Acute kidney injury, contrast & TMA — MRCP Part 1 flashcards

Question 1

What creatinine change defines KDIGO stage 1 AKI?

Accepted Answer

A rise of ≥26.5 µmol/L within 48 hours, or 1.5–1.9 times baseline within 7 days. — KDIGO (used by NICE NG148) stages AKI by the worse of the creatinine or urine-output criteria.

Question 2

Name the creatinine criteria for KDIGO stage 3 AKI.

Accepted Answer

Creatinine 3 times baseline or more, OR creatinine ≥354 µmol/L, OR starting renal replacement therapy. — Stage 2 is 2.0–2.9 times baseline. Stage 3 carries the highest mortality and needs urgent renal input.

Question 3

KDIGO urine-output criteria: stage 1 AKI is <0.5 mL/kg/h for ______; stage 3 is <0.3 mL/kg/h for 24 hours or anuria for 12 hours.

Accepted Answer

more than 6 hours — Stage 2 is <0.5 mL/kg/h for more than 12 hours. Urine output often falls before creatinine rises.

Question 4

KDIGO urine-output criteria: stage 1 AKI is <0.5 mL/kg/h for more than 6 hours; stage 3 is <0.3 mL/kg/h for ______.

Accepted Answer

24 hours or anuria for 12 hours — Stage 2 is <0.5 mL/kg/h for more than 12 hours. Urine output often falls before creatinine rises.

Question 5

What fractional excretion of sodium (FENa) suggests pre-renal AKI rather than acute tubular necrosis?

Accepted Answer

FENa below 1% (urine sodium usually <20 mmol/L). — In pre-renal AKI the tubules still work and avidly retain sodium. Damaged tubules in ATN cannot, so FENa is above 1% and urine sodium above 40 mmol/L.

Question 6

A patient with AKI has been taking furosemide. Which urinary index is more reliable than FENa for detecting a pre-renal state?

Accepted Answer

Fractional excretion of urea (FEUrea) — below 35% suggests pre-renal AKI. — Diuretics force sodium into the urine and falsely raise FENa. Urea handling is much less affected by diuretics.

Question 7

What is the classic urine microscopy finding in acute tubular necrosis?

Accepted Answer

Muddy brown granular casts (renal tubular epithelial cell casts). — They are made of sloughed, necrotic tubular cells. Pre-renal AKI has a bland urinalysis; glomerulonephritis gives red cell casts.

Question 8

Name three nephrotoxic drugs that classically cause acute tubular necrosis.

Accepted Answer

Any three of: aminoglycosides (gentamicin), vancomycin, amphotericin B, cisplatin, iodinated contrast. — These injure tubular epithelial cells directly. Aminoglycoside toxicity is related to trough levels, so monitor levels and renal function.

Question 9

Name four drugs that commonly cause acute interstitial nephritis.

Accepted Answer

Any four of: PPIs (omeprazole, lansoprazole), penicillins, cephalosporins, NSAIDs, rifampicin, ciprofloxacin, diuretics. — Drugs cause most cases of AIN (a type IV hypersensitivity reaction). It can occur weeks after starting the drug, especially with PPIs.

Question 10

A 68-year-old woman started omeprazole 3 weeks ago. Her creatinine has doubled. She has a faint rash and a blood eosinophil count of 1.2 × 10⁹/L. Urine shows leucocytes with a negative culture. What urinary casts are typical of the likely diagnosis?

Accepted Answer

White cell casts (with sterile pyuria ± eosinophiluria). — This is drug-induced acute interstitial nephritis. Inflammatory cells infiltrate the interstitium and tubules, so white cells (not red cell casts) appear in the urine.

Question 11

What is the definitive (gold-standard) investigation for acute interstitial nephritis?

Accepted Answer

Renal biopsy — interstitial oedema with lymphocytes, plasma cells and eosinophils (tubulitis). — Urine eosinophils are suggestive but neither sensitive nor specific; histology confirms the diagnosis.

Question 12

What is the first-line management of drug-induced acute interstitial nephritis?

Accepted Answer

Stop the offending drug; consider oral corticosteroids if renal function does not improve. — Most cases recover once the drug is withdrawn. Steroids are used if creatinine keeps rising; delay risks permanent interstitial fibrosis.

Question 13

Name three drugs that can cause AKI through intratubular crystal deposition.

Accepted Answer

Any three of: aciclovir, methotrexate, indinavir, triamterene (also sulfonamides). — These drugs precipitate in the tubules, especially when the patient is dehydrated. Hydration before high-dose methotrexate or IV aciclovir reduces the risk.

Question 14

In AKI with no obvious cause, or suspected urinary tract obstruction, what imaging does NICE recommend and how quickly?

Accepted Answer

Urgent renal tract ultrasound within 24 hours of assessment (immediate, within 6 hours, if pyonephrosis — an infected obstructed kidney — is suspected). — Obstruction is reversible and needs prompt drainage. An infected obstructed kidney is a urological emergency.

Question 15

Name four types of medicine that should usually be withheld when a patient develops AKI or is acutely unwell and dehydrated ('sick day rules').

Accepted Answer

Any four of: ACE inhibitors, ARBs, diuretics, NSAIDs, metformin, SGLT2 inhibitors, sulfonylureas. — ACEi/ARBs, NSAIDs and diuretics reduce glomerular perfusion. Metformin (lactic acidosis), sulfonylureas (hypoglycaemia) and SGLT2 inhibitors (ketoacidosis) become dangerous as renal clearance falls.

Question 16

How does trimethoprim cause hyperkalaemia and a rise in serum creatinine?

Accepted Answer

It blocks ENaC in the collecting duct (amiloride-like) and inhibits tubular secretion of creatinine. — The creatinine rise does not always mean a true fall in GFR. Hyperkalaemia is more likely with ACEi/ARBs, spironolactone or CKD.

Question 17

In suspected rhabdomyolysis, which blood test confirms the diagnosis?

Accepted Answer

Creatine kinase (CK) — markedly raised, typically more than 5 times the upper limit of normal. — Myoglobin released from damaged muscle is toxic to tubules and causes ATN. Treat with aggressive IV fluids.

Question 18

A high-risk inpatient (e.g. eGFR below 30) needs iodinated contrast. What does NICE suggest to reduce the risk of contrast-induced AKI?

Accepted Answer

Consider IV volume expansion with isotonic sodium bicarbonate or 0.9% sodium chloride, and consider temporarily stopping ACE inhibitors/ARBs. — NICE (2024) counts eGFR below 30, a kidney transplant, large contrast volumes and intra-arterial contrast with first-pass renal exposure as high risk. Other risks include diabetes with CKD, heart failure and age over 75.

Question 19

What is the classic triad of haemolytic uraemic syndrome (HUS)?

Accepted Answer

Microangiopathic haemolytic anaemia, thrombocytopenia and acute kidney injury. — Thrombi in small vessels shear red cells (schistocytes) and consume platelets; the kidney is the main target. TTP adds fever and neurological features (pentad).

Question 20

What is the most common cause of typical (diarrhoea-associated) HUS?

Accepted Answer

Shiga toxin–producing Escherichia coli, classically O157:H7. — It mainly affects children after bloody diarrhoea. Shigella dysenteriae is another Shiga-toxin cause.

Question 21

What is the mechanism of eculizumab, the treatment for atypical HUS?

Accepted Answer

A monoclonal antibody against complement C5, blocking formation of the membrane attack complex. — Atypical HUS is driven by uncontrolled activation of the alternative complement pathway. Ravulizumab is a longer-acting C5 inhibitor.

Question 22

Deficiency of which enzyme causes thrombotic thrombocytopenic purpura (TTP)?

Accepted Answer

ADAMTS13 (the von Willebrand factor–cleaving protease). — Without ADAMTS13, ultra-large vWF multimers build up and trigger platelet thrombi. Acquired TTP is due to anti-ADAMTS13 antibodies and is treated with urgent plasma exchange.

Acute kidney injury, contrast & TMA flashcards

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