usual mechanism of chronic analgesic nephropathy.

7 / 10

A patient receiving an immune checkpoint inhibitor (anti‑PD‑1) for melanoma develops a rise in creatinine from 90 to 260 µmol/L over 10 days. There are sterile pyuria and modest proteinuria; no systemic infection is found. What is the most appropriate immediate action?

Continue the checkpoint inhibitor and monitor renal function closely

Obtain urgent renal biopsy before any change to therapy

Start haemodialysis immediately

Administer cyclophosphamide and continue checkpoint inhibitor

Withhold the checkpoint inhibitor and start systemic corticosteroids

For suspected immune checkpoint inhibitor–associated AIN, withhold the immunotherapy and start corticosteroids for significant renal impairment; biopsy is reserved for diagnostic uncertainty.

Immune checkpoint inhibitors can cause acute interstitial nephritis. The recommended immediate action is to withhold the offending immunotherapy and start systemic corticosteroids for significant renal injury (moderate to severe AKI). Urgent biopsy may be helpful in atypical cases or before prolonged immunosuppression if the diagnosis is uncertain, but it is not mandatory before initiating steroids when the clinical picture is typical. Continuing the drug risks further renal injury; dialysis is reserved for standard renal indications; cyclophosphamide is not first‑line therapy for this toxicity.

8 / 10

A factory worker with chronic occupational lead exposure has gout, microcytic anaemia and progressive renal impairment. Which urinary finding best supports a diagnosis of lead‑induced proximal tubular dysfunction?

Glycosuria with normal blood glucose

Heavy orthostatic proteinuria >2 g/day

Selective albuminuria with preserved tubular function

Very low urine osmolality only

Isolated glucosuria that resolves with improved glycaemic control

Proximal tubular dysfunction (Fanconi features) such as normoglycaemic glycosuria suggests toxic injury to proximal tubules (eg lead exposure).

Lead nephropathy preferentially affects the proximal tubules and can cause a Fanconi-like proximal tubulopathy with impaired reabsorption: glycosuria despite normoglycaemia, phosphate wasting, aminoaciduria and bicarbonate loss. Heavy orthostatic proteinuria or selective albuminuria are glomerular patterns and not characteristic of proximal tubule toxin-induced dysfunction. Isolated glucosuria that resolves with glycaemic control indicates diabetic glucosuria rather than tubular dysfunction.

9 / 10

An elderly patient presents with AKI after self‑medicating with very high‑dose vitamin C for several weeks. Kidney biopsy demonstrates numerous intratubular birefringent oxalate crystals with tubular obstruction and interstitial inflammation. Which immediate management step is most appropriate to address the acute kidney injury?

Intravenous calcium to precipitate oxalate intravascularly

Administer fomepizole to inhibit alcohol dehydrogenase

Urgent renal replacement therapy (dialysis) if standard dialysis indications present

High‑dose corticosteroids to treat interstitial inflammation

Start oral potassium citrate only

In oxalate nephropathy stop the source of oxalate; use supportive care and institute dialysis for standard indications while awaiting renal recovery.

Secondary oxalate nephropathy (eg from massive vitamin C intake) can cause intratubular crystal deposition and AKI. Immediate steps include stopping the offending agent, supportive care and when standard indications for renal replacement therapy (refractory hyperkalaemia, acidosis, volume overload, uremia) exist, urgent dialysis is appropriate — it can also help remove small molecules and manage complications while renal recovery is assessed. Fomepizole is used for ethylene glycol poisoning to prevent oxalate formation and is not indicated for vitamin C–induced oxalate nephropathy. Intravenous calcium is not an appropriate treatment to manage intrarenal oxalate crystals. Corticosteroids have no proven role acutely for crystal-induced tubular obstruction. Potassium citrate may be used chronically to reduce stone risk but is not the immediate treatment for severe AKI.

10 / 10

A 45‑year‑old woman has progressive creatinine rise from 90 to 320 µmol/L over 2 weeks after starting an antibiotic. Urine microscopy is unremarkable and there is no clear systemic allergic picture. The drug was stopped 72 hours ago but creatinine continues to rise and the diagnosis remains uncertain. What is the most appropriate next step?

Continue conservative management and recheck creatinine in 2 weeks

Start high‑dose systemic corticosteroids empirically without further evaluation

Proceed to percutaneous kidney biopsy to establish diagnosis

Start empirical antibiotics for occult infection

Refer urgently for renal transplantation assessment

Renal biopsy is indicated when AKI is progressive and the diagnosis is uncertain and will influence therapy (eg to decide about immunosuppression).

When there is progressive AKI of uncertain aetiology despite stopping a suspected offending drug, or when there is diagnostic uncertainty that will change management (for example to decide on immunosuppression), a renal biopsy is indicated to establish the histological diagnosis (eg AIN vs ATN vs other). Continuing conservative management risks further irreversible injury if the process is treatable. Empirical high‑dose corticosteroids without histological confirmation may be reasonable in some clear-cut cases but is not appropriate when the diagnosis is uncertain and a biopsy will influence treatment. Empirical antibiotics are not indicated without evidence of infection. Transplant referral is inappropriate at this stage.

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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.

Thrombotic Microangiopathy

Advanced clinical MCQs on diagnosis, interpretation, acute and chronic management, complications and special situations in thrombotic microangiopathy (TMA).

1 / 10

A 36-year-old previously well woman presents with 48 hours of confusion and fluctuating visual disturbance. Lab tests: Hb 78 g/L, platelet count 18 x10^9/L, creatinine 90 μmol/L, bilirubin 45 μmol/L, LDH markedly elevated. Peripheral blood film shows schistocytes. ADAMTS13 activity returns at 6%. What is the most appropriate immediate management?

Start eculizumab immediately without plasma exchange

Transfuse platelets and begin intravenous antibiotics

Commence urgent plasma exchange (plasmapheresis) and start corticosteroids

Obtain an urgent renal biopsy to guide therapy

Observe and repeat ADAMTS13 testing in 24 hours before treating

Severe ADAMTS13 deficiency (<10%) with MAHA and thrombocytopenia mandates urgent plasma exchange and immunosuppression for TTP.

This presentation is classical for thrombotic thrombocytopenic purpura (TTP): severe thrombocytopenia, MAHA with schistocytes, neurological symptoms and critically low ADAMTS13 activity (<10%). The immediate, life‑saving therapy for acquired TTP is urgent plasma exchange together with immunosuppression (commonly high‑dose corticosteroids) while further antibody testing is obtained. Eculizumab targets complement-mediated TMA (aHUS) and is not first‑line for TTP. Platelet transfusion is contraindicated unless there is life‑threatening bleeding because it may exacerbate microvascular thrombosis. Renal biopsy is unnecessary and potentially hazardous in the acute unstable thrombocytopenic patient and will not change the urgent need for plasma exchange. Waiting to repeat ADAMTS13 delays critical treatment and is inappropriate in suspected TTP.

2 / 10

A 24-year-old man presents with acute kidney injury (creatinine 420 μmol/L), microangiopathic haemolytic anaemia and thrombocytopenia. There are no neurological features. ADAMTS13 activity is 60%. Complement assays suggest activation; STEC (Shiga toxin) PCR is negative. He is dialysis dependent and haemodynamically stable. What is the most appropriate next step in acute management?

Proceed with immediate therapeutic plasma exchange alone

Conservative management only; do not start targeted therapy until spontaneous recovery

Start high‑dose intravenous methylprednisolone as sole therapy

Delay treatment pending full genetic testing of complement genes

Initiate complement blockade (eculizumab) after ensuring meningococcal vaccination/prophylaxis and excluding active infection

In suspected complement‑mediated aHUS with significant renal involvement, prompt initiation of complement blockade (with appropriate infectious prophylaxis) is indicated and should not be deferred for genetic results.

This clinical picture (TMA with AKI, ADAMTS13 not severely deficient, negative STEC) is typical of complement‑mediated aHUS. The disease can progress rapidly to organ failure; targeted therapy with terminal complement blockade (eculizumab or similar agents) is indicated in aHUS after excluding active infection and providing meningococcal vaccination and appropriate antibiotic prophylaxis. Plasma exchange has limited efficacy in typical complement‑mediated aHUS and is not preferred as sole long‑term therapy. Genetic testing is important but should not delay urgent initiation of complement blockade when clinically indicated. High‑dose steroids alone are ineffective as monotherapy in aHUS.

3 / 10

A 29-year-old pregnant woman at 34 weeks presents with new hypertension, platelet count 85 x10^9/L, Hb 100 g/L and schistocytes on blood film. Coagulation studies (PT/APTT) are normal and ALT is mildly elevated. ADAMTS13 activity is 58%. Which is the most likely diagnosis?

Warm autoimmune haemolytic anaemia

Thrombotic microangiopathy (pregnancy‑related: pre‑eclampsia / HELLP rather than TTP)

Vitamin B12 deficiency causing macroangiopathic haemolysis

Disseminated intravascular coagulation (DIC)

Mechanical haemolysis from a prosthetic valve

In pregnancy with MAHA and thrombocytopenia, normal ADAMTS13 and normal coagulation point towards pre‑eclampsia/HELLP rather than TTP; management focuses on maternal/fetal delivery and supportive care.

In pregnancy, thrombocytopenia with haemolysis and schistocytes can reflect pregnancy‑associated TMA syndromes. Normal coagulation studies and an ADAMTS13 activity that is not severely deficient (58%) make acquired TTP unlikely. HELLP (Haemolysis, Elevated Liver enzymes, Low Platelets) or severe pre‑eclampsia commonly present around this gestation with hypertension, elevated liver enzymes and MAHA; these are pregnancy‑related TMAs. Warm autoimmune haemolysis is typically Coombs (direct antiglobulin) positive and does not cause schistocytes or thrombocytopenia. Vitamin B12 deficiency causes macrocytosis and hypersegmented neutrophils, not schistocytes. DIC would usually show abnormal PT/APTT and hypofibrinogenaemia. Mechanical haemolysis from a prosthetic valve is unlikely in this context.

4 / 10

A 48-year-old man presents with features of TMA. His ADAMTS13 activity returns as 12% (measured while on steroids). What is the most appropriate immediate interpretation and management decision?

Treat as TTP and start or continue plasma exchange and immunosuppression while searching for an inhibitor or secondary cause

ADAMTS13 12% excludes TTP; do not give plasma exchange and treat as aHUS

ADAMTS13 level is uninterpretable while on steroids; discontinue immunosuppression and await repeat testing

Platelet transfusion is required to correct thrombocytopenia before invasive procedures

Immediate initiation of long‑term eculizumab is mandatory

Low ADAMTS13 activity consistent with TTP should prompt urgent plasma exchange and immunosuppression; do not delay therapy awaiting additional confirmatory tests.

An ADAMTS13 activity around 10–20% is strongly suggestive of TTP in the right clinical context; many guidelines use a threshold <10% as diagnostic of severe deficiency, but values around 10–20% still warrant treatment as TTP if clinical features match. The correct action is to treat as TTP with plasma exchange and immunosuppression while further testing for inhibitor and secondary causes continues. ADAMTS13 does not 'exclude' TTP at 12% — rather it supports it. Steroids do not invalidate the measurement to the point of withholding therapy. Platelet transfusion is generally avoided unless there is life‑threatening haemorrhage. Eculizumab is not first‑line in TTP.

5 / 10

When is a native kidney biopsy most appropriate in a patient presenting with thrombotic microangiopathy?

Always perform biopsy before any therapy to obtain a definitive diagnosis

Never perform biopsy because it rarely changes management

Only perform biopsy if platelet count is >150 x10^9/L

Consider biopsy when diagnosis remains uncertain after initial stabilisation, or to assess chronicity and guide long‑term renal prognosis

Perform biopsy immediately in all patients with AKI on dialysis to determine whether to continue dialysis

Perform renal biopsy selectively in TMA when it will influence management or prognosis and after patient stabilisation; it is not mandatory before initiating urgent therapy.

Kidney biopsy can provide useful diagnostic and prognostic information in TMA (e.g. distinguishing chronic changes, thrombi, complement deposition) but it is not required in every acute case and is often impractical or unsafe while the patient is thrombocytopenic or haemodynamically unstable. Biopsy is most appropriate after initial stabilisation if the diagnosis is unclear, if renal disease persists or to determine chronicity and guide long‑term management. It should not routinely precede urgent life‑saving therapy (e.g. plasma exchange or complement blockade), nor is an absolute platelet threshold of 150 x10^9/L required. Immediate biopsy in all dialysis patients is unnecessary.

6 / 10

Regarding genetic testing for complement pathway abnormalities in a patient with suspected complement‑mediated aHUS, which statement is most appropriate?

Genetic testing is not useful as it rarely alters management

Only children should undergo complement genetic testing; adults do not benefit

Obtain comprehensive complement genetic and functional testing early (after initial stabilisation), as results inform prognosis and transplant planning though they should not delay acute therapy

Start lifelong eculizumab only if genetic testing shows a defined mutation

Complement genetic testing can predict immediate response to plasma exchange and should guide acute decisions

Arrange complement genetic and functional testing early for prognosis and transplant planning, but do not delay acute treatment while awaiting results.

Genetic and functional complement testing in suspected complement‑mediated aHUS is important for prognosis, recurrence risk assessment and transplant planning (e.g. recurrence risk post‑renal transplant differs by mutation). These investigations should be arranged early once the patient is stabilised but must not delay urgent therapy (e.g. eculizumab). Genetic abnormalities occur in both adults and children and can meaningfully influence long‑term decisions. Lack of an identifiable mutation does not exclude complement dysregulation. Genetic results do not reliably predict immediate response to plasma exchange.

7 / 10

A woman develops TMA in the third trimester. After delivery her ADAMTS13 activity is 72% and renal function progressively worsens with rising creatinine and ongoing haemolysis. Which immediate management is most appropriate postpartum?

Consider complement‑mediated aHUS and initiate complement blockade (eculizumab) after ensuring appropriate vaccination/prophylaxis

Treat with repeated urgent plasma exchange as primary therapy indefinitely

Initiate high‑dose corticosteroids alone and observe for recovery

Perform immediate kidney transplantation as renal function will not recover

Start lifelong anticoagulation to prevent further microthrombi

In postpartum TMA with preserved ADAMTS13 and ongoing renal failure after delivery, suspect aHUS and initiate complement blockade with appropriate infection prophylaxis.

Postpartum TMA with normal ADAMTS13 and persistent renal failure despite delivery suggests complement‑mediated aHUS. Complement blockade (eculizumab) is indicated in this scenario, with appropriate meningococcal vaccination and prophylaxis. Plasma exchange is not reliably effective for aHUS and is not the preferred definitive therapy. Corticosteroids alone are not effective. Immediate kidney transplantation is inappropriate in the acute setting. Lifelong anticoagulation is not an accepted therapy for TMA and is not indicated to treat microvascular thrombosis in this context.

8 / 10

A renal transplant recipient develops a de novo TMA with rising creatinine, schistocytes and thrombocytopenia two months post‑transplant. Background: tacrolimus‑based immunosuppression. What is the most appropriate initial management step?

Immediately switch tacrolimus to an alternative agent and investigate for antibody‑mediated rejection and viral triggers

Start lifelong dialysis and stop all immunosuppression permanently

Empirically start high‑dose intravenous steroids only and continue tacrolimus

Proceed directly to splenectomy to control microangiopathy

Always start eculizumab without assessing reversible causes

In transplant‑associated TMA first address reversible triggers (e.g. CNI toxicity, rejection, infection); consider complement blockade if TMA persists or if complement dysregulation is identified.

Post‑transplant TMA has multiple potential causes: calcineurin inhibitor toxicity (tacrolimus), antibody‑mediated rejection, infections (e.g. CMV), recurrence of primary disease or de novo complement dysregulation. The initial appropriate step is to address reversible causes — reduce or change the calcineurin inhibitor and evaluate/treat antibody‑mediated rejection and infectious triggers. Dialysis may be required if severe but stopping all immunosuppression permanently risks graft loss and infection. High‑dose steroids alone without addressing the likely trigger are inadequate. Splenectomy is not standard. Eculizumab may be considered if complement‑mediated disease is confirmed or if TMA persists despite addressing reversible causes, but it should not automatically replace evaluation of reversible causes.

9 / 10

A patient with a history of acquired TTP treated successfully with plasma exchange 2 years ago is in clinical remission. Which follow‑up strategy best reduces the risk of relapse?

No further follow‑up is required once normal platelet count is documented

Annual complement genetic testing to monitor for new mutations

Regular clinical review with periodic ADAMTS13 activity monitoring and pre‑emptive rituximab if activity falls significantly

Continue lifelong plasma exchange at decreasing frequency

Start lifelong low‑dose aspirin to prevent relapse

Monitor ADAMTS13 activity during remission of acquired TTP; consider pre‑emptive immunotherapy (e.g. rituximab) if activity drops to levels associated with relapse.

Patients with a history of acquired TTP are at risk of relapse. Regular clinical follow‑up with periodic measurement of ADAMTS13 activity is recommended because falling ADAMTS13 activity often precedes clinical relapse; pre‑emptive rituximab in patients with persistent or recurrent severe ADAMTS13 deficiency can reduce relapse risk. Routine annual complement genetic testing is not relevant for acquired TTP. Lifelong plasma exchange is unnecessary and impractical. Low‑dose aspirin has not been shown to prevent TTP relapses.

10 / 10

A 35‑year‑old man had an episode of complement‑mediated aHUS requiring dialysis in the acute phase and recovered to CKD stage 3. He is now being evaluated for living donor kidney transplantation. Which approach best minimises the risk of disease recurrence in the graft?

Proceed to transplant without specific measures; recurrence is uncommon and unpredictable

Use intensified plasma exchange only in the peri‑operative period

Perform transplantation only if complement genetic testing is negative; otherwise decline transplant

Perform complement genetic testing and, for those with high‑risk complement mutations or prior aggressive disease, plan prophylactic peri‑operative and early post‑transplant complement blockade (eculizumab) with close monitoring

Switch immunosuppression from calcineurin inhibitors to lifelong high‑dose steroids to prevent recurrence

Use complement genetic testing to stratify recurrence risk and consider peri‑transplant prophylactic complement blockade in high‑risk aHUS patients to protect the graft.

Recurrence risk of complement‑mediated aHUS after kidney transplant depends on the underlying complement abnormality; some mutations (e.g. factor H) confer high recurrence risk. Best practice is to perform complement genetic/functional testing and use that information to plan transplant strategy. In high‑risk patients, prophylactic complement blockade with eculizumab around the time of transplant reduces recurrence and preserves graft function. Plasma exchange alone is often insufficient as prophylaxis. Saying transplant only if genetic testing is negative is overly restrictive — many patients can be transplanted with peri‑transplant complement blockade. Altering immunosuppression to high‑dose steroids is not evidence‑based for preventing aHUS recurrence.

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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.

ANCA Vasculitis and Anti-GBM Disease

Ten advanced, board-style single-best-answer questions covering diagnosis, pathology, acute and chronic management, complications and prognostication in ANCA-associated vasculitis and anti-GBM disease.

1 / 10

A 58-year-old man presents with rapidly progressive renal impairment and new haemoptysis. An indirect immunofluorescence (IIF) ANCA test shows a cytoplasmic pattern (c-ANCA). Which test is most appropriate to determine the ANCA antigen specificity?

Enzyme-linked immunosorbent assay (ELISA) for proteinase-3 (PR3) and myeloperoxidase (MPO) antibodies

Repeat the IIF ANCA on a fresh sample and defer further testing until renal biopsy

Anti-glomerular basement membrane (anti-GBM) antibody titre

Complement C3 and C4 levels

Antinuclear antibody (ANA) by immunofluorescence

Use antigen-specific PR3 and MPO immunoassays after ANCA IIF; send anti-GBM antibodies in parallel when a pulmonary–renal syndrome is present.

After a positive IIF ANCA, antigen-specific immunoassays for PR3 and MPO are the appropriate next tests to define the target antigen and improve diagnostic specificity. Because haemoptysis creates a pulmonary–renal syndrome, anti-GBM antibodies should also be sent urgently in parallel; however, the question asks specifically which test determines ANCA antigen specificity. Repeating IIF does not identify the antigen, and complement or ANA testing is not the key next test for this purpose.

2 / 10

Which renal biopsy finding is most characteristic of ANCA-associated (pauci-immune) crescentic glomerulonephritis?

Granular immune complex deposition along the GBM with subendothelial deposits

Diffuse linear IgG staining along the GBM on immunofluorescence

Necrotising lesions with crescent formation and little or no immune complex deposition on immunofluorescence

Mesangial IgA-dominant immune complex deposition

Thrombotic microangiopathy with fibrin thrombi in glomerular capillaries

Pauci-immune necrotising crescentic GN with minimal IF staining is the histological hallmark of ANCA-associated renal vasculitis.

ANCA-associated renal vasculitis classically produces a necrotising, crescentic glomerulonephritis with a 'pauci-immune' immunofluorescence pattern (minimal or absent immunoglobulin and complement deposits). Granular immune complex deposition suggests immune-complex GN (e.g. lupus, infection-related GN). Linear IgG on IF is the hallmark of anti-GBM disease. Mesangial IgA-dominant deposits are typical of IgA nephropathy/HSP. Thrombotic microangiopathy has a different aetiology (eg TTP/HUS) and distinct histology.

3 / 10

A 42-year-old woman has haemoptysis, rapidly progressive renal failure and a strongly positive anti-GBM antibody assay. Which of the following biopsy/immunofluorescence findings would confirm the diagnosis of anti-GBM (Goodpasture) disease?

Mesangial proliferation with IgA deposition

Segmental sclerosing lesions with few immune deposits

Granular subepithelial 'humps' on electron microscopy

Linear deposition of IgG along the glomerular basement membrane on immunofluorescence

Linear C1q deposition without IgG

Anti-GBM disease is confirmed by linear IgG deposition along the GBM on immunofluorescence.

The definitive immunopathological hallmark of anti-GBM disease is linear IgG staining along the glomerular basement membrane on immunofluorescence. Mesangial IgA indicates IgA nephropathy. Segmental sclerosis with paucity of immune deposits is typical of ANCA-associated pauci-immune GN. Granular subepithelial 'humps' are seen in post-infectious GN. Linear C1q without IgG is not the pattern seen in anti-GBM disease; anti-GBM characteristically shows strong linear IgG (often with linear light chains) across the GBM.

4 / 10

A 63-year-old patient presents with severe haemoptysis, hypoxia, and rapidly progressive renal failure. Blood tests show both high‑titer anti-GBM antibodies and MPO‑ANCA (a 'double-positive' result). Which is the most appropriate immediate management strategy?

High-dose intravenous methylprednisolone alone and urgent renal biopsy before any other therapy

Plasma exchange combined with high-dose glucocorticoids and cyclophosphamide

Oral prednisolone and azathioprine only, with outpatient follow-up

Rituximab monotherapy without glucocorticoids or plasma exchange

Conservative management with haemodynamic support while awaiting antibody titres to fall

Double-positive disease with pulmonary haemorrhage requires urgent plasma exchange plus immunosuppression (steroids and cyclophosphamide) to remove anti‑GBM antibodies and suppress further production.

Double-positive patients (ANCA and anti-GBM) commonly present with severe renal injury and pulmonary haemorrhage and are managed initially like anti-GBM disease: urgent plasma exchange to remove circulating anti-GBM antibodies, together with high-dose glucocorticoids and cyclophosphamide to suppress antibody production and inflammation. Immediate high‑dose steroids without plasma exchange is inadequate for anti-GBM disease with pulmonary haemorrhage. Oral prednisolone and azathioprine alone are insufficient in life‑threatening pulmonary–renal syndrome. Rituximab is effective in AAV induction but as monotherapy without steroids or plasma exchange it is inappropriate in acute anti-GBM presentations. Conservative management delaying disease‑directed therapy risks irreversible renal injury and ongoing alveolar haemorrhage.

5 / 10

Following successful induction of remission in a PR3‑ANCA positive patient with generalised AAV (induced with rituximab), which maintenance strategy is most supported by current evidence to reduce relapse risk?

No maintenance therapy; observe clinically and treat relapses as they occur

Continue low‑dose oral glucocorticoid monotherapy indefinitely

Oral methotrexate for maintenance

Scheduled rituximab infusions for maintenance

Switch to intravenous cyclophosphamide for long‑term maintenance

In patients at high risk of relapse (eg PR3‑ANCA), scheduled rituximab maintenance is an effective relapse‑prevention strategy.

For PR3‑ANCA positive patients, scheduled rituximab maintenance has been shown to reduce relapse risk compared with azathioprine in several trials and is an accepted maintenance strategy, particularly for patients at high relapse risk. No maintenance carries an unacceptable relapse risk. Long‑term low‑dose glucocorticoid monotherapy is not recommended as sole maintenance. Methotrexate is used for maintenance in patients with non‑severe renal disease but is less preferred in those with prior severe disease or PR3 positivity and higher relapse risk. Long‑term cyclophosphamide is avoided due to cumulative toxicity; it is not used for maintenance.

6 / 10

Renal histology in ANCA-associated vasculitis can be classified by the Berden classification. Which histological class is associated with the best long-term renal survival?

Focal class (majority normal glomeruli)

Crescentic class (predominant crescents)

Sclerotic class (predominant global sclerosis)

Mixed class (no dominant pattern)

Membranous class

Berden histological classification predicts renal outcome: focal has the best prognosis, sclerotic the worst.

The Berden classification divides ANCA GN into focal, crescentic, mixed and sclerotic classes. The focal class (predominantly normal glomeruli) has the best renal prognosis. Sclerotic class has the worst prognosis. Crescentic and mixed have intermediate outcomes. 'Membranous class' is not part of the Berden classification and would imply immune complex–mediated membranous nephropathy rather than pauci‑immune ANCA GN.

7 / 10

Which of the following drugs is most classically implicated as a cause of drug‑induced ANCA‑associated vasculitis, especially with MPO‑ANCA positivity and possible pulmonary–renal involvement?

Allopurinol

Methimazole

Hydralazine

Amoxicillin

Amlodipine

Hydralazine is a classic trigger of drug‑induced MPO‑ANCA vasculitis and should be stopped if suspected.

Hydralazine is a well‑recognised cause of drug‑induced ANCA vasculitis, often associated with anti‑MPO antibodies and can present with pulmonary–renal syndrome. Other drugs classically implicated include propylthiouracil and certain antithyroid and anti‑arrhythmic agents. Allopurinol, amoxicillin and amlodipine are not typical causes of ANCA‑associated vasculitis; methimazole is less commonly implicated than propylthiouracil but is not the classic offender.

8 / 10

Regarding patients who are 'double‑positive' (both ANCA and anti‑GBM antibodies), which statement is most accurate concerning their clinical course and management?

They behave clinically like ANCA vasculitis and rarely require plasma exchange

They have a lower risk of relapse than patients with isolated anti‑GBM disease

Anti‑GBM positivity in a double‑positive patient indicates that immunosuppression alone (no plasma exchange) is adequate

They should not receive cyclophosphamide because of increased toxicity when both antibodies are present

They often present with severe renal injury/pulmonary haemorrhage and are treated with plasma exchange plus immunosuppression; relapse risk is higher than isolated anti‑GBM

Double‑positive disease requires acute plasma exchange plus immunosuppression and carries a higher relapse risk than isolated anti‑GBM disease.

Double‑positive patients often present with severe renal disease and pulmonary haemorrhage similar to anti‑GBM disease and therefore are typically treated with plasma exchange plus immunosuppression (steroids and cyclophosphamide). Unlike isolated anti‑GBM disease, double‑positive patients have a higher longer‑term relapse risk (more similar to ANCA vasculitis), so close follow‑up for relapse is required. They do not have lower relapse risk, and plasma exchange is generally indicated in the acute setting. Cyclophosphamide is commonly used and not contraindicated because both antibodies are present—indeed it is part of standard therapy in severe presentations.

9 / 10

A novel therapy, avacopan, targets the complement system in AAV. Which of the following best describes its mechanism and current role in AAV management?

An anti‑C5 monoclonal antibody used to treat refractory anti‑GBM disease

A C5a receptor (C5aR) antagonist used as a steroid‑sparing agent in induction therapy for AAV

A complement C3 inhibitor used for long‑term maintenance in MPO‑ANCA disease

A B‑cell depleting agent that replaces rituximab for maintenance therapy

An anticoagulant used to prevent thrombotic complications in active vasculitis

Avacopan is a C5aR antagonist used to reduce glucocorticoid exposure during induction therapy for AAV, not a replacement for B‑cell depletion or complement C5 blockade.

Avacopan is an oral C5a receptor antagonist that interferes with C5a‑mediated neutrophil activation and has been studied as a steroid‑sparing agent in induction therapy for AAV. It is not an anti‑C5 monoclonal antibody (that would be eculizumab), nor a C3 inhibitor, nor a B‑cell depleting agent. It does not replace rituximab for B‑cell depletion and is not an anticoagulant. Trials have shown avacopan can reduce steroid exposure as part of induction regimens, but its incorporation into routine practice should follow guideline recommendations and individual patient considerations.

10 / 10

In the outpatient follow‑up of a patient in remission from PR3‑ANCA positive vasculitis, what is the best interpretation of a rising PR3‑ANCA titre in an otherwise asymptomatic patient?

Immediately re‑start induction‑dose immunosuppression solely because the titre has risen

Recognise that ANCA titres are never useful and ignore the change

Treat with a single high‑dose steroid bolus and reassess ANCA titres

Consider the titre rise as a risk indicator that warrants closer clinical monitoring and investigation, but not automatic escalation without clinical evidence of relapse

Switch maintenance therapy from azathioprine to cyclophosphamide based on titre rise alone

Rising PR3‑ANCA titres warrant heightened surveillance and evaluation for clinical relapse but do not alone justify re‑starting intensive immunosuppression.

Rising PR3‑ANCA titres may precede clinical relapse more often than MPO‑ANCA, but increases in titre alone, in an asymptomatic patient, should not be the sole trigger for re‑induction of immunosuppression. The appropriate action is closer clinical monitoring, re‑examination for symptoms/signs of active disease and targeted investigations. Immediate re‑induction, steroid boluses or escalation to cyclophosphamide based on titres alone is not recommended due to toxicity risk and imperfect predictive value of titres. It is also incorrect to ignore ANCA changes completely; they provide useful adjunctive information when combined with clinical assessment.

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Lupus Nephritis and Immune-Complex Disease

Advanced MRCP-style single-best-answer questions on diagnosis, pathology interpretation, acute and chronic management, complications and special situations in lupus nephritis and immune-complex kidney disease.

1 / 10

Which of the following clinical scenarios is least likely to require an immediate diagnostic renal biopsy to evaluate for lupus nephritis?

New nephrotic-range proteinuria with active urinary sediment in a patient with recent-onset systemic lupus erythematosus (SLE).

Rapid (< weeks) decline in estimated glomerular filtration rate with dysmorphic red cells and red-cell casts in a patient with established SLE.

Isolated low-grade proteinuria (small urinary dipstick, stable low-level proteinuria) with inactive urine sediment and stable serum creatinine for several months in a patient with known quiescent SLE.

New heavy proteinuria accompanied by rising anti-dsDNA titres and falling complement levels.

New nephritic syndrome (oedema, hypertension, haematuria) developing in a patient with SLE and no prior renal disease.

Active urinary sediment, rapid renal function decline, nephrotic-range proteinuria or serological flares in SLE are indications for prompt renal biopsy; stable low-grade proteinuria with inactive sediment may be monitored.

Renal biopsy is indicated promptly for presentations suggesting active, potentially progressive glomerular disease: nephrotic-range proteinuria with active sediment (A), rapid loss of kidney function with RBC casts (B), new heavy proteinuria with serological evidence of activity (D), and new nephritic syndrome (E) — all warrant biopsy to determine class, activity and chronicity and guide immunosuppression. By contrast (C) an isolated, low-grade, stable proteinuria with inactive sediment and stable renal function in a patient with otherwise quiescent SLE can usually be monitored clinically and biochemically rather than proceeding immediately to biopsy. The decision must always be individualised, but (C) is the least likely scenario to require immediate biopsy. Alternatives: A, B, D and E all represent situations where histological classification will change management and therefore biopsy is appropriate.

2 / 10

Which renal histopathological description is most consistent with ISN/RPS class V (membranous) lupus nephritis?

Granular subepithelial immune-complex deposits along the glomerular basement membrane with a ‘spike-and-dome’ appearance on silver stain and granular IgG on immunofluorescence.

Widespread subendothelial immune-complex deposits with endocapillary hypercellularity and 'wire-loop' lesions.

Mesangial hypercellularity with mesangial immune-complex deposition only.

Linear IgG staining along the GBM on immunofluorescence consistent with anti-GBM disease.

A pauci-immune pattern with little or no immune-complex deposition and crescentic necrotising lesions (ANCA-associated pattern).

Class V LN shows subepithelial immune-complex deposition with granular IgG staining and characteristic ultrastructural features; subendothelial deposits point to proliferative classes.

ISN/RPS class V (membranous) LN is characterised by predominantly subepithelial immune-complex deposition along the GBM producing a granular immunofluorescence pattern and the so-called ‘spike-and-dome’ appearance on silver stain/electron microscopy. Choice A describes this and is therefore correct. Choice B describes subendothelial deposition and endocapillary proliferation typical of proliferative (class III/IV) LN. Choice C corresponds to isolated mesangial lupus nephritis (class II). Choice D indicates linear IgG along the GBM seen in anti-GBM disease, not immune-complex membranous LN. Choice E is typical of pauci-immune ANCA-associated GN rather than immune-complex LN. Correct interpretation of deposit location and associated light-microscopy changes is essential for classifying LN and directing therapy.

3 / 10

Regarding induction immunosuppressive therapy for severe proliferative (class III/IV) lupus nephritis, which statement best reflects current evidence and guideline recommendations?

Intravenous cyclophosphamide is the only induction regimen shown to produce meaningful renal remissions in class III/IV LN.

High-dose corticosteroids alone are as effective as combination immunosuppressive induction in severe proliferative LN.

Mycophenolate mofetil (MMF) has demonstrated at least similar efficacy to cyclophosphamide for induction of remission in proliferative lupus nephritis in multiple trials and is an accepted first-line option.

Azathioprine is the preferred induction agent for class III/IV LN because of its superior efficacy and safety.

Calcineurin inhibitors are contraindicated during induction of proliferative lupus nephritis because of high risk of irreversible nephrotoxicity.

Both MMF and cyclophosphamide are recommended induction options for severe proliferative LN; steroids alone are insufficient and azathioprine is primarily a maintenance agent.

Randomised trials and guideline syntheses indicate that MMF is at least as effective as intravenous cyclophosphamide for induction therapy in proliferative (class III/IV) LN and is widely accepted as a first-line option alongside cyclophosphamide (thus option C is true). Option A is incorrect because cyclophosphamide is not the only effective induction agent; MMF is an established alternative. Option B is incorrect — high‑dose corticosteroids alone are inadequate for most cases of severe proliferative LN. Option D is incorrect — azathioprine is used for maintenance therapy but has inferior induction efficacy compared with MMF/cyclophosphamide. Option E is false as stated here — calcineurin inhibitors are not absolutely contraindicated and can be used in some induction/combination regimens (though use must consider nephrotoxicity); however they are not the universally preferred induction agents for severe proliferative disease. Therefore the best-supported statement is that MMF and cyclophosphamide are evidence-based induction options (C).

4 / 10

A kidney biopsy from a patient with lupus nephritis shows a high chronicity index (extensive glomerulosclerosis, interstitial fibrosis and tubular atrophy) and low activity indices. Which of the following is the most accurate implication for patient management and prognosis?

High chronicity index predicts excellent responsiveness to aggressive immunosuppression and rapid recovery of renal function.

High chronicity index indicates chronic irreversible damage and a reduced likelihood that additional immunosuppression will restore renal function.

High chronicity index has no prognostic significance and should not influence therapy decisions.

High chronicity index suggests that escalating doses of cyclophosphamide will produce substantial improvement.

High chronicity index indicates active immune-complex deposition and requires immediate plasmapheresis.

High chronicity on renal biopsy signals irreversible damage and predicts limited benefit from further aggressive immunosuppression; focus should shift to CKD care and balancing treatment risks.

A high chronicity index denotes established irreversible structural damage (glomerulosclerosis, interstitial fibrosis, tubular atrophy). Such changes predict a limited likelihood that intensified immunosuppression will recover renal function; management shifts towards supportive care for chronic kidney disease and careful consideration of risks vs benefits of further immunosuppression. Thus option B is correct. Option A is false — high chronicity predicts poor, not excellent, response. Option C is incorrect because chronicity does have prognostic significance and should influence management decisions. Option D is incorrect — further cyclophosphamide is unlikely to reverse chronic scarring and may cause harm. Option E is wrong — chronicity reflects scarring rather than active immune-mediated deposits that would be cleared by plasmapheresis. Biopsy activity versus chronicity indices guide expectations and therapy selection.

5 / 10

Which immunosuppressant is generally regarded as acceptable for maintenance therapy in pregnancy when treatment of lupus nephritis is required?

Mycophenolate mofetil (MMF)

Cyclophosphamide

Methotrexate

Azathioprine

Leflunomide

Azathioprine is an accepted maintenance immunosuppressant in pregnancy for SLE/LN; MMF, methotrexate and leflunomide are teratogenic and should be avoided.

Azathioprine is considered acceptable for use in pregnancy when immunosuppression is required for SLE or lupus nephritis; it has a well-documented safety profile in pregnancy at usual doses (option D correct). MMF (A) is teratogenic and should be stopped preconception. Cyclophosphamide (B) is strongly teratogenic, particularly in the first trimester, and associated with gonadotoxicity; it may be used in life‑threatening situations with specialist input but is not regarded as acceptable routine maintenance in pregnancy. Methotrexate (C) and leflunomide (E) are teratogenic and contraindicated. When immunosuppression is needed in pregnancy, azathioprine and some calcineurin inhibitors are considered among the safer options in specialist guidance; drug changes should ideally be made prior to conception.

6 / 10

Antiphospholipid syndrome (APS) nephropathy is an important cause of renal impairment in patients with SLE. Which of the following statements best describes the usual long-term management approach for APS nephropathy?

High-dose corticosteroids and cyclophosphamide are the mainstay long-term therapy to prevent progressive renal scarring.

Lifelong anticoagulation with warfarin (or other long-term anticoagulation where indicated) is central to management because the lesion is primarily thrombotic microangiopathy.

Plasmapheresis is indicated as first-line long-term therapy to remove antiphospholipid antibodies.

No specific therapy is indicated because APS nephropathy is always self-limiting.

Only antiplatelet therapy (aspirin) is required and anticoagulation is contraindicated.

APS nephropathy is primarily a thrombotic microvascular disease; long‑term anticoagulation is the cornerstone of management rather than immunosuppression.

APS nephropathy is characterised by thrombotic lesions in small renal arteries, arterioles and capillaries leading to chronic ischaemic damage. Long-term anticoagulation (typically warfarin for thrombotic APS) is central in preventing recurrent thrombotic events and progression (B correct). High-dose immunosuppression (A) is not the primary long-term therapy unless there are superimposed immune-mediated lesions. Plasmapheresis (C) is not used routinely as long-term therapy for APS nephropathy. Statement D is false; APS nephropathy can cause progressive CKD. Statement E is incorrect — antiplatelet therapy alone is insufficient for most patients with thrombotic APS who generally require anticoagulation. Management must be individualised and coordinated with rheumatology/haematology specialists.

7 / 10

In monitoring for lupus nephritis flare, which of the following statements about serological markers is most accurate?

Trends in complement levels (C3/C4) and anti-dsDNA titres over time are more useful than a single isolated result for predicting renal flare.

A single normal complement and normal anti-dsDNA level reliably excludes active lupus nephritis.

Anti-dsDNA titres are entirely insensitive to renal disease activity and therefore should not be measured.

Complement levels rise prior to a renal flare and are a reliable early indicator when elevated.

Urine sediment examination has no role; serology alone is sufficient to decide on renal biopsy.

Use serial trends in anti-dsDNA and complement alongside urine examination and clinical assessment; isolated single results are of limited value.

Serial measurements of complement (C3/C4) and anti-dsDNA have greater clinical utility than isolated values because trends (falling complements, rising anti-dsDNA) often precede or accompany disease flares, including renal flares (A correct). A single normal complement and anti-dsDNA (B) does not reliably exclude active LN — false negatives occur. Statement C is incorrect — anti-dsDNA can correlate with disease activity, albeit imperfectly. Statement D is wrong — complements characteristically fall (not rise) in active disease. Statement E is incorrect — urine sediment and quantitative proteinuria are essential in assessment; serology alone is insufficient to decide biopsy. Clinical context and trends guide decisions about investigation and biopsy.

8 / 10

A patient with class IV lupus nephritis is to receive induction therapy including high-dose corticosteroids and cyclophosphamide. Which prophylactic measure is generally recommended to reduce a common opportunistic infection associated with such immunosuppression?

Prescribe oral valacyclovir for CMV prophylaxis routinely.

Give daily oral co-trimoxazole for Pneumocystis jirovecii pneumonia (PCP) prophylaxis while on intensive immunosuppression.

Administer monthly intravenous immunoglobulin to prevent bacterial infection.

Routine antifungal prophylaxis with fluconazole is recommended for all patients on induction therapy.

No prophylaxis is needed; infectious risk is low with modern regimens.

Consider PCP prophylaxis with co-trimoxazole for patients receiving intensive immunosuppression for lupus nephritis; tailor other prophylaxis to individual risk.

The correct option is B: guideline recommendations and expert consensus commonly recommend co-trimoxazole prophylaxis against Pneumocystis jirovecii pneumonia for patients receiving intensive immunosuppression (high‑dose steroids, cyclophosphamide, MMF or combined therapy). Choice A (valacyclovir) is not routinely used for CMV prophylaxis in this setting unless there is a specific risk or prior CMV disease. Choice C (routine IVIG) is not standard for prophylaxis against infection in LN induction. Choice D (routine fluconazole) is not routinely recommended and may cause interactions; antifungal prophylaxis is reserved for specific circumstances. Choice E is false — immunosuppressive induction confers a significant infectious risk and selected prophylactic measures (notably PCP prophylaxis) are standard. (Note: local policies and individual risk assessments guide prophylaxis decisions.)

9 / 10

Regarding lupus nephritis after kidney transplantation, which statement is most accurate?

Recurrent lupus nephritis in the renal allograft is very common and is the leading cause of graft loss.

Recurrent lupus nephritis occurs infrequently and when it does occur it only rarely leads to graft failure; overall graft outcomes are more often influenced by rejection and infection.

Active extra-renal SLE activity at time of transplantation has no bearing on post-transplant outcomes and can be ignored.

Standard transplant immunosuppression should be stopped in patients transplanted for lupus nephritis to prevent recurrence.

Patients with previous lupus nephritis are universally excluded from transplantation because of high recurrence risk.

Recurrent LN in the transplant is uncommon and seldom the primary cause of graft loss; standard transplant immunosuppression and individualised timing of transplant are important.

Recurrent lupus nephritis in the allograft does occur but is uncommon and rarely the dominant cause of graft loss; graft survival is generally determined more by immunological rejection, infection and other complications (B correct). Statement A is incorrect — recurrence is not very common nor the leading cause of graft loss. Statement C is false — active SLE at the time of transplantation may affect timing and peri-transplant management and should not be ignored. Statement D is incorrect — standard transplant immunosuppression is not routinely stopped to prevent recurrence; suppression is required to prevent rejection and may also control SLE. Statement E is wrong — prior lupus nephritis is not an absolute contraindication to transplantation; many patients receive successful transplants. Pre‑transplant disease quiescence and individual assessment are important.

10 / 10

A patient with severe proliferative lupus nephritis presents with life‑threatening diffuse alveolar haemorrhage and rapidly progressive renal failure. Which immediate management approach is most appropriate while arranging definitive therapy?

Begin high-dose oral prednisone alone and await biopsy results before further therapy.

Commence high-dose intravenous methylprednisolone and urgent cyclophosphamide, and consider adjunctive plasmapheresis if alveolar haemorrhage is severe or there is uncertainty about anti-GBM disease.

Treat conservatively with haemodynamic support alone because immunosuppression is contraindicated in pulmonary haemorrhage.

Immediate rituximab monotherapy is the evidence-based first-line option for simultaneous severe pulmonary and renal involvement.

Defer systemic immunosuppression and proceed to urgent renal replacement therapy as the only necessary acute intervention.

Life‑threatening pulmonary–renal syndrome in SLE needs immediate high‑dose IV corticosteroids and cytotoxic therapy (often cyclophosphamide); consider plasmapheresis for severe alveolar haemorrhage or suspected anti‑GBM/other antibody-mediated disease.

In life‑threatening pulmonary–renal syndrome from severe lupus nephritis (diffuse alveolar haemorrhage with rapidly progressive GN), immediate aggressive therapy is required. The recommended urgent approach is high‑dose intravenous corticosteroids and cytotoxic therapy such as cyclophosphamide; plasmapheresis is considered when alveolar haemorrhage is severe or when anti‑GBM or other antibody-mediated disease is suspected/possible. Thus option B is the appropriate immediate strategy (correct). Option A (oral prednisone alone) is inadequate for life‑threatening disease. Option C is incorrect — immunosuppression is often lifesaving in pulmonary haemorrhage due to SLE. Option D is incorrect — while rituximab can be used, it is not established as the sole immediate first-line monotherapy in this acute setting; cyclophosphamide plus steroids is the standard initial combination in many guidelines, with rituximab considered in refractory cases or particular circumstances. Option E is wrong — renal replacement therapy may be required for kidney failure but does not treat the underlying immunological process causing haemorrhage. Management should be urgent, multidisciplinary (renal, respiratory, rheumatology, ICU) and individualised.

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Nephritic Syndrome and Rapidly Progressive GN

Board-level MCQs covering diagnosis, pathophysiology, biopsy interpretation, acute and chronic management, complications and guideline-based decision-making in nephritic syndromes and rapidly progressive (crescentic) GN.

1 / 10

A 58-year-old man presents with 2 weeks of dark urine, periorbital oedema and new hypertension. He had a sore throat 3 weeks ago that settled without antibiotics. Serum creatinine has risen from baseline 90 to 240 µmol/L. Urinalysis: haematuria with red cell casts, protein 1.2 g/day. Complement levels: low C3, normal C4. Which diagnosis is most likely?

IgA nephropathy

Post-infectious (post-streptococcal) glomerulonephritis

Anti-neutrophil cytoplasmic antibody (ANCA)-associated pauci-immune GN

Anti-GBM disease (Goodpasture's syndrome)

Class V lupus nephritis

Low C3 with normal C4 in a nephritic syndrome occurring 1–3 weeks after infection strongly suggests post-infectious GN.

Post-infectious GN commonly follows an infection (classically streptococcal pharyngitis or skin infection) with a latency of 1–3 weeks in adults and presents with nephritic features (haematuria, RBC casts, oedema, hypertension). Complement profile typically shows low C3 with normal or near-normal C4 because the alternative complement pathway is activated. IgA nephropathy classically presents with synpharyngitic haematuria (concurrent with infection) and usually normal complement levels. ANCA-associated GN is pauci-immune and typically has normal complement levels. Anti-GBM disease shows rapidly progressive GN often with pulmonary haemorrhage and IF demonstrates linear IgG; complement is usually not characteristically low. Class V lupus nephritis (membranous) would more commonly have nephrotic-range proteinuria and both C3 and C4 are often low in active lupus.

2 / 10

A 45-year-old man develops rapidly progressive renal impairment over 10 days with serum creatinine rising from 80 to 650 µmol/L. He develops haemoptysis and hypoxia. ANCA and anti-GBM results are pending. Which immediate management step is most appropriate while awaiting serology and biopsy?

Wait for serology and biopsy results before initiating immunosuppression

Start oral prednisolone alone and reassess

Begin intravenous antibiotics and defer immunomodulation until cultures return

Start cyclophosphamide monotherapy without plasma exchange

Commence high‑dose intravenous methylprednisolone and urgent plasma exchange in addition to immunosuppression as indicated

In a patient with life‑threatening pulmonary haemorrhage and rapidly progressive renal failure where anti‑GBM disease or small‑vessel vasculitis is strongly suspected, immediate treatment should not be delayed for confirmatory tests. High‑dose intravenous steroids and urgent plasma exchange are indicated when anti‑GBM disease is suspected, particularly with alveolar haemorrhage, because plasma exchange removes pathogenic antibodies. Concurrent immunosuppression (cyclophosphamide or rituximab according to the clinical scenario) is usually given. Waiting for tests risks deterioration. Antibiotics are not indicated unless there is clear infection. Monotherapy with cyclophosphamide without steroids/plasma exchange is inadequate for life‑threatening pulmonary haemorrhage.

3 / 10

Immunofluorescence microscopy of a renal biopsy shows a strong, smooth, linear deposition of IgG along the glomerular basement membrane. Which diagnosis does this pattern most strongly support?

Anti-glomerular basement membrane (anti-GBM) disease

Post-infectious glomerulonephritis

IgA nephropathy

C3 glomerulopathy

ANCA-associated pauci-immune glomerulonephritis

Linear IgG on renal IF is diagnostic for anti‑GBM disease and distinguishes it from immune‑complex and pauci‑immune causes.

Linear, smooth, diffuse IgG staining along the glomerular basement membrane on immunofluorescence is the hallmark of anti‑GBM disease (Goodpasture’s). Post‑infectious GN and immune complex diseases (e.g. IgA nephropathy) show granular 'lumpy-bumpy' immune complex deposition. C3 glomerulopathy is characterised by dominant C3 staining (often without strong IgG), reflecting alternative pathway activation. ANCA‑associated GN is typically pauci‑immune with little or no immune complex deposition on IF.

4 / 10

Regarding the role of therapeutic plasma exchange (PLEX) in ANCA‑associated vasculitis with rapidly progressive glomerulonephritis (RPGN), which statement is most correct?

PLEX is recommended routinely for all patients with ANCA‑associated RPGN to reduce progression to end‑stage kidney disease

PLEX is indicated only when there is concurrent severe infection

PLEX is reserved for patients with life‑threatening alveolar haemorrhage or selected patients with very severe renal failure

PLEX has been shown to be harmful and should be avoided in ANCA‑associated disease

PLEX should be given instead of induction immunosuppression in ANCA‑vasculitis

PLEX is not routinely indicated for all ANCA‑associated RPGN; use is reserved for life‑threatening alveolar haemorrhage and selected severe renal presentations.

Randomised evidence (e.g. trials synthesised in guideline updates) has not supported routine use of plasma exchange for all patients with severe ANCA‑associated renal disease to prevent end‑stage kidney disease. Current practice is to reserve PLEX for patients with life‑threatening pulmonary haemorrhage and consider it selectively in very severe renal failure (though routine use is not recommended). PLEX is not indicated because of infection alone, is not considered harmful in general when used appropriately, and should not replace induction immunosuppression; rather it may be used in addition to immunosuppressive therapy in selected cases.

5 / 10

A 32-year-old woman with known systemic lupus erythematosus presents with nephritic syndrome: serum creatinine 220 µmol/L, urine protein 3.2 g/day, active urinary sediment and low C3 and low C4. Renal biopsy most likely to show which of the following features characteristic of diffuse proliferative (class IV) lupus nephritis?

Predominantly subepithelial 'hump'-shaped deposits with endocapillary proliferation

Mesangial hypercellularity with mesangial-only immune deposits

Extensive crescentic necrotising lesions with paucity of immune complexes

Diffuse endocapillary hypercellularity with subendothelial immune complex 'wire-loop' deposits

Thickened glomerular basement membranes with granular deposits along capillary walls only

Diffuse endocapillary proliferation with subendothelial immune complexes ('wire‑loop' lesions) is characteristic of class IV lupus nephritis and usually requires aggressive induction therapy.

Class IV (diffuse proliferative) lupus nephritis is characterised by diffuse endocapillary proliferation affecting >50% of glomeruli and prominent subendothelial immune complex deposition, often visualised as 'wire-loop' lesions on light microscopy and granular immune complexes on immunofluorescence. Subepithelial humps are more typical of post‑infectious GN. Mesangial‑only deposits typify class II. Paucity of immune complexes suggests pauci‑immune (ANCA) disease, not lupus. Thickened GBMs with capillary wall granular deposits alone are more typical of membranous (class V) lupus nephritis.

6 / 10

A 70-year-old man with rapidly progressive GN is found to have a serum potassium of 6.8 mmol/L and peaked T waves on ECG. Which of the following is the most appropriate immediate treatment to reduce the risk of fatal arrhythmia?

Nebulised salbutamol alone

Intravenous calcium (e.g. calcium gluconate or calcium chloride)

Oral potassium-binding resin (sodium polystyrene sulfonate)

Intravenous sodium bicarbonate as single immediate therapy

Start urgent haemodialysis only

In hyperkalaemia with ECG changes, give IV calcium immediately to stabilise the myocardium before potassium-lowering measures or dialysis.

When hyperkalaemia is associated with ECG changes (peaked T waves, widening QRS), the immediate priority is to stabilise the cardiac membrane with intravenous calcium (calcium gluconate or chloride). This does not lower serum potassium but reduces the risk of malignant arrhythmia while potassium‑lowering measures are instituted (insulin/dextrose, nebulised salbutamol, bicarbonate if acidotic) and preparations are made for definitive therapy such as diuretics or dialysis. Nebulised salbutamol or insulin/dextrose are temporising measures to shift potassium intracellularly but are not the immediate membrane stabiliser. Oral resins act slowly and are not suitable for immediate stabilisation. Dialysis may be required urgently but one should stabilise the patient first and institute measures to lower potassium while arranging dialysis.

7 / 10

A 60-year-old man with Staphylococcus aureus infective endocarditis develops new haematuria, proteinuria and rising creatinine. Blood cultures remain positive and echocardiography shows vegetations. Which management approach is most appropriate for his glomerulonephritis?

Start high-dose corticosteroids immediately to preserve renal function

Begin plasmapheresis to remove immune complexes and antibodies

Commence long-term immunosuppression with cyclophosphamide

Focus on appropriate intravenous antibiotics and treat the underlying infection; defer immunosuppression unless GN persists after infection control

Start ACE inhibitor therapy and avoid treating the infection aggressively due to renal risk

In infective endocarditis–associated GN, treat the infection first; immunosuppression is avoided until infection is controlled.

In infection‑associated (eg. infective endocarditis) immune-complex GN, the primary intervention is eradication of the underlying infection with appropriate intravenous antibiotics ± surgical source control. Immunosuppression (steroids, cyclophosphamide) is generally contraindicated while infection is active because it may worsen infection. Plasmapheresis is not routinely used for infective endocarditis–related GN and carries risk. ACE inhibitors may be used cautiously for blood pressure/proteinuria control but do not replace treating the infection and should not preclude aggressive infection management. Therefore, treat the infection first and reassess renal disease once infection is controlled.

8 / 10

Renal biopsy in rapidly progressive GN demonstrates that most crescents are cellular with minimal interstitial fibrosis and only focal tubular atrophy. Which statement about prognosis and treatment response is most accurate?

Predominantly cellular crescents with little chronic change predict a better chance of renal recovery with aggressive therapy

Cellular crescents indicate irreversible disease and immunosuppression is futile

Presence of cellular crescents mandates withholding immunosuppression due to high infection risk

Degree of interstitial fibrosis is unimportant once there are crescents

Fewer than 10% crescents predicts the need for immediate dialysis regardless of creatinine

Predominantly cellular crescents with minimal chronic change indicate potentially reversible disease and warrant aggressive treatment to maximise recovery.

Cellular crescents represent an acute, potentially reversible stage of crescent formation. When crescents are predominantly cellular and chronic changes (interstitial fibrosis, tubular atrophy) are minimal, there is a higher likelihood of renal recovery with timely and appropriate aggressive immunosuppressive therapy. Fibrous crescents and extensive chronic tubulo‑interstitial damage predict poor recovery. Cellular crescents do not mandate withholding immunosuppression; rather they often indicate a window for effective treatment. Statements that minimize the importance of chronicity or assert immediate dialysis based solely on low crescent fraction are incorrect.

9 / 10

A 50-year-old man with PR3‑ANCA positive pauci‑immune rapidly progressive GN achieved remission after induction with rituximab and steroids. For relapse prevention, which maintenance strategy is supported by recent evidence and commonly used in practice, particularly for patients at higher relapse risk?

Switch immediately to long‑term oral cyclophosphamide

No maintenance therapy is required after rituximab induction

Fixed-interval rituximab infusions (eg. 6-monthly) for a defined maintenance period

Lifelong high‑dose corticosteroids alone

Short (2–4 week) course of mycophenolate only

Fixed-interval rituximab maintenance is an evidence-supported option to prevent relapse in higher‑risk ANCA‑associated vasculitis after remission induction.

For ANCA‑associated vasculitis, maintenance therapy is usually required after induction to reduce relapse risk. Rituximab given at fixed intervals (eg. 6‑monthly) has been shown to be effective for maintenance and is commonly used, especially in patients with PR3‑ANCA or those at higher risk of relapse. Long‑term cyclophosphamide is avoided because of cumulative toxicity. No maintenance is inappropriate due to relapse risk. Lifelong high‑dose steroids is not a recommended strategy owing to adverse effects. Short mycophenolate alone is not optimal maintenance for higher‑risk PR3‑ANCA patients.

10 / 10

A 35-year-old woman with crescentic GN presents with severe uraemia (marked fatigue, nausea), refractory pulmonary oedema despite diuretics, and persistent hyperkalaemia despite medical therapy. Which of the following is the clearest indication for initiating urgent renal replacement therapy (dialysis)?

Asymptomatic serum creatinine of 800 µmol/L with stable fluid status

Proteinuria of 4 g/day without uraemic symptoms

Controlled hyperkalaemia responding to insulin and salbutamol

Refractory pulmonary oedema causing hypoxia despite diuretic therapy

Low haemoglobin of 75 g/L in the absence of bleeding

Refractory pulmonary oedema despite medical therapy is an accepted urgent indication for initiating dialysis in RPGN.

Absolute (urgent) indications for dialysis include refractory fluid overload (pulmonary oedema) despite maximal medical therapy, life‑threatening hyperkalaemia unresponsive to medical measures, severe metabolic acidosis, and overt uraemic complications (pericarditis, encephalopathy). Refractory pulmonary oedema causing hypoxia despite diuretics is thus a clear indication for urgent dialysis. Elevated creatinine alone without symptoms or uncontrolled metabolic disturbances does not mandate immediate dialysis. Proteinuria and anaemia without other complications are not urgent dialysis indications.

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Nephrotic Syndrome and Podocytopathies

Board-level MCQs covering diagnosis, pathophysiology, complications and management decisions in nephrotic syndrome and podocytopathies.

1 / 10

A 55-year-old man presents with new nephrotic-range proteinuria and preserved renal function. Serology is negative for hepatitis B, C and ANA. Which one of the following is the most useful next investigation to distinguish primary (idiopathic) membranous nephropathy from secondary causes?

Serum anti-phospholipase A2 receptor (anti-PLA2R) antibody measurement

Serum complement C3 and C4 levels

Serum anti–thrombospondin type-1 domain–containing 7A (anti-THSD7A) antibody

Monoclonal protein screen including serum and urine immunofixation

Percutaneous renal biopsy with light and immunofluorescence microscopy

Anti-PLA2R serology is a sensitive and specific non‑invasive test that supports the diagnosis and activity assessment of primary membranous nephropathy.

Anti-PLA2R antibody testing is the most useful non‑invasive test to support a diagnosis of primary (autoimmune) membranous nephropathy: a positive test strongly suggests primary disease and correlates with disease activity. Complement levels (option B) are more helpful in complement‑mediated glomerulopathies and are typically normal in primary membranous nephropathy. Anti-THSD7A (option C) is another autoantibody that can be positive in a minority of primary membranous cases but is less sensitive than anti-PLA2R and is not the first-line test. Monoclonal protein screening (option D) is appropriate when secondary causes such as light‑chain amyloidosis or monoclonal gammopathy are suspected, but it does not distinguish primary membranous disease specifically. Renal biopsy (option E) remains the diagnostic gold standard and will confirm membranous nephropathy and exclude other histologies, but in many adults with suspected membranous disease a positive anti-PLA2R result informs diagnosis and may guide timing of biopsy and management; therefore serology is a useful next investigation. In summary, anti-PLA2R is the best initial test to support primary membranous nephropathy in this context.

2 / 10

A 42-year-old woman presents with new-onset nephrotic syndrome (oedema, heavy proteinuria, hypoalbuminaemia). She is normotensive and has normal renal function. Which of the following is the most appropriate next step before starting immunosuppressive therapy?

Start high-dose oral corticosteroids empirically for presumed minimal change disease

Start an ACE inhibitor and defer further investigations for 3 months

Perform a percutaneous renal biopsy to establish histological diagnosis

Commence rituximab immediately because of heavy proteinuria

Arrange genetic testing for podocytopathy genes prior to therapy

Adults with new nephrotic syndrome usually require renal biopsy to define histology before commencing immunosuppression.

In adults with new‑onset nephrotic syndrome, a renal biopsy is indicated to establish the histological diagnosis before instituting disease‑directed immunosuppression because the differential includes multiple histologies (membranous nephropathy, FSGS, minimal change, amyloid, etc.) that require different therapies. Empirical high‑dose steroids (option A) are appropriate in many children but not adults without biopsy confirmation. Starting an ACE inhibitor (option B) is good supportive care for proteinuria but does not replace the need for histological diagnosis if immunosuppression is being considered. Immediate rituximab (option D) without histological confirmation or serological markers (e.g., anti‑PLA2R) is not appropriate. Routine upfront genetic testing (option E) is not the initial step in an adult without features suggestive of monogenic disease (early onset, family history, extrarenal features); genetic testing is considered in steroid‑resistant disease or when the clinical picture suggests a genetic cause. Therefore, renal biopsy is the correct next step prior to disease‑specific immunosuppression.

3 / 10

A 63-year-old man with long-standing nephrotic syndrome has tense peripheral oedema and large-volume ascites. He has low serum albumin and has been taking high-dose oral furosemide with minimal response. What is the next best therapeutic manoeuvre to mobilise oedema?

Increase oral furosemide dose further and wait 48 hours

Start spironolactone alone

Switch to an oral thiazide-type diuretic alone

Administer intravenous albumin followed immediately by intravenous loop diuretic

Referral for immediate extracorporeal ultrafiltration

In severe hypoalbuminaemic diuretic‑resistant nephrotic oedema, IV albumin followed by an IV loop diuretic and sequential nephron blockade can mobilise fluid; reserve ultrafiltration for refractory cases.

In nephrotic patients with diuretic resistance related to severe hypoalbuminaemia, a commonly used strategy is to give intravenous albumin to restore intravascular oncotic pressure followed promptly by an intravenous loop diuretic to increase natriuresis and fluid mobilization. This approach can transiently improve diuretic effectiveness. Simply increasing oral furosemide (option A) while the patient is diuretic‑resistant and likely has poor bioavailability is unlikely to be effective. Spironolactone alone (option B) or a thiazide‑type diuretic alone (option C) may be used as part of sequential nephron blockade (combination therapy) but are less effective as single agents in tense oedema and do not address hypoalbuminaemia. Extracorporeal ultrafiltration (option E) is a rescue therapy for severe refractory fluid overload and generally reserved for cases unresponsive to aggressive medical management or when there are contraindications; it is not the immediate next step. Note that albumin infusion should be used selectively and with close monitoring of intravascular volume and renal function.

4 / 10

Which single clinical or laboratory feature most strongly increases the risk of venous thromboembolism (VTE) in patients with nephrotic syndrome?

Severe hypoalbuminaemia

History of remote minor haematuria

Hypertension controlled on ACE inhibition

Low-density lipoprotein elevation

Microscopic urinary sediment

Low serum albumin in nephrotic syndrome is a key predictor of venous thromboembolism and should prompt heightened vigilance for thrombosis.

Severe hypoalbuminaemia is the most important and reproducible risk factor for venous thromboembolism in nephrotic syndrome; low oncotic pressure, loss of anticoagulant proteins in the urine and increased hepatic synthesis of procoagulant factors contribute to a prothrombotic state. A history of minor haematuria (option B) or controlled hypertension (option C) are not major drivers of VTE risk in this context. Elevated LDL (option D) is associated with atherothrombotic risk but not the acute venous thromboembolism risk seen in nephrotic syndrome. A bland or microscopic urinary sediment (option E) does not predict VTE risk. Additionally, certain histologies such as membranous nephropathy confer higher thrombotic risk, but among measurable parameters, low serum albumin best correlates with thrombotic events.

5 / 10

An adult patient has biopsy‑proven focal segmental glomerulosclerosis (FSGS) and has failed an adequate trial of high-dose oral corticosteroids (steroid‑resistant). Which one of the following is the next most appropriate investigation before escalating to further immunosuppression?

Start a calcineurin inhibitor immediately

Begin rituximab therapy

Commence plasmapheresis

Proceed to empiric cyclophosphamide

Perform genetic testing for monogenic podocytopathy

Consider genetic testing in steroid‑resistant FSGS because a monogenic diagnosis often predicts non‑responsiveness to further immunosuppression and changes management.

In steroid‑resistant FSGS, especially when presenting at a younger age or with features suggesting a genetic cause, testing for monogenic podocytopathy is important because a confirmed genetic diagnosis alters management: many monogenic forms do not respond to immunosuppression and immunosuppressive toxicity can be avoided. Starting a calcineurin inhibitor (option A) or rituximab (option B) may be considered if a genetic cause is unlikely, but genetic testing should be considered prior to committing to further toxic immunosuppression. Plasmapheresis (option C) is reserved for antibody‑mediated diseases (e.g., recurrent FSGS post‑transplant in selected cases) rather than routine steroid‑resistant primary FSGS. Empiric cyclophosphamide (option D) is not the preferred next step without excluding a genetic cause. Therefore, genetic testing is the correct next investigation in steroid‑resistant FSGS.

6 / 10

A 28-year-old woman with biopsy-proven minimal change disease (MCD) has had multiple steroid‑dependent relapses causing significant steroid toxicity. Which steroid‑sparing agent has the strongest contemporary evidence for inducing and maintaining remission while reducing steroid exposure in adults with steroid‑dependent MCD?

Oral cyclophosphamide

Calcineurin inhibitor (e.g., tacrolimus or cyclosporin)

Mycophenolate mofetil

Azathioprine

Rituximab

Rituximab is an effective steroid‑sparing therapy for steroid‑dependent minimal change disease in adults and reduces steroid exposure and relapses.

Rituximab has emerged as a highly effective steroid‑sparing agent in steroid‑dependent or frequently relapsing MCD in adults, with good evidence for inducing sustained remission and reducing cumulative steroid exposure. Cyclophosphamide (option A) and calcineurin inhibitors (option B) are also effective steroid‑sparing options; cyclophosphamide is effective for inducing longer‑term remission but carries fertility and toxicity concerns, and calcineurin inhibitors require monitoring and relapse is common after withdrawal. Mycophenolate (option C) and azathioprine (option D) have less robust evidence compared with rituximab and the other options. Therefore, rituximab is the most evidence‑supported choice to reduce steroid burden in adult steroid‑dependent MCD.

7 / 10

Which lipid-lowering strategy is most appropriate for reducing long‑term atherosclerotic cardiovascular risk in an adult patient with persistent nephrotic syndrome?

Initiate fibrate therapy as first-line to treat severe hypertriglyceridaemia

Begin bile acid sequestrant therapy

Start a high‑intensity statin (unless contraindicated) as primary/secondary prevention based on overall cardiovascular risk

Defer lipid therapy until the nephrotic state resolves

Use ezetimibe monotherapy

Use statins to reduce atherosclerotic risk in adults with nephrotic syndrome according to cardiovascular risk assessment; treat hypertriglyceridaemia separately if needed.

Statins are first‑line therapy to reduce atherosclerotic cardiovascular risk in adults with chronic kidney disease and in nephrotic syndrome when indicated by overall cardiovascular risk; they reduce major atherosclerotic events. Fibrates (option A) may be used selectively for severe hypertriglyceridaemia to reduce pancreatitis risk but are not primary agents for atherosclerotic risk reduction and have increased myopathy risk when combined with statins. Bile acid sequestrants (option B) have limited efficacy and are poorly tolerated in many patients. Deferring lipid therapy until nephrotic remission (option D) risks prolonged exposure to high atherogenic lipoproteins; treating based on risk assessment is appropriate. Ezetimibe monotherapy (option E) is less effective than statin therapy; it may be used as an adjunct or if statin intolerance occurs. Therefore, statin therapy is the most appropriate evidence-based strategy.

8 / 10

A 67-year-old man with new nephrotic syndrome has low-level monoclonal gammopathy detected on serum protein electrophoresis. You suspect AL amyloidosis as the cause of nephrotic syndrome. Which initial laboratory panel is the single best choice to evaluate for a monoclonal light chain (AL) process?

Serum free light chain assay combined with serum and urine immunofixation electrophoresis

Urine dipstick for protein and microscopy

Serum complement C3 and C4 levels

Anti-nuclear antibody and dsDNA testing

Hepatitis B and C serology

In suspected AL amyloidosis, use serum free light chains plus serum and urine immunofixation as the initial diagnostic panel for detecting a monoclonal light‑chain process.

When AL amyloidosis or monoclonal gammopathy is suspected in a nephrotic patient, the optimal initial laboratory evaluation is a serum free light chain assay together with serum and urine immunofixation electrophoresis. This combination maximises sensitivity for detecting a monoclonal light‑chain process. Urine dipstick (option B) is insensitive for light chains and does not replace immunofixation. Complement levels (option C), ANA/dsDNA (option D) and viral serology (option E) may be relevant in other causes of nephrotic syndrome but are not the best initial tests when AL amyloidosis is suspected. If these tests suggest a monoclonal process, referral to haematology and tissue diagnosis (e.g., fat pad or organ biopsy with Congo red and typing) are required.

9 / 10

A 54-year-old patient with biopsy‑proven anti‑PLA2R‑positive membranous nephropathy has persistent heavy proteinuria despite optimal renin–angiotensin blockade and is at high risk of progressive renal disease. Which immunosuppressive regimen is currently preferred by many guidelines as a first‑line targeted therapy in this scenario?

Long‑term high‑dose glucocorticoids alone

Combined monthly cyclophosphamide and high‑dose oral corticosteroid (Ponticelli regimen)

Oral mycophenolate mofetil monotherapy

B cell depleting therapy with rituximab

Immediate plasmapheresis

Rituximab is a guideline‑supported first-line immunotherapy for many patients with high‑risk anti‑PLA2R‑positive membranous nephropathy; cyclophosphamide/steroid regimens remain an alternative.

For high‑risk patients with primary membranous nephropathy, contemporary guidelines increasingly support B‑cell depletion with rituximab as a first‑line targeted immunotherapy because of favourable efficacy and toxicity compared with older regimens. The Ponticelli regimen (option B: cyclophosphamide plus steroids) remains an effective alternative, particularly where rituximab is contraindicated or unavailable, but rituximab is often preferred due to a better safety profile. High‑dose glucocorticoids alone (option A) are not effective as monotherapy for membranous nephropathy. Mycophenolate (option C) has variable evidence and is not the preferred first‑line choice in high‑risk membranous disease. Plasmapheresis (option E) is not a standard primary therapy for membranous nephropathy.

10 / 10

Which of the following is an absolute contraindication to performing a percutaneous renal biopsy in a patient being investigated for nephrotic syndrome?

Solitary kidney

Uncorrected bleeding diathesis (e.g., INR above target that cannot be corrected)

Moderate hypertension controlled with two agents

Concurrent urinary tract infection

Advanced age

Uncorrected coagulopathy is an absolute contraindication to percutaneous renal biopsy; correct clotting abnormalities prior to biopsy where possible.

An uncorrected bleeding diathesis (coagulopathy) is an absolute contraindication to percutaneous renal biopsy because of the high risk of life‑threatening haemorrhage; coagulopathy should be corrected before biopsy or an alternative diagnostic approach used. A solitary kidney (option A) is not an absolute contraindication—biopsy can be done with informed consent and experienced operators when the diagnostic benefit outweighs risk. Moderate controlled hypertension (option C) is a relative risk factor but not an absolute contraindication; it should be optimised before biopsy. A urinary tract infection (option D) may necessitate treatment before biopsy to reduce infection risk but is not an absolute contraindication in all circumstances. Advanced age (option E) increases procedural risk but is not an absolute contraindication.

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Glomerular Syndromes and Diagnostic Approach

Board-style single-best-answer questions on nephritic and nephrotic presentations, diagnostic testing, biopsy indications, acute and chronic management, complications, and interpretation of histology and serology in glomerular disease.

1 / 10

A 45-year-old man presents with acute onset haematuria, oedema and hypertension. Blood tests show serum C3 low, C4 normal. Which one of the following diagnostic conclusions is most consistent with this complement pattern?

Classical pathway activation due to immune-complex mediated disease (eg, lupus nephritis)

Isolated lectin-pathway activation

Alternative pathway activation, classically seen in post-infectious GN or C3 glomerulopathy

Combined classical and alternative pathway activation (both C3 and C4 low) typical of cryoglobulinaemic GN

Normal complement levels do not help differentiate GN aetiologies

A low C3 with normal C4 points to alternative pathway activation (eg, post-infectious GN, C3 glomerulopathy) and should prompt complement-focused investigations and immunofluorescence assessment.

Low C3 with normal C4 most commonly reflects activation of the alternative complement pathway. This pattern is classically seen in post-infectious (post-streptococcal) glomerulonephritis and in complement-mediated diseases such as C3 glomerulopathy. Classical pathway activation (eg, lupus, cryoglobulinaemia with immune complexes) tends to reduce both C3 and C4. Isolated lectin pathway activation is uncommon and not characterised by this specific pattern. The option that complement levels do not help is incorrect: complement profiles provide useful diagnostic clues in glomerular disease.

2 / 10

A 29-year-old man presents with rapidly progressive renal failure over 2 weeks and haemoptysis. Serology results return showing very high anti-glomerular basement membrane (anti-GBM) antibody titres. Which immediate management step is most appropriate?

Delay therapy until a renal biopsy confirms crescentic GN

Start high-dose oral prednisolone alone and await further tests

Start oral cyclophosphamide only

Treat conservatively with blood pressure control and monitor

Initiate urgent plasma exchange in addition to immunosuppression

In anti-GBM disease with pulmonary haemorrhage and severe renal involvement, start plasma exchange urgently alongside immunosuppression; do not delay for biopsy.

Anti-GBM disease (Goodpasture syndrome) with pulmonary haemorrhage and rapidly progressive renal failure is a medical emergency; urgent plasma exchange (plasmapheresis) with concomitant immunosuppression (corticosteroids ± cyclophosphamide) is indicated to remove pathogenic antibodies and limit ongoing alveolar and glomerular damage. Waiting for a biopsy risks irreversible injury. Steroids and cyclophosphamide alone without plasma exchange are insufficient in the acute setting with alveolar haemorrhage. Conservative measures or steroid monotherapy are inappropriate for fulminant anti-GBM disease.

3 / 10

A 36-year-old patient presents with nephrotic syndrome (proteinuria >3.5 g/24 h) and normal renal function. Light microscopy is inconclusive. Which is the best initial therapy if electron microscopy confirms diffuse podocyte foot-process effacement consistent with minimal change disease (MCD)?

High-dose systemic corticosteroids as first-line induction

Immediate cyclophosphamide induction

Conservative therapy only (salt restriction and diuretics) with no immunosuppression

Immediate rituximab as first-line therapy

Renal transplantation

Adult MCD is treated initially with high-dose corticosteroids; use steroid-sparing agents for relapse or steroid dependence/resistance.

Minimal change disease is usually highly steroid-sensitive even in adults; first-line therapy is high-dose systemic corticosteroids to induce remission. Cyclophosphamide or calcineurin inhibitors are reserved for steroid-dependent, frequently relapsing, or steroid-resistant disease. Rituximab can be used in relapsing or steroid-dependent cases but is not first-line. Conservative therapy alone is inadequate for induction of remission in typical MCD presenting with nephrotic syndrome. Renal transplantation is irrelevant here.

4 / 10

A 54-year-old woman presents with nephrotic-range proteinuria. Serum anti-PLA2R antibody titre is markedly elevated. Which statement best reflects the clinical implication of a high anti-PLA2R titre in this context?

A high anti-PLA2R titre excludes primary membranous nephropathy and suggests secondary causes

Anti-PLA2R titre is unrelated to disease activity and has no prognostic value

A high titre indicates membranoproliferative glomerulonephritis (MPGN)

High anti-PLA2R titres are associated with active primary membranous nephropathy and a higher likelihood of progressive disease

Anti-PLA2R antibodies are diagnostic of IgA nephropathy

High anti-PLA2R antibody titres support active primary membranous nephropathy and predict a higher risk of persistent nephrotic-range proteinuria; titres can be used to monitor response to therapy.

Anti-PLA2R antibodies are implicated in primary membranous nephropathy; higher antibody titres correlate with disease activity and greater risk of persistent proteinuria and progression, and they can be used to monitor response to therapy. A positive anti-PLA2R supports primary rather than secondary membranous disease (though clinical correlation to exclude secondary causes is still required). Anti-PLA2R is not associated with MPGN or IgA nephropathy. It therefore has prognostic and monitoring value.

5 / 10

Which glomerular disease carries the highest relative risk of venous thromboembolism (especially renal vein thrombosis) and should prompt heightened vigilance for thrombotic complication in the nephrotic state?

Minimal change disease

Membranous nephropathy

IgA nephropathy

Alport syndrome

Thin basement membrane disease

Membranous nephropathy confers the highest risk of venous thromboembolism among nephrotic syndromes — maintain vigilance and consider thromboprophylactic strategies when appropriate.

Membranous nephropathy is associated with the highest risk of venous thromboembolism among nephrotic disorders, including renal vein thrombosis and pulmonary embolism. The hypercoagulable state in nephrotic syndrome is multifactorial (loss of antithrombin III, increased fibrinogen, platelet hyperreactivity). While all causes of nephrotic syndrome increase thrombotic risk, membranous disease has the strongest association. Minimal change disease also increases risk but less so; IgA nephropathy, Alport and thin basement membrane disease are not typically associated with a high VTE risk.

6 / 10

A patient with biopsy-confirmed C3 glomerulopathy has progressive proteinuria and declining renal function despite supportive care. Which targeted therapeutic option is mechanistically most appropriate for refractory disease driven by complement activation?

Rituximab (anti-CD20) to deplete B cells

High-dose intravenous immunoglobulin (IVIG)

Terminal complement inhibition with a C5 inhibitor (eg, eculizumab)

Mycophenolate mofetil as anti-proliferative therapy

Azathioprine alone

In progressive C3 glomerulopathy refractory to standard measures, consider complement-directed therapy (eg, C5 inhibition) because the disease is driven by alternative pathway dysregulation.

C3 glomerulopathy is caused by dysregulation of the alternative complement pathway; terminal complement blockade with a C5 inhibitor such as eculizumab can be considered in selected, refractory cases to interrupt complement-mediated injury. Rituximab or conventional immunosuppressants are not specifically targeted at alternative pathway dysregulation and have variable efficacy. IVIG, mycophenolate and azathioprine are not mechanistically directed at complement activation; they may be used in other immune-mediated conditions but are not the primary targeted therapy for complement-mediated GN.

7 / 10

A 32-year-old man has lifelong microscopic haematuria and a family history of hearing loss and end-stage kidney disease. Which single investigation is the most appropriate next step to establish the diagnosis before proceeding to renal biopsy?

Urinary protein electrophoresis

Serum ANCA and anti-GBM testing

C3 and C4 complement levels

Skin biopsy for immune complex deposition

Genetic testing for collagen IV (COL4A3/COL4A4/COL4A5) mutations

In suspected Alport syndrome, perform genetic testing for COL4A gene mutations as first-line investigation; this may avoid biopsy and informs prognosis and family counselling.

A family history of haematuria with sensorineural hearing loss and progressive renal disease is highly suggestive of Alport syndrome (collagen IV gene mutations). Genetic testing for COL4A3/COL4A4/COL4A5 is the most appropriate next step and may obviate the need for a diagnostic renal biopsy. The other tests listed are not directed at diagnosing inherited collagen IV disorders: ANCA/anti-GBM and complement tests investigate immune causes; urinary protein electrophoresis is for paraprotein-associated disease; skin biopsy is not a standard diagnostic test for Alport.

8 / 10

A 58-year-old patient with long-standing nephrotic syndrome and marked hypoalbuminaemia is oliguric despite high-dose loop diuretics. Which immediate intervention is most appropriate to attempt improved diuresis?

Administer an intravenous albumin bolus followed immediately by intravenous loop diuretic

Increase oral loop diuretic dose only and wait 48 hours for response

Start intravenous thiazide diuretics alone

Start full anticoagulation empirically to treat nephrotic hypercoagulability

Immediate initiation of haemodialysis

In diuretic-resistant nephrotic oedema with severe hypoalbuminaemia, an IV albumin bolus followed immediately by a loop diuretic can improve diuresis; use cautiously and monitor haemodynamics.

In nephrotic patients with severe hypoalbuminaemia, diuretic resistance may occur because loop diuretics are highly protein-bound and less effective. Administering intravenous albumin followed by a loop diuretic can transiently increase intravascular volume of distribution for the diuretic and enhance natriuresis and diuresis in diuretic-resistant oedema. Simply increasing oral diuretics may be ineffective; thiazide diuretics are sometimes used in combination with loop diuretics but are less appropriate alone in the hypoalbuminaemic, oliguric patient. Empiric anticoagulation and immediate dialysis are not first-line measures to overcome diuretic resistance.

9 / 10

Which of the following is the most appropriate preventive measure to reduce the risk of serious infection in an adult patient with active nephrotic syndrome receiving immunosuppression?

No specific prophylaxis is needed beyond standard hand hygiene

Annual influenza vaccine only

Pneumococcal vaccination (conjugate and polysaccharide as per schedule) and ensure appropriate vaccinations before significant immunosuppression when possible

Lifelong prophylactic co-trimoxazole for all patients with nephrotic syndrome

Immediate commencement of broad-spectrum prophylactic antifungal therapy

Ensure pneumococcal vaccination and other routine immunisations in patients with nephrotic syndrome, especially before initiating substantial immunosuppression.

Nephrotic patients (particularly with heavy proteinuria and those on immunosuppression) have increased susceptibility to infections with encapsulated organisms due to urinary losses of immunoglobulins and complement proteins. Pneumococcal vaccination (both conjugate and appropriate polysaccharide vaccines following local schedules) should be ensured before or during immunosuppression. Influenza vaccination is important but insufficient alone. Lifelong co-trimoxazole prophylaxis is not routinely indicated for nephrotic syndrome (it is used selectively to prevent Pneumocystis jirovecii in certain immunosuppressed regimens). Routine prophylactic antifungal therapy is not indicated.

10 / 10

A 48-year-old woman with biopsy-proven IgA nephropathy has persistent proteinuria of 1.6 g/day despite six months of maximally tolerated ACE inhibitor therapy and good blood-pressure control. According to recent guideline-based CKD management principles, which additional therapy should now be considered to reduce proteinuria and slow progression?

Switch ACE inhibitor to a beta-blocker

Add an SGLT2 inhibitor as an adjunct to RAAS blockade

Immediately start high-dose corticosteroids

Start long-term warfarin anticoagulation for nephrotic-range proteinuria

No further therapy; proceed to renal biopsy repeat

In patients with persistent proteinuria despite maximally tolerated RAAS blockade, add an SGLT2 inhibitor (if not contraindicated) to reduce proteinuria and slow CKD progression.

Recent KDIGO and contemporary CKD guidance support the use of sodium–glucose cotransporter 2 (SGLT2) inhibitors to reduce progression of proteinuric CKD and to lower proteinuria when used in addition to maximally tolerated RAAS blockade, irrespective of diabetes status, provided eGFR is sufficient for their use. Switching to a beta-blocker does not reduce proteinuria. High-dose corticosteroids are not routinely indicated for IgA nephropathy unless specific histological or clinical features indicate steroid-responsive disease; they carry significant risks. Anticoagulation is not a treatment for proteinuria. A repeat biopsy is not routinely required before adding SGLT2 therapy.

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Kidney Transplantation

Ten board-style single-best-answer questions covering donor selection, HLA sensitisation, immunosuppression, perioperative complications, rejection types and management, viral nephropathy, drug toxicity, post-transplant malignancy and infection prophylaxis. Each item tests clinical reasoning applicable to postgraduate nephrology exams.

1 / 10

A 52-year-old woman with prior blood transfusions is being considered for deceased-donor kidney transplantation. Pre-transplant immunology results: complement-dependent cytotoxicity (CDC) crossmatch positive, flow cytometric crossmatch negative, and single-antigen Luminex shows high mean fluorescence intensity (MFI) donor-specific HLA class I antibodies. Which of the following statements is most accurate regarding the immediate transplant risk?

A negative flow cytometric crossmatch makes hyperacute rejection very unlikely despite a positive CDC crossmatch.

High MFI donor-specific antibodies on Luminex with a negative CDC crossmatch indicate no increased risk of rejection.

A positive CDC crossmatch indicates a high risk of hyperacute rejection and is generally considered an absolute contraindication to immediate transplantation.

A positive CDC crossmatch with negative flow crossmatch can be managed by routine induction therapy and standard maintenance immunosuppression.

Virtual crossmatch results supersede CDC crossmatch findings and you should proceed as long as virtual crossmatch is acceptable.

A positive CDC crossmatch signifies complement-fixing anti-donor antibodies and high immediate graft loss risk; it mandates avoidance of straightforward transplantation without specific desensitisation or strategies.

Correct answer: C. A positive complement-dependent cytotoxicity (CDC) crossmatch indicates the presence of cytotoxic, complement-fixing anti-donor antibodies and is associated with a high risk of hyperacute rejection; historically it has been considered a contraindication to transplantation without desensitisation or other measures. A negative flow cytometric crossmatch does not negate the prognostic importance of a positive CDC result. High MFI on Luminex indicates circulating anti-HLA antibodies and increases risk, but the CDC result specifically shows complement-fixing capability and immediate graft injury risk. Option A is incorrect because a negative flow cytometry does not reliably exclude the risk indicated by a positive CDC. Option B is incorrect: high MFI DSA increases rejection risk. Option D is unsafe—standard induction is inadequate when CDC is positive. Option E is incorrect: virtual crossmatch (based on antibody specificities) informs compatibility but does not supplant a positive CDC crossmatch which demonstrates functional cytotoxicity.

2 / 10

Which of the following is considered an absolute contraindication to living kidney donation?

Active, untreated malignancy in the prospective donor

History of a single episode of nephrolithiasis 10 years ago with no recurrence

Age greater than 70 years with otherwise normal health assessment

Body mass index (BMI) of 36 without other comorbidities (centre-dependent assessment)

Well-controlled type 2 diabetes mellitus with microalbuminuria absent after 2 years of stable glycaemic control

Active, untreated malignancy precludes living kidney donation; many other factors are assessed as relative contraindications and require individual assessment.

Correct answer: A. Active, untreated malignancy is an absolute contraindication to living kidney donation because of the risk of tumour transmission and the donor's own health risks. Options B, C, D and E are considerations that may be acceptable or relative contraindications depending on centre-specific evaluation and risk assessment: a remote solitary stone may be allowed, older age is assessed on fitness rather than an absolute cutoff, high BMI is often a relative contraindication and managed case by case, and well-controlled diabetes may preclude donation if there is evidence of end-organ damage but isolated well-controlled diabetes without complications may be handled variably. Thus only active untreated cancer is an absolute contraindication.

3 / 10

A 46-year-old woman awaiting deceased-donor transplant has a calculated panel-reactive antibody (cPRA) reported as 80%. Which interpretation best describes the clinical meaning of a cPRA of 80%?

The probability that she will develop acute rejection in the first month post-transplant is 80%.

She has antibodies against 80% of HLA antigens within her family members.

Eighty percent of prior transfusions produced a positive crossmatch.

Her chance of immediate graft loss is 80% irrespective of donor selection.

Approximately 80% of potential donors would be incompatible because of unacceptable HLA antibodies; roughly 20% of donors would be expected to be compatible.

cPRA expresses the estimated fraction of donors against whom the recipient has unacceptable HLA antibodies; higher cPRA implies greater difficulty finding a compatible donor.

Correct answer: E. cPRA estimates the proportion of donors in the donor pool who would be incompatible because the recipient has unacceptable HLA antibodies; a cPRA of 80% implies that about 80% of potential donors carry one or more unacceptable antigens and approximately 20% would be compatible. It does not directly quantify immediate rejection risk (A), is not limited to family members (B), is not a statement about transfusions (C), nor does it predict immediate graft loss irrespective of donor-specific matching or desensitisation (D).

4 / 10

A 38-year-old man is scheduled for deceased-donor kidney transplantation. He has had a prior transplant and a panel-reactive antibody (PRA) of 70%. Which induction immunosuppressive strategy is most appropriate for minimising early cellular rejection risk in this high-immunological-risk recipient?

Basiliximab (IL-2 receptor antagonist) induction

T-cell-depleting induction with rabbit antithymocyte globulin (rATG)

Belatacept-based induction without calcineurin inhibitor

No induction but high-dose maintenance steroids only

Single-dose monoclonal anti-IL-6 receptor antibody induction

High-immunologic-risk recipients commonly receive T-cell-depleting induction (e.g., rATG) to reduce early rejection risk; IL-2 receptor antagonists are for lower-risk patients.

Correct answer: B. For patients at high immunological risk (retransplantation, high PRA), guidelines commonly recommend T-cell-depleting induction such as rabbit antithymocyte globulin (rATG) because it provides greater lymphocyte depletion and lower early rejection rates than IL-2 receptor antagonists. Basiliximab (A) is typically used for lower-risk recipients. Belatacept (C) is an alternative maintenance agent in some contexts but is not the standard induction choice for high immunological risk. High-dose steroids alone (D) are generally inferior to lymphocyte-depleting agents in high-risk patients. Option E (anti-IL-6) is not established as standard induction in this setting.

5 / 10

On the first postoperative day after a deceased-donor kidney transplant the patient is oliguric and serum creatinine remains high. Urine output is reduced despite fluid optimisation and blood pressure is adequate. Which immediate investigation is the most appropriate next step to distinguish surgical and vascular causes from other causes of poor graft perfusion?

Immediate allograft biopsy at bedside without imaging

Start empirical high-dose intravenous methylprednisolone for presumed rejection

Send for urgent nuclear medicine renal scan (MAG3) as the first-line test

Urgent Doppler ultrasound of the renal transplant to assess perfusion, resistive indices and vascular flow

Measure trough tacrolimus level and withhold tacrolimus pending result

In early postoperative oliguria, urgent Doppler ultrasound is the first-line investigation to assess for vascular complications before biopsy or empiric anti-rejection therapy.

Correct answer: D. In the immediate post-transplant period with oliguria and concern for poor graft perfusion, an urgent Doppler ultrasound is the best initial test to assess vascular complications (arterial/venous thrombosis, stenosis, cortical perfusion) and can be performed rapidly at the bedside. Option A (immediate biopsy) risks bleeding if a vascular complication is present and is not first-line. Empirical high-dose steroids (B) are inappropriate without evidence of rejection and may worsen infection risk; biopsy-directed therapy is preferred. A nuclear medicine scan (C) can be useful but is less readily available and slower than Doppler in most centres. Checking tacrolimus level (E) is reasonable but will not rapidly exclude a vascular surgical cause and should not delay imaging.

6 / 10

A 55-year-old transplant recipient presents 3 months after transplantation with rising creatinine. Renal biopsy shows microvascular inflammation with peritubular capillaritis, C4d deposition in peritubular capillaries, and circulating donor-specific anti-HLA antibodies (DSA) are detected. What is the most appropriate initial treatment strategy?

Plasmapheresis combined with IV immunoglobulin (IVIG), with consideration of adjunctive rituximab

High-dose intravenous methylprednisolone alone

Increase baseline calcineurin inhibitor dose to maximise suppression of T-cell activation

Observation and repeat biopsy in 2 weeks as many cases will resolve spontaneously

Start high-dose intravenous acyclovir and monitor response

Antibody-mediated rejection is treated by antibody removal/neutralisation (plasmapheresis ± IVIG) and adjunctive B-cell/plasma-cell–targeted therapies, whereas steroids mainly address cellular rejection.

Correct answer: A. The biopsy findings and presence of DSA are diagnostic of antibody-mediated rejection (AMR). Initial treatment typically targets removal and neutralisation of pathogenic antibodies with plasmapheresis (or therapeutic plasma exchange) combined with IVIG; adjunctive agents (e.g., rituximab) may be used in many protocols. High-dose steroids alone (B) are the mainstay for acute cellular rejection but are generally insufficient for AMR. Increasing calcineurin inhibitor dose (C) is not the priority and may be harmful. Observation (D) is inappropriate for AMR because it usually progresses without active therapy. Acyclovir (E) is irrelevant to AMR.

7 / 10

A 62-year-old kidney transplant recipient is screened for BK virus and has a plasma BK viral load rising from 3,000 copies/mL to 50,000 copies/mL over four weeks but serum creatinine is stable and urinalysis without haematuria. What is the most appropriate next step in management?

Start empiric intravenous ganciclovir for presumed BK nephropathy

Immediate allograft biopsy to confirm BK virus nephropathy before any change in management

Reduce immunosuppression (e.g., lower antimetabolite dose) and intensify viral monitoring; consider biopsy if renal function declines

Add cidofovir as first-line antiviral therapy for BK virus

Increase steroid dose to prevent immune-mediated injury and allow viral clearance

Rising BK viraemia is managed initially by stepwise reduction of immunosuppression and close monitoring; biopsy is indicated when graft function declines or diagnosis is unclear.

Correct answer: C. The initial and evidence-based step for BK viraemia is to reduce immunosuppression (commonly reducing or holding the antimetabolite such as mycophenolate) and monitor viral load and renal function closely. Biopsy is generally reserved for cases where renal function is worsening or to confirm BK nephropathy. There is no proven role for ganciclovir (A) which targets herpesviruses, and cidofovir (D) is nephrotoxic and not routinely first-line. Increasing steroids (E) would worsen viral replication and is contraindicated.

8 / 10

A 47-year-old man 4 years post-kidney transplant develops progressive decline in eGFR and a protocol biopsy shows chronic tubulointerstitial fibrosis, arteriolar hyalinosis and isometric vacuolisation of tubular epithelium consistent with calcineurin inhibitor (CNI) toxicity. He is clinically stable otherwise. Which management approach is most appropriate to attempt to preserve long-term graft function?

Increase the calcineurin inhibitor dose to overcome presumed under-immunosuppression

Immediate cessation of immunosuppression and initiation of haemodialysis planning

Switch to high-dose prednisone monotherapy permanently

Add mycophenolate without changing CNI dose

Reduce CNI exposure (lower trough target) and consider conversion to an mTOR inhibitor if not contraindicated and proteinuria is acceptable

Chronic CNI nephrotoxicity is managed by reducing CNI exposure and, where suitable, considering conversion to mTOR inhibitors while weighing risks such as increased proteinuria.

Correct answer: E. Histologic changes consistent with chronic CNI nephrotoxicity warrant strategies to reduce CNI exposure, such as lowering trough targets or converting to an mTOR inhibitor (sirolimus/everolimus) where appropriate. Conversion may slow progression of chronic injury; however conversion must be considered carefully because mTOR inhibitors can worsen wound healing and increase proteinuria. Increasing CNI (A) would worsen toxicity. Immediate cessation of all immunosuppression (B) is unsafe. High-dose prednisone monotherapy (C) is not an effective long-term strategy and increases adverse effects. Adding mycophenolate without addressing CNI exposure (D) will not reverse CNI-induced structural injury.

9 / 10

A 60-year-old renal transplant recipient develops multiple non-melanoma skin cancers (squamous cell carcinomas) over three years while on tacrolimus-based immunosuppression. Which of the following management steps is most likely to reduce future cutaneous squamous cell carcinoma risk while preserving graft function?

Increase tacrolimus dose to reduce immune activation against tumours

Convert from a calcineurin inhibitor to a mammalian target of rapamycin (mTOR) inhibitor (e.g., sirolimus) where clinically appropriate

Start long-term high-dose systemic corticosteroids to suppress inflammation

Stop all immunosuppression immediately and arrange urgent re-transplant assessment

Begin lifelong azathioprine monotherapy as it reduces cancer risk

For recurrent post-transplant skin cancers, consider conversion from CNI to mTOR inhibitors to reduce subsequent skin cancer risk, after multidisciplinary discussion.

Correct answer: B. Conversion from calcineurin inhibitors to mTOR inhibitors (sirolimus/everolimus) has been associated with a reduced incidence of certain skin malignancies and may be considered in patients with multiple skin cancers, balancing benefits against side effects (e.g., impaired wound healing, dyslipidaemia, proteinuria). Increasing tacrolimus (A) would likely increase cancer risk. High-dose corticosteroids (C) worsen long-term complications and do not reduce cancer risk. Stopping all immunosuppression (D) risks graft loss. Azathioprine (E) is not used specifically to reduce cancer risk and in some contexts may increase photosensitivity and cancer risk. Management should be individualised with dermatology and transplant teams.

10 / 10

A 34-year-old man is scheduled for kidney transplantation. Donor and recipient CMV serology are as follows: donor CMV IgG positive, recipient CMV IgG negative (D+/R-). Which CMV prevention strategy is recommended for this serostatus combination?

No CMV-specific prophylaxis is required; monitor clinically only

Pre-emptive strategy only (weekly PCR monitoring without prophylaxis) is preferred in D+/R-

Initiate lifelong acyclovir prophylaxis starting post-transplant

Administer antiviral prophylaxis (e.g., valganciclovir) for a defined post-transplant period rather than relying solely on pre-emptive therapy

Administer high-dose intravenous immunoglobulin weekly as sole prophylaxis

CMV D+/R− transplant recipients are high risk and are typically managed with antiviral prophylaxis (valganciclovir) rather than observation or pre-emptive-only approaches.

Correct answer: D. Donor-positive/recipient-negative (D+/R−) is the highest CMV risk constellation; most guidelines recommend antiviral prophylaxis (commonly valganciclovir) for a defined post-transplant period rather than relying solely on pre-emptive PCR monitoring. No prophylaxis (A) is unsafe. Pre-emptive monitoring (B) is an option for intermediate-risk groups but D+/R− generally benefits from prophylaxis. Lifelong acyclovir (C) is not appropriate; acyclovir has limited CMV activity compared with ganciclovir/valganciclovir. IVIG (E) is not used as sole CMV prophylaxis.

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Hemodialysis and Acute Renal Replacement Therapy

Advanced MCQs on modality selection, anticoagulation, complications, access problems, prescribing and monitoring of acute and chronic haemodialysis and CRRT.

1 / 10

A 68-year-old man with septic shock (norepinephrine 0.25 mcg/kg/min) develops oliguric acute kidney injury with pulmonary oedema and a serum potassium of 6.8 mmol/L with peaked T waves. He is intubated and sedated. Which renal replacement strategy is the most appropriate next step?

Immediate intermittent haemodialysis (4-hour conventional session) in the ICU dialysis machine

Peritoneal dialysis via urgent temporary catheter

Continuous renal replacement therapy (CRRT) in the ICU with regional anticoagulation as required

Single prolonged low-efficiency dialysis (SLED) for 8–10 hours

Conservative management with insulin/glucose, nebulised salbutamol and diuretics while awaiting haemodynamic stabilization

CRRT is the preferred modality for haemodynamically unstable patients requiring urgent fluid and solute removal.

This patient is haemodynamically unstable on vasopressor support with life-threatening indications for RRT (pulmonary oedema and severe hyperkalaemia with ECG changes). Intermittent haemodialysis may cause rapid fluid and solute shifts and further haemodynamic deterioration. Peritoneal dialysis is slow and inadequate for rapid correction of life-threatening hyperkalaemia and pulmonary oedema in this context. SLED may be better tolerated than conventional intermittent HD but in a patient requiring ongoing vasopressor support CRRT provides the most haemodynamically stable, continuous fluid removal and gradual correction of electrolytes and volume. Conservative measures (insulin/glucose, salbutamol, calcium) are needed immediately for ECG protection, but definitive extra-renal clearance is required. CRRT with appropriate anticoagulation (or no anticoagulation if bleeding risk) is therefore the most appropriate next step.

2 / 10

During CRRT, which prescription parameter most directly determines small-solute (urea) clearance delivered to the patient?

Total effluent flow rate (sum of dialysate and ultrafiltrate flow)

Anticoagulation type (regional citrate versus systemic heparin)

Dialyser membrane surface area alone

Duration of each interruption of therapy

Patient body mass index

In CRRT, set and monitor effluent flow rate to control small-solute clearance (urea).

In CRRT the principal determinant of small-solute clearance is the effluent flow rate (for continuous therapies, clearance approximates the effluent rate): higher effluent flows produce greater small-molecule removal. Anticoagulation affects circuit patency and therefore delivered therapy but does not directly set solute clearance. Dialyser surface area influences clearance but in CRRT the effluent flow is the primary control. Frequent interruptions reduce delivered dose but the question asks for the parameter that most directly determines clearance in the prescription. Patient BMI influences distribution and dosing considerations but is not a direct prescription parameter controlling instantaneous clearance.

3 / 10

A 55-year-old woman with recent spontaneous intracerebral haemorrhage requires CRRT for oliguric AKI. Anticoagulation of the extracorporeal circuit is needed. Which anticoagulation strategy is most appropriate?

Systemic unfractionated heparin infusion adjusted to an activated partial thromboplastin time target

Low-molecular-weight heparin subcutaneous prophylactic dosing

No anticoagulation; run the circuit without any anticoagulant

Systemic direct thrombin inhibitor (e.g., argatroban) infusion

Regional citrate anticoagulation with careful monitoring of calcium and acid–base status

Regional citrate anticoagulation is preferred for CRRT in patients at high bleeding risk, with strict monitoring for calcium and citrate accumulation.

In patients with high bleeding risk (recent intracranial haemorrhage) regional citrate anticoagulation is preferred for CRRT because it provides effective circuit anticoagulation while minimising systemic anticoagulant exposure. Systemic unfractionated heparin or LMWH increases bleeding risk and is therefore undesirable. Running circuit without any anticoagulant may be possible but commonly results in frequent circuit clotting and inadequate therapy. Systemic direct thrombin inhibitors avoid heparin but still expose the patient to systemic anticoagulation and bleeding risk; they may be used when citrate is contraindicated but are not preferred in active bleeding. Citrate requires monitoring for ionised calcium (systemic and post-filter), total calcium/ionised calcium ratio for citrate accumulation, and acid–base status.

4 / 10

A patient starting haemodialysis for the first time is at risk of dialysis disequilibrium syndrome (DDS). Which of the following measures is most effective to reduce the risk of DDS during the first dialysis session?

Use a high dialysate sodium concentration and cold dialysate

Minimise the rate of urea removal by using a small dialyser, low blood flow and/or prolonged gentle dialysis (or CRRT)

Give a rapid large-volume ultrafiltration to remove cerebral oedema

Start with high-dose ultrafiltration to normalise weight quickly

Give high-dose loop diuretics prior to dialysis

Prevent DDS by limiting rapid urea reduction: use lower blood flow, smaller dialyser or gentler/continuous modalities for the first dialysis sessions.

DDS results from rapid reduction in plasma osmolality (urea) leading to cerebral fluid shifts. The most effective prevention is to minimise the rate of urea removal at the initial session—achieved by using a small surface area dialyser, low blood flow, lower dialysate flow, shorter or more gentle sessions, or use of CRRT/slow low-efficiency dialysis. Increasing dialysate sodium or using cooler dialysate may help haemodynamic stability but are not the primary preventive strategy for DDS. Rapid or high-volume ultrafiltration will worsen cerebral perfusion and is contraindicated. Loop diuretics are ineffective in anuric patients and do not prevent DDS.

5 / 10

A haemodialysis patient has recurrent failure to aspirate blood from a tunnelled dialysis catheter despite good inflow pressure on the arterial lumen. A contrast venogram demonstrates a fibrin sheath encasing the catheter. What is the next best management step to restore catheter function?

Repeat instillation of alteplase (tPA) into the catheter lumens and reassess

Replace the catheter over a guidewire at the same site at bedside without imaging

Start systemic anticoagulation with warfarin to dissolve the sheath

Refer for radiological fibrin sheath disruption/stripping or catheter exchange under imaging guidance

Remove the catheter and wait 2 weeks before inserting a new catheter at the same site

Refractory catheter dysfunction from a fibrin sheath is best managed by interventional radiological fibrin-sheath disruption or guided catheter exchange.

A fibrin sheath often causes refractory inability to aspirate blood. While intraluminal tPA may temporarily restore function if thrombus is intraluminal, a mature fibrin sheath often requires radiological intervention: venography-guided fibrin-sheath disruption/stripping or exchange under imaging. Bedside over-the-wire exchange without imaging may reintroduce a catheter into the same sheath and fail. Systemic anticoagulation does not reliably resolve a fibrin sheath. Immediate removal and waiting 2 weeks is not necessary and delays dialysis access; radiological management is the preferred next step.

6 / 10

A chronic haemodialysis patient presents with chest pain and ECG showing peaked T waves and widened QRS. Serum potassium is 7.2 mmol/L. He is hypotensive. Which immediate action is the most critical first step?

Begin emergency haemodialysis immediately and arrange vascular access

Administer intravenous 10% calcium chloride (or calcium gluconate) to stabilise myocardial membrane

Give intravenous insulin and glucose to shift potassium intracellularly

Nebulised salbutamol and oral potassium binders only

Intravenous sodium bicarbonate as first-line stabilisation

For hyperkalaemia with ECG changes, give IV calcium immediately, start temporising therapy, and arrange urgent dialysis when definitive potassium removal is required.

With severe hyperkalaemia and ECG changes, intravenous calcium is the immediate first step because it stabilises the myocardial membrane. At the same time, give temporising potassium-shifting therapy such as insulin with glucose and nebulised salbutamol, and arrange urgent haemodialysis as definitive potassium removal in a dialysis-dependent patient. Calcium does not lower serum potassium, so definitive therapy and close monitoring must follow without delay.

7 / 10

A haemodialysis patient with a falling platelet count is suspected of having heparin-induced thrombocytopenia (HIT). Which of the following anticoagulants is preferred to anticoagulate dialysis circuits in a patient with suspected or confirmed HIT and severe renal failure?

Continue unfractionated heparin but reduce the dose

Subcutaneous low-molecular-weight heparin (LMWH)

Fondaparinux at standard dosing

Bivalirudin infusion adjusted for renal function

Argatroban infusion (hepatic metabolism) for circuit anticoagulation

In HIT with severe renal failure, use a non-heparin anticoagulant with hepatic metabolism (argatroban) to anticoagulate dialysis circuits.

In suspected or confirmed HIT all heparin products must be stopped. In patients with severe renal failure, anticoagulants that are predominantly renally cleared (e.g., bivalirudin, fondaparinux) accumulate and may be problematic. Argatroban is hepatically metabolised and is therefore the preferred intravenous alternative for anticoagulating extracorporeal circuits in severe renal impairment (dose adjustment for hepatic impairment needed). Fondaparinux is renally cleared and contraindicated in severe renal failure. LMWH and continuing heparin are contraindicated. Bivalirudin is partially renally cleared and requires dose adjustment but is less favourable compared with argatroban in severe renal impairment.

8 / 10

Which pharmacokinetic property of a drug is the best single predictor of how much will be removed by intermittent haemodialysis?

Plasma protein binding percentage

Molecular weight of the drug molecule

Apparent volume of distribution (Vd)

Hepatic metabolic clearance

pKa of the drug

Small volume of distribution predicts high dialysis clearance; consider Vd when deciding whether dialysis will remove a drug.

Although several factors influence dialysability (molecular size, protein binding, water solubility), the apparent volume of distribution is the best single predictor: drugs with a small Vd (largely confined to the intravascular space, e.g., Vd < 1 L/kg) are more readily removed by dialysis. Highly protein-bound drugs are less dialysable, and very large molecules are less dialysable, but Vd integrates distribution and is most useful clinically when predicting removal. Hepatic clearance and pKa influence overall drug handling but are not primary predictors of acute dialysability.

9 / 10

In haemodialysis-related intradialytic hypotension, which physiological factor most directly determines the patient's tolerance to ultrafiltration during a session?

Dialysate sodium concentration

Rate of plasma refill from the interstitial compartment relative to ultrafiltration rate

Core body temperature during dialysis

Residual renal urine output

Systemic haemoglobin concentration

Match ultrafiltration rate to the patient's plasma refill capacity to reduce intradialytic hypotension.

Tolerance to ultrafiltration is primarily determined by the capacity of the vascular compartment to be refilled from the interstitial fluid (plasma refill rate). If ultrafiltration rate exceeds plasma refill capacity, intravascular volume falls and hypotension ensues. Dialysate sodium, temperature, residual urine output and haemoglobin all influence haemodynamic stability but the direct determinant of UF tolerance is the balance between UF rate and plasma refilling.

10 / 10

A patient with severe acute liver failure is started on CRRT for metabolic acidosis and kidney injury. Regional citrate anticoagulation is contraindicated because of concern about citrate accumulation. Which replacement-fluid strategy is generally preferred?

Bicarbonate-based replacement fluid without citrate anticoagulation

Regional citrate anticoagulation with standard citrate dosing and monitoring

No anticoagulation and frequent circuit changes

Systemic heparin with close monitoring of bleeding

Use of lower citrate dose with very close monitoring for citrate accumulation

Separate CRRT buffer choice from anticoagulation choice; in severe hepatic failure with citrate accumulation risk, use bicarbonate-based fluid and individualise anticoagulation.

When citrate anticoagulation is contraindicated because of severe hepatic failure and concern about citrate accumulation, bicarbonate-based replacement or dialysate fluid without citrate is generally preferred. The separate anticoagulation decision should be individualised: CRRT may be run without anticoagulation with frequent circuit changes, or a systemic agent may be considered after assessing bleeding risk. Routine citrate dosing should not be used in this setting; if citrate is considered in a selected centre, intensive monitoring and dose adjustment are required.

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Peritoneal Dialysis and Home Kidney Replacement Therapy

Ten advanced single-best-answer MCQs covering peritoneal dialysis (PD) and home kidney replacement therapies: catheter issues, peritonitis, adequacy, ultrafiltration failure, encapsulating peritoneal sclerosis, APD prescription, post-insertion complications, patient selection for home therapies, PD for AKI, and using PD for acute hyperkalaemia.

1 / 10

A 58-year-old patient on continuous ambulatory peritoneal dialysis (CAPD) presents with a painful, erythematous exit site and purulent discharge. Swab culture grows Pseudomonas aeruginosa. There is no tunnel involvement and no systemic sepsis. What is the most appropriate first-line management?

Immediate catheter removal and switch to haemodialysis

Oral flucloxacillin for 7 days and topical mupirocin

Oral ciprofloxacin combined with topical gentamicin at the exit site

Intraperitoneal vancomycin for 14 days

Intravenous piperacillin–tazobactam for 5 days

Pseudomonas exit-site infections are usually treated with oral ciprofloxacin plus topical gentamicin; catheter removal is reserved for tunnel involvement, peritonitis, or refractory infection.

Pseudomonas exit-site infections are optimally treated with anti-pseudomonal systemic therapy. Oral ciprofloxacin is an effective agent for Pseudomonas exit-site infections and is recommended when there is no systemic sepsis or tunnel infection; topical aminoglycoside (gentamicin) applied to the exit site can augment local control and reduce recurrence. Immediate catheter removal is not mandatory for isolated exit-site infection without tunnel or peritonitis unless infection is refractory. Flucloxacillin and mupirocin target Staphylococcus species and are ineffective against Pseudomonas. Intraperitoneal vancomycin is primarily for Gram‑positive peritonitis rather than exit-site Pseudomonas. Intravenous piperacillin–tazobactam would provide anti‑pseudomonal coverage but is overly invasive for a non-systemic exit-site infection and systemic antibiotics with oral ciprofloxacin are appropriate first-line; IV therapy is reserved for systemic or deep infection.

2 / 10

A 46-year-old CAPD patient presents with cloudy effluent, abdominal pain, and dialysis fluid leukocyte count 1,200 cells/µL with 90% neutrophils. No organisms are seen on Gram stain. Which empiric antibiotic regimen is most appropriate to start immediately (assuming intraperitoneal administration is available)?

Intraperitoneal cefazolin plus ceftazidime

Oral amoxicillin–clavulanate alone

Intravenous vancomycin alone

Intraperitoneal flucloxacillin plus metronidazole

Oral doxycycline and topical exit-site gentamicin

Start empiric intraperitoneal antibiotics covering both Gram‑positive and Gram‑negative organisms (e.g., cefazolin plus ceftazidime) while awaiting culture results.

Empiric therapy for PD-associated peritonitis should cover both Gram-positive and Gram-negative organisms. Intraperitoneal administration achieves high local antibiotic concentrations and is preferred. A first-generation cephalosporin such as cefazolin provides Gram‑positive coverage (including many staphylococci), and an anti‑pseudomonal cephalosporin such as ceftazidime (or cefepime) provides Gram‑negative coverage; this combination is a widely accepted empiric regimen. Oral amoxicillin–clavulanate alone does not provide sufficient Gram‑negative/pseudomonal coverage and oral route is suboptimal in PD peritonitis. Intravenous vancomycin alone lacks Gram‑negative coverage and intraperitoneal administration is preferred where feasible. Flucloxacillin plus metronidazole misses Gram‑negative aerobes and anaerobes are rarely the primary cause. Oral doxycycline and topical measures are inappropriate for peritonitis.

3 / 10

A 65-year-old anuric patient on CAPD (four 2-L exchanges daily) has persistently low weekly Kt/V urea of 1.3 (target ≥1.7). Which of the following is the most appropriate next step to improve dialysis adequacy?

Start erythropoiesis-stimulating agent to improve urea kinetics

Increase dwell glucose concentration to 4.25% for all exchanges

Begin long-term intermittent haemodialysis instead of PD

Attempt to restore residual renal function by stopping diuretics

Increase the total peritoneal dialysate volume per 24 hours (more exchanges or larger volumes) or convert to automated PD to increase total clearance

When PD adequacy is inadequate in anuric patients, increase total peritoneal dialysate volume (more exchanges or larger fills) or convert to APD before abandoning PD.

In anuric patients, peritoneal clearance must provide the entire solute removal. The most direct way to raise weekly Kt/V is to increase total dialysate volume per week — by increasing number of exchanges, using larger fill volumes if tolerated, or switching to automated PD (APD) to increase total exchanges/clearance. Erythropoiesis-stimulating agents affect anaemia, not dialysis solute clearance. Routinely using very high glucose concentrations for all exchanges risks metabolic and peritoneal membrane damage and does not optimally increase small‑molecule clearance relative to increasing total volume. Converting to haemodialysis may be necessary if PD cannot meet targets despite optimisation, but the next step should be to intensify PD first. Restoring residual renal function is not possible in an anuric patient and stopping diuretics would not increase Kt/V.

4 / 10

A long-term PD patient develops progressive peripheral and peritoneal fluid overload with rising ultrafiltration (UF) failure on standard glucose exchanges. Peritoneal equilibration test suggests a high transporter membrane. Which immediate prescription change is most likely to improve long-dwell ultrafiltration?

Switch all exchanges to 4.25% dextrose solutions

Use icodextrin for the long (daytime) dwell

Decrease dwell volumes to shorten transit time

Add oral loop diuretics and reduce dialysate sodium

Stop PD and transfer immediately to haemodialysis

Icodextrin is the preferred intervention to improve ultrafiltration during the long dwell in high peritoneal transporters.

High peritoneal transporters absorb glucose rapidly, which limits osmotic UF during long dwells; icodextrin provides sustained colloid osmotic effect and is specifically effective for the long dwell (typically daytime) in high transporters to improve UF. Repeated use of high glucose (4.25%) can increase risks of metabolic complications and may still be ineffective for long dwell in high transporters. Decreasing dwell volumes or shortening dwells might help solute clearance strategies but will not improve long-dwell UF; short dwells favour sodium sieving and may paradoxically worsen net fluid removal for the long dwell. Oral loop diuretics help patients with residual renal function but do not address peritoneal UF failure. Immediate transfer to haemodialysis is a later option if medical/prescription measures fail; the first-line prescription change for long-dwell UF failure is icodextrin.

5 / 10

A 52-year-old man with 8 years of PD presents with progressive abdominal pain, weight loss, nausea, increasing ultrafiltration failure and loculated ascites. CT abdomen shows peritoneal thickening and bowel tethering (‘cocooning’). What is the management most likely to improve outcome in established encapsulating peritoneal sclerosis (EPS)?

Increase PD exchanges with hypertonic glucose to clear ascites

Long-term broad-spectrum antibiotics and retain PD catheter

Immediate transfer to automated peritoneal dialysis and monitor

Stop PD, commence corticosteroids and consider tamoxifen ± surgical intervention

No change; conservative therapy only because interventions worsen prognosis

EPS requires stopping PD and early institution of anti-inflammatory therapy (often corticosteroids ± tamoxifen); surgery is considered for obstructive complications.

Encapsulating peritoneal sclerosis is a serious, potentially life‑threatening complication of long-term PD. Management includes stopping PD, nutritional support, anti-inflammatory/immunomodulatory therapy (corticosteroids often used acutely) and tamoxifen has been used to stabilise disease; surgical adhesiolysis or enterolysis may be required for obstructive complications. Increasing PD exchanges or hypertonic glucose will not treat the fibrotic process and may worsen outcomes. Long-term antibiotics are not effective unless infection is documented. Switching to automated PD does not address EPS; stopping PD is generally necessary. While prognosis can be poor, active treatment (steroids, tamoxifen, and surgery when indicated) improves outcomes in many cases.

6 / 10

A 70-year-old patient with refractory congestive heart failure on CAPD has persistent interdialytic fluid overload. You are asked to modify the PD prescription using automated PD (APD) to improve sodium and water removal. Which strategy is most appropriate?

Use a long daytime icodextrin dwell combined with nocturnal APD with short, frequent cycles to increase convection/fluid removal

Replace all exchanges with icodextrin to maximise ultrafiltration

Reduce total nightly exchange volume to shorten dwell times and increase sodium removal

Use only low-glucose (1.36%) solutions to avoid fluid shifts

Stop using icodextrin and rely on hypertonic glucose nocturnal exchanges only

For volume-overloaded PD patients, combine a long dwell with icodextrin and nocturnal short-cycle APD to maximise sustained UF and sodium removal.

In patients with refractory volume overload, combining a long daytime icodextrin dwell with nocturnal APD using shorter, more frequent cycles can increase total ultrafiltration and improve sodium removal because icodextrin provides sustained long-dwell UF and short nocturnal cycles enhance convection and net sodium removal. Replacing all exchanges with icodextrin is impractical and not recommended due to cost and formulation limits. Reducing nightly volume may decrease overall clearance and UF. Using only low-glucose solutions will reduce osmotic UF. Reliance on hypertonic glucose alone without icodextrin increases glucose exposure and may be less effective for long-dwell UF; icodextrin is the preferred long-dwell solution for fluid-overloaded patients.

7 / 10

A patient developed severe abdominal pain and faeculent PD effluent 24 hours after laparoscopic PD catheter insertion. He is febrile and tachycardic. What is the single most important immediate action?

Start intraperitoneal antibiotics and observe for 48 hours

Perform bedside PD catheter flushes to clear effluent and continue PD

Urgent surgical review with cessation of PD, remove catheter, make nil by mouth and start broad-spectrum IV antibiotics

Increase PD exchanges to dilute contaminated effluent and monitor

Replace the catheter under local anaesthesia and resume dialysis

Suspected bowel perforation after PD catheter placement requires immediate cessation of PD, nil by mouth, broad-spectrum IV antibiotics, urgent surgical review and catheter removal.

Faeculent effluent soon after catheter insertion strongly suggests bowel perforation. Immediate priorities are to stop PD (to avoid ongoing contamination), make the patient nil by mouth, start broad-spectrum intravenous antibiotics, obtain urgent surgical review and imaging, and usually remove the catheter. Continuing PD, flushing the catheter, or attempting to replace it locally risks worsening contamination and sepsis. Increasing exchanges would distribute contamination. Definitive surgical management is often required.

8 / 10

Which of the following patient factors is most likely to make a person unsuitable for ambulatory peritoneal dialysis at home (without reliable caregiver support)?

Age > 70 years with preserved cognition and reliable home environment

Significant cognitive impairment with inability to self-manage or lack of caregiver

History of well-controlled type 2 diabetes mellitus

Previous single uncomplicated appendicectomy 20 years ago

Body mass index of 28 kg/m2

The inability to perform PD safely at home because of cognitive impairment or lack of caregiver support is a strong contra-indication to unsupervised home PD.

Peritoneal dialysis performed at home requires the ability to perform aseptic technique and manage exchanges, or reliable caregiver support. Significant cognitive impairment without a capable caregiver is a major contraindication to unsupervised home PD because of infection risk and treatment errors. Advanced age alone is not a contraindication if the patient is cognitively intact and has suitable environment/support. Diabetes, prior uncomplicated intra-abdominal surgery remote in time, and BMI in the overweight range are not absolute contra-indications; specific surgical adhesions or extensive previous abdominal surgery may pose problems but a remote uncomplicated appendicectomy usually does not.

9 / 10

In which of the following acute kidney injury (AKI) scenarios is peritoneal dialysis (PD) least appropriate compared with extracorporeal therapies (CRRT/haemodialysis)?

AKI in a low‑resource setting in a haemodynamically stable patient without major metabolic derangements

AKI in a neonate or small infant where vascular access for haemodialysis is difficult

AKI in a patient with severe coagulopathy where anticoagulation for CRRT is contraindicated

AKI in an immunocompetent patient with isolated uraemic symptoms but stable haemodynamics

AKI in a critically ill, hypercatabolic patient with life‑threatening hyperkalaemia and pulmonary oedema requiring immediate high‑efficiency solute and fluid removal

PD is generally unsuitable when immediate, high-efficiency solute and fluid removal is required (e.g., life‑threatening hyperkalaemia with pulmonary oedema); haemodialysis/CRRT is preferred.

PD is valuable in many AKI situations (especially paediatric/neonatal cases, low-resource settings, patients with bleeding risk) because it avoids vascular access and systemic anticoagulation. However, PD provides lower instantaneous solute and fluid clearance than haemodialysis/CRRT and is therefore least appropriate for patients needing very rapid, high-efficiency removal of potassium and fluid (life‑threatening hyperkalemia and pulmonary oedema) where haemodialysis or CRRT is preferred. The other scenarios listed are situations where PD can be appropriate or even advantageous.

10 / 10

A 60-year-old anuric PD patient presents with serum potassium 7.2 mmol/L and ECG changes. The team consider using PD for rapid potassium removal because haemodialysis access will take time. Which PD prescription is most appropriate to remove potassium quickly?

Single long daytime icodextrin dwell lasting 10–12 hours

Standard CAPD exchanges every 6 hours with 2-L fills and no change in dialysate potassium

One immediate intraperitoneal injection of insulin plus glucose into the peritoneal cavity

Use haemofiltration instead — PD is never effective for hyperkalaemia

Use potassium-free (0 mmol/L) dialysate with short dwells and frequent exchanges (e.g., repeated 1–2 hour exchanges) to maximise transperitoneal potassium removal

For acute hyperkalaemia using PD, use potassium‑free dialysate and short, frequent exchanges to maximise rapid potassium removal; give standard temporising measures (IV insulin–glucose) concurrently.

To use PD for acute hyperkalaemia, potassium-free dialysate (commercial PD fluids typically contain no potassium) and a strategy of short dwells with frequent exchanges increases transperitoneal clearance of potassium because potassium diffuses down its gradient into the dialysate. A long icodextrin dwell is not optimal for rapid potassium removal because its slower solute clearance and long dwell time limit immediate K removal. Standard CAPD intervals are too long for acute emergency removal. Insulin–glucose should be given intravenously (not injected into the peritoneal cavity) as immediate temporising therapy. Haemodialysis is the fastest modality and preferable if available urgently, but PD can be used with potassium‑free solutions and frequent exchanges if HD access is delayed.

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