Prometric Exam Questions for Nephrology Specialists 2026: 20 MCQs with Answers on Acute Kidney Injury, Chronic Kidney Disease, Glomerulonephritis, Nephrotic Syndrome, Electrolytes, Dialysis, Transplantation, Hypertension and Diabetic Kidney Disease

The specialist nephrology paper (NEP5991 at DHA, and the equivalents at SCFHS, QCHP, NHRA and the other authorities) is 100 to 150 single-best-answer questions in up to three hours with a pass mark of about 60%. The Gulf has among the highest rates of diabetes and dialysis dependence in the world, and the paper reflects it: diabetic kidney disease, dialysis prescription and complications, and transplantation sit alongside the classic glomerular diseases and electrolyte emergencies. The licensing route is in the nephrologist guide.

Acute kidney injury

Question 1

A patient's creatinine rises from 90 to 200 micromol/L over 48 hours with urine output of 0.4 mL/kg/h for 14 hours. The KDIGO AKI stage is:

1. Stage 1
2. Stage 2 (creatinine 2.0 to 2.9 times baseline, or urine output below 0.5 mL/kg/h for 12 hours or more)
3. Stage 3
4. Not AKI

Answer: B. Stage 3 is a threefold rise, creatinine above 354 micromol/L, initiation of dialysis, or anuria for 12 hours.

Question 2

A 75-year-old on an ACE inhibitor, a thiazide and an NSAID becomes dehydrated with gastroenteritis and develops AKI. Urinalysis is bland. The most likely mechanism and initial management are:

1. Glomerulonephritis; steroids
2. Haemodynamic (pre-renal) AKI from volume depletion with loss of autoregulation ("triple whammy"); stop the nephrotoxins, correct volume with isotonic fluid, monitor potassium and treat the cause
3. Obstruction; nephrostomy
4. Acute interstitial nephritis; biopsy

Answer: B. Sick-day rules (holding ACE inhibitors, diuretics, metformin and NSAIDs during dehydrating illness) are a tested patient-education point.

Question 3

A patient started on omeprazole and a new antibiotic three weeks ago develops AKI with fever, rash, eosinophilia and sterile pyuria with white cell casts. The most likely diagnosis is:

1. Acute tubular necrosis
2. Acute interstitial nephritis, drug-induced; stop the offending drug and consider glucocorticoids if there is no early recovery
3. Post-streptococcal glomerulonephritis
4. Renal vein thrombosis

Answer: B. Proton pump inhibitors, antibiotics (beta-lactams, sulfonamides, rifampicin), NSAIDs and checkpoint inhibitors are the common culprits.

Question 4

Which measure best reduces contrast-associated AKI in a high-risk patient with CKD stage 3b before a coronary angiogram?

1. N-acetylcysteine
2. Intravenous isotonic saline hydration before and after, the lowest necessary volume of iso- or low-osmolar contrast, and holding nephrotoxins; sodium bicarbonate and N-acetylcysteine add no proven benefit
3. Prophylactic haemodialysis after contrast
4. Furosemide before the procedure

Answer: B. Metformin is held around contrast in patients with reduced eGFR because of lactic acidosis risk if AKI develops.

Chronic kidney disease

Question 5

A 58-year-old with type 2 diabetes has an eGFR of 45 mL/min/1.73 m² and a urine albumin-to-creatinine ratio of 60 mg/mmol. Beyond glucose and blood pressure control, which therapy reduces progression and cardiovascular events?

1. A sulfonylurea
2. Maximal tolerated ACE inhibitor or ARB plus an SGLT2 inhibitor, with finerenone or a GLP-1 receptor agonist considered for residual albuminuria
3. A thiazolidinedione
4. Dual ACE inhibitor and ARB therapy

Answer: B. SGLT2 inhibitors slow CKD progression regardless of diabetes status (DAPA-CKD, EMPA-KIDNEY); dual RAAS blockade increases hyperkalaemia and AKI without benefit.

Question 6

A patient with CKD stage 4 has a haemoglobin of 92 g/L, ferritin 80 µg/L and transferrin saturation 14%. The first step in managing the anaemia is:

1. Start an erythropoiesis-stimulating agent immediately
2. Correct iron deficiency first (intravenous iron is often needed in CKD), target ferritin above 100 µg/L and saturation above 20%, then an ESA if haemoglobin remains below 100 g/L, aiming for 100 to 115 g/L and avoiding normalisation
3. Transfuse to a haemoglobin of 120 g/L
4. Oral vitamin B12

Answer: B. Targeting normal haemoglobin with ESAs increases stroke and thrombosis; blood transfusion is minimised in transplant candidates because of sensitisation.

Question 7

A dialysis patient has a phosphate of 2.4 mmol/L, calcium 2.1 mmol/L and PTH 95 pmol/L. Management of the mineral bone disorder includes:

1. Calcium-based binders in unlimited doses
2. Dietary phosphate restriction and dialysis adequacy, phosphate binders (non-calcium binders such as sevelamer or lanthanum preferred where calcium is high or vascular calcification is present), active vitamin D or a calcimimetic such as cinacalcet for secondary hyperparathyroidism, with parathyroidectomy for refractory cases
3. High-dose calcium supplements
4. No treatment

Answer: B. Calciphylaxis and vascular calcification are the feared consequences; PTH is kept at about two to nine times the upper limit of normal in dialysis patients.

Glomerular disease

Question 8

A 28-year-old man has recurrent episodes of visible haematuria after upper respiratory infections, persistent microscopic haematuria, proteinuria of 1.2 g/day and normal complement. The most likely diagnosis and first-line management are:

1. Minimal change disease; steroids
2. IgA nephropathy; maximal supportive care with ACE inhibitor or ARB, blood pressure control, SGLT2 inhibitor, and consideration of glucocorticoids or newer agents (targeted-release budesonide, sparsentan) for persistent proteinuria above 0.75 to 1 g/day after optimised supportive care
3. Alport syndrome; genetic testing only
4. Post-infectious glomerulonephritis; antibiotics

Answer: B. Biopsy shows mesangial IgA deposits; the MEST-C Oxford score and proteinuria predict progression.

Question 9

A 6-year-old has sudden periorbital and leg oedema, proteinuria of 4+ on dipstick, serum albumin 18 g/L and normal blood pressure, creatinine and complement. Appropriate management is:

1. Renal biopsy before any treatment
2. Empirical oral prednisolone (60 mg/m² per day) for presumed minimal change disease, with salt restriction, cautious diuretics, pneumococcal vaccination and monitoring for infection and thrombosis; biopsy is reserved for steroid resistance, atypical features or age outside 1 to 12 years
3. Cyclophosphamide first line
4. Albumin infusions daily

Answer: B. Over 90% of childhood nephrotic syndrome is minimal change disease and steroid-responsive; frequent relapsers may need levamisole, mycophenolate, calcineurin inhibitors or rituximab.

Question 10

A 40-year-old man has nephrotic syndrome with a biopsy showing membranous nephropathy and positive anti-PLA2R antibodies. Which statement is correct?

1. Secondary causes are more likely than primary disease
2. Anti-PLA2R positivity indicates primary membranous nephropathy; after a period of supportive therapy, immunosuppression (rituximab, or cyclophosphamide-based regimens for high-risk disease) is given to patients with persistent nephrotic proteinuria or declining function, and anticoagulation is considered when albumin is very low
3. Steroids alone cure most cases
4. Dialysis is inevitable within a year

Answer: B. Malignancy, hepatitis B, lupus and drugs cause secondary membranous disease and are screened for when antibodies are negative.

Question 11

A 25-year-old woman with lupus has new proteinuria of 2.5 g/day, haematuria with red cell casts and a rising creatinine. Biopsy shows class IV lupus nephritis. Induction treatment is:

1. Hydroxychloroquine alone
2. Glucocorticoids plus mycophenolate mofetil or low-dose intravenous cyclophosphamide, with belimumab or voclosporin as add-on options, and hydroxychloroquine continued; maintenance with mycophenolate or azathioprine for at least three years
3. Methotrexate
4. Rituximab alone

Answer: B. Mycophenolate is preferred for fertility preservation in young women; azathioprine is the pregnancy-compatible maintenance agent.

Question 12

A 68-year-old presents with a rapidly rising creatinine over three weeks, haematuria, pulmonary haemorrhage and a positive MPO-ANCA. Biopsy shows pauci-immune crescentic glomerulonephritis. Management is:

1. Supportive care only
2. High-dose glucocorticoids plus rituximab or cyclophosphamide, with plasma exchange considered for severe renal failure or pulmonary haemorrhage, and PJP prophylaxis
3. Antibiotics for pneumonia
4. Anticoagulation

Answer: B. Anti-GBM disease, by contrast, requires plasma exchange routinely; linear IgG staining on biopsy distinguishes it.

Electrolytes and acid-base

Question 13

A dialysis patient who missed a session has a potassium of 7.2 mmol/L with peaked T waves and a widened QRS. The immediate sequence is:

1. Oral potassium binder and recheck tomorrow
2. Intravenous calcium gluconate 10% to stabilise the myocardium, then insulin with dextrose and nebulised salbutamol to shift potassium into cells, and urgent haemodialysis for definitive removal; potassium binders and loop diuretics have minor roles
3. Sodium bicarbonate alone
4. Emergency pacing

Answer: B. Calcium does not lower potassium but protects the heart within minutes; dialysis is the only reliable removal in anuric patients.

Question 14

A 70-year-old on a thiazide has a sodium of 118 mmol/L, is confused and has had a seizure. The correct treatment is:

1. Fluid restriction alone
2. Hypertonic 3% saline bolus (for example 100 to 150 mL over 10 to 20 minutes, repeated if needed) to raise sodium by 4 to 6 mmol/L and stop seizures, then a controlled correction of no more than 8 to 10 mmol/L in 24 hours to avoid osmotic demyelination
3. Rapid normalisation with 0.9% saline
4. Desmopressin

Answer: B. Severe symptoms justify hypertonic saline regardless of cause; overcorrection is reversed with dextrose water and desmopressin.

Question 15

Arterial blood gas: pH 7.22, bicarbonate 10 mmol/L, PaCO₂ 3.3 kPa, sodium 138, chloride 100, potassium 5.0, glucose 25 mmol/L, urine ketones strongly positive. The acid-base disorder is:

1. Normal anion gap metabolic acidosis
2. High anion gap metabolic acidosis (gap 28) with appropriate respiratory compensation, consistent with diabetic ketoacidosis
3. Respiratory acidosis
4. Metabolic alkalosis

Answer: B. Anion gap = Na − (Cl + HCO₃) = 138 − 110 = 28. Normal gap acidosis points to diarrhoea or renal tubular acidosis; the urine anion gap separates them.

Dialysis and transplantation

Question 16

Which patient has an absolute indication for urgent renal replacement therapy?

1. A creatinine of 400 micromol/L in a stable patient
2. Refractory pulmonary oedema, refractory hyperkalaemia, severe acidosis unresponsive to treatment, uraemic pericarditis or encephalopathy, or certain dialysable toxins (lithium, methanol, salicylate, metformin-associated lactic acidosis)
3. An eGFR of 15 mL/min with no symptoms
4. Mild hyperphosphataemia

Answer: B. In CKD, dialysis starts for symptoms and complications, usually at an eGFR of 5 to 10, not for a number alone; a fistula is planned when eGFR falls below about 15 to 20.

Question 17

A peritoneal dialysis patient has abdominal pain, fever and cloudy effluent with 450 white cells/µL, 70% neutrophils. The management is:

1. Oral antibiotics and continue dialysis unchanged
2. Diagnose PD peritonitis (effluent WCC above 100/µL with over 50% neutrophils), send effluent for cell count, Gram stain and culture, start empirical intraperitoneal antibiotics covering Gram-positive and Gram-negative organisms, and remove the catheter for refractory, relapsing or fungal peritonitis
3. Immediate catheter removal in all cases
4. Switch to haemodialysis permanently

Answer: B. Exit-site care and training reduce rates; fungal peritonitis mandates catheter removal.

Question 18

Three weeks after a deceased-donor kidney transplant, a patient's creatinine rises from 110 to 190 micromol/L. Tacrolimus level is 7 ng/mL. Ultrasound shows no obstruction and good perfusion. The next step is:

1. Increase tacrolimus empirically
2. Check for donor-specific antibodies and BK virus, then transplant biopsy to distinguish acute T-cell-mediated rejection (treated with pulsed steroids, or thymoglobulin if severe), antibody-mediated rejection (plasma exchange, IVIG, consideration of rituximab) and calcineurin inhibitor toxicity
3. Stop all immunosuppression
4. Start dialysis

Answer: B. Standard maintenance is tacrolimus, mycophenolate and low-dose prednisolone; CMV prophylaxis and PJP prophylaxis are given early; skin cancer surveillance is lifelong.

Question 19

A 45-year-old has recurrent calcium oxalate stones. Twenty-four-hour urine shows hypercalciuria with normal serum calcium and low urine volume. Preventive advice includes:

1. Restrict dietary calcium severely
2. Fluid intake to achieve over 2 to 2.5 litres of urine a day, normal dietary calcium with reduced sodium and animal protein, reduced oxalate-rich foods, citrate supplementation if urinary citrate is low, and a thiazide for persistent hypercalciuria
3. High-dose vitamin C
4. Cranberry juice

Answer: B. Low dietary calcium paradoxically increases oxalate absorption and stones. Heat and dehydration make stone disease very common in the Gulf.

Question 20

A 50-year-old has a blood pressure of 165/100 mmHg despite three agents including a diuretic, with potassium 3.2 mmol/L and an aldosterone-to-renin ratio markedly raised. The most likely diagnosis and next steps are:

1. Essential hypertension; add a fourth agent randomly
2. Primary aldosteronism; confirm with a suppression test, adrenal CT and adrenal vein sampling where surgery is considered, then unilateral adrenalectomy for a lateralising adenoma or a mineralocorticoid receptor antagonist (spironolactone or eplerenone) for bilateral disease
3. Phaeochromocytoma; alpha blockade
4. Renal artery stenosis; stenting

Answer: B. Primary aldosteronism is the commonest secondary cause of resistant hypertension; spironolactone is also the preferred fourth drug in resistant hypertension generally (PATHWAY-2).

How to practise

• Learn the staging and targets: KDIGO AKI and CKD stages, albuminuria categories, anaemia and mineral bone targets, dialysis adequacy.
• Know the glomerular diseases by pattern: haematuria-predominant versus nephrotic, complement levels, serology and biopsy findings.
• Practise electrolyte emergencies as sequences: hyperkalaemia, hyponatraemia, acidosis.
• Practise under time in the Nephrology bank with the error-log method.

Related sets: internal medicine, urology and endocrinology. Dialysis staff should see the dialysis technician questions.

Frequently asked questions

How many questions are in the Prometric nephrology specialist exam?

Typically 100 to 150 single-best-answer MCQs in up to three hours, with a pass mark of about 60%, varying by authority.

Which nephrology topics come up most?

AKI and CKD management, diabetic kidney disease, glomerulonephritis and nephrotic syndrome, electrolyte emergencies, dialysis indications and complications, and transplantation.

Does the exam include acid-base and electrolyte calculations?

Yes. Expect anion gap, sodium correction rates and potassium management questions.

Which guidelines does the exam follow?

Current KDIGO guidelines for AKI, CKD, glomerular disease, anaemia, mineral bone disorder and transplantation, with ESC/ESH hypertension guidance.

Are these real exam questions?

No. They are original practice questions written to the published blueprint. Real exam content is confidential.