Renal Medicine MCQs: MRCP Part 2

Test yourself

Pick an answer to reveal the explanation.

• Question 1

  A 68-year-old man on long-term omeprazole is given a course of flucloxacillin for cellulitis. Ten days later his creatinine has risen sharply. Urinalysis shows sterile pyuria with white cell casts, and he has a peripheral eosinophilia. What is the most likely diagnosis?

  • AAcute tubular necrosis
  • BAcute interstitial nephritis
  • CPrerenal acute kidney injury
  • DPost-streptococcal glomerulonephritis
  • EMinimal change disease

  Answer: B

  The combination of a rising creatinine after starting drugs (here a PPI and an antibiotic), sterile pyuria with white cell casts and peripheral eosinophilia is characteristic of acute interstitial nephritis, an immune-mediated, usually drug-induced injury. Acute tubular necrosis gives muddy-brown granular casts, not white cell casts. Prerenal AKI has a bland sediment and responds to fluids. Post-streptococcal GN causes a nephritic picture roughly two weeks after streptococcal infection with a low C3. Management is to stop the offending drug, with corticosteroids often added.

• Question 2

  A 74-year-old woman is admitted with vomiting and reduced oral intake. She is hypotensive and her creatinine is elevated. Urine sodium is 12 mmol/L, urine osmolality 640 mOsm/kg, and the fractional excretion of sodium is 0.4%. The sediment is bland. What is the most likely cause of her acute kidney injury?

  • AAcute tubular necrosis
  • BPrerenal (pre-renal) uraemia
  • CAcute interstitial nephritis
  • DObstructive uropathy
  • ERapidly progressive glomerulonephritis

  Answer: B

  A low urine sodium (under 20 mmol/L), high urine osmolality (over 500 mOsm/kg), fractional excretion of sodium below 1% and a bland sediment indicate an intact kidney that is avidly retaining sodium and water in response to hypoperfusion — prerenal AKI. In acute tubular necrosis the damaged tubules cannot concentrate urine or reclaim sodium, so urine sodium and osmolality move in the opposite direction and muddy-brown casts appear. Restoring perfusion with fluids should improve her function.

• Question 3

  A 34-year-old man with autosomal dominant polycystic kidney disease has a father who died of a subarachnoid haemorrhage. He is asymptomatic. Which investigation is most appropriate to screen for the relevant extrarenal complication?

  • AEchocardiography
  • BCT of the abdomen
  • CMagnetic resonance angiography of the cerebral vessels
  • DCarotid Doppler ultrasound
  • ELumbar puncture

  Answer: C

  ADPKD is associated with intracranial (berry) aneurysms, which can rupture to cause a subarachnoid haemorrhage. Screening with MR angiography of the cerebral vessels is appropriate in those with a family history of subarachnoid haemorrhage or aneurysm. Echocardiography would assess for valvular disease (also associated) but not the aneurysm risk implied by the family history. A lumbar puncture and carotid Doppler are not screening tools for unruptured intracranial aneurysms.

• Question 4

  A 26-year-old man presents with haemoptysis and rapidly worsening renal function. Renal biopsy shows a crescentic glomerulonephritis with linear IgG deposition along the glomerular basement membrane, and serum anti-GBM antibodies are positive. Which treatment is most important?

  • AOral prednisolone alone
  • BAn ACE inhibitor
  • CPlasma exchange with corticosteroids and cyclophosphamide
  • DRituximab monotherapy
  • EObservation with repeat biopsy

  Answer: C

  This is anti-GBM (Goodpasture) disease — a pulmonary-renal syndrome from antibodies to type IV collagen, confirmed by linear IgG on biopsy and positive anti-GBM antibodies. Urgent plasma exchange removes circulating antibody, combined with corticosteroids and cyclophosphamide to suppress its production. Speed is critical to preserve renal function and prevent life-threatening pulmonary haemorrhage. An ACE inhibitor or observation would allow progression, and steroids alone are insufficient.

• Question 5

  A 22-year-old man develops visible ('cola-coloured') haematuria one day after the onset of a sore throat. His complement C3 is normal and renal function is preserved. What is the most likely diagnosis?

  • APost-streptococcal glomerulonephritis
  • BIgA nephropathy
  • CAnti-GBM disease
  • DMinimal change disease
  • EMembranous nephropathy

  Answer: B

  Visible haematuria occurring within 1–2 days of an upper respiratory tract infection ('synpharyngitic'), with a normal complement, is typical of IgA nephropathy. Post-streptococcal glomerulonephritis develops around two weeks after infection and characteristically has a transiently low C3. Timing and complement are the discriminators. Minimal change and membranous disease present with nephrotic syndrome, not visible haematuria, and anti-GBM disease would cause rapidly progressive renal failure often with lung involvement.

• Question 6

  A haemodialysis patient is found to have a potassium of 7.2 mmol/L. The ECG shows tall, tented T waves. What is the most appropriate immediate first step?

  • AIntravenous insulin with dextrose
  • BNebulised salbutamol
  • CIntravenous calcium gluconate
  • DOral potassium binder
  • EUrgent haemodialysis

  Answer: C

  With ECG changes, the first priority is to stabilise the myocardium using intravenous calcium (gluconate or chloride). It acts within minutes but does not lower the potassium itself. Insulin-dextrose and salbutamol then shift potassium into cells, and definitive removal (a potassium binder or, in this dialysis patient, haemodialysis) follows. Giving a shifting agent or dialysis first, without cardioprotection, leaves the heart vulnerable while those measures take effect.

• Question 7

  A 6-year-old boy presents with periorbital oedema and heavy proteinuria. Renal biopsy would be expected to show normal glomeruli on light microscopy with effacement of the podocyte foot processes on electron microscopy. What is the most appropriate first-line treatment?

  • ACorticosteroids
  • BCyclophosphamide
  • CAn ACE inhibitor only
  • DRituximab
  • EPlasma exchange

  Answer: A

  This is minimal change disease, the commonest cause of nephrotic syndrome in children, characterised by normal light microscopy and foot-process effacement on electron microscopy. The great majority of children respond to corticosteroids, which are first-line (and often started empirically without biopsy in typical cases). Cyclophosphamide or a calcineurin inhibitor is reserved for frequent relapsers or steroid-dependent disease. Plasma exchange has no role here.

• Question 8

  A 62-year-old man presents with nephrotic syndrome. Serum anti-phospholipase A2 receptor (anti-PLA2R) antibodies are positive. What is the most likely underlying diagnosis?

  • AMinimal change disease
  • BFocal segmental glomerulosclerosis
  • CMembranous nephropathy
  • DIgA nephropathy
  • EAmyloidosis

  Answer: C

  Anti-PLA2R antibodies are present in the majority of cases of primary membranous nephropathy, the commonest cause of nephrotic syndrome in older adults. Their presence in a patient with nephrotic syndrome strongly supports the diagnosis. Membranous nephropathy also carries the highest risk of venous thromboembolism, including renal vein thrombosis, of the glomerular diseases. Anti-PLA2R is not a feature of minimal change disease, FSGS, IgA nephropathy or amyloidosis.

• Question 9

  A 4-year-old girl develops acute kidney injury a few days after an illness with bloody diarrhoea. Investigations show anaemia with schistocytes on the blood film, thrombocytopenia, and normal coagulation studies. What is the most likely diagnosis?

  • ADisseminated intravascular coagulation
  • BImmune thrombocytopenic purpura
  • CHaemolytic uraemic syndrome
  • DHenoch–Schönlein purpura
  • EAcute tubular necrosis

  Answer: C

  The triad of microangiopathic haemolytic anaemia (schistocytes), thrombocytopenia and acute kidney injury following bloody diarrhoea in a child is typical of haemolytic uraemic syndrome, usually caused by Shiga-toxin-producing E. coli. Normal coagulation distinguishes it from DIC. Management is supportive, and antibiotics are generally avoided as they may increase toxin release. ITP causes isolated thrombocytopenia without haemolysis or AKI, and HSP causes a palpable purpura with normal platelets.

• Question 10

  A 58-year-old man with type 2 diabetes is found to have a raised urinary albumin:creatinine ratio. His blood pressure is 124/78 mmHg. Which intervention is most appropriate to slow progression of his diabetic kidney disease?

  • ANo treatment, as he is normotensive
  • BStart an ACE inhibitor
  • CStart both an ACE inhibitor and an ARB
  • DStart a dihydropyridine calcium-channel blocker
  • EStart a loop diuretic

  Answer: B

  An ACE inhibitor (or ARB) should be started once albuminuria is present in diabetic kidney disease, even when blood pressure is normal, because it reduces intraglomerular pressure and albuminuria and slows progression. An SGLT2 inhibitor would also be added for its renal benefit. ACE inhibitors and ARBs must not be combined because of the risk of hyperkalaemia and acute kidney injury. Withholding treatment because he is normotensive misses the renoprotective indication.