Master Renal Medicine
for MRCP Part 1
Access 50+ high-yield questions tailored for the 2026 syllabus. Includes AI-powered explanations and performance tracking.
What the MRCP Part 1 Tests in Renal Medicine
MRCP Part 1 Renal Medicine tests the ability to diagnose and manage acute kidney injury (AKI), chronic kidney disease (CKD), glomerulonephritis, tubular disorders, and electrolyte/acid-base disturbances. Candidates must apply KDIGO AKI criteria (creatinine rise ≥26.5 µmol/L in 48h or ≥1.5× baseline within 7 days), differentiate prerenal from intrinsic AKI using urine sodium (<20 mmol/L prerenal, >40 mmol/L intrinsic) and fractional excretion of sodium (FENa <1% prerenal, >2% intrinsic). They must know CKD staging by eGFR (G1 ≥90, G2 60-89, G3a 45-59, G3b 30-44, G4 15-29, G5 <15 mL/min/1.73m²) and albuminuria categories (A1 <3, A2 3-30, A3 >30 mg/mmol). Questions often present with urinalysis, renal biopsy results, or acid-base nomograms. Emphasis is on first-line treatments: ACEi/ARB for proteinuric CKD, steroids for minimal change disease, rituximab for ANCA vasculitis, and managing complications like hyperkalaemia (calcium gluconate, insulin/dextrose, salbutamol, then calcium resonium or patiromer).
High-Yield Concepts
- AKI Classification and Causes: KDIGO criteria: Stage 1: creatinine rise ≥26.5 µmol/L in 48h or 1.5-1.9× baseline; Stage 2: 2.0-2.9×; Stage 3: ≥3× or ≥353.6 µmol/L or initiation of RRT. Common prerenal causes: hypovolaemia, NSAIDs, ACEi. Intrinsic: acute tubular necrosis (ATN) from ischaemia or nephrotoxins (aminoglycosides, contrast), acute interstitial nephritis (AIN) from drugs (penicillins, PPIs, NSAIDs), glomerulonephritis. Postrenal: obstruction (BPH, stones, tumour).
- Nephrotic Syndrome Management: Defined by proteinuria >3.5 g/24h, hypoalbuminaemia <30 g/L, oedema, hyperlipidaemia. First-line for minimal change disease: prednisolone 1 mg/kg/day (max 80 mg) for 4-16 weeks. For membranous nephropathy: conservative (ACEi, statins) plus rituximab 1 g IV on days 1 and 15 if PLA2R antibody-positive. Focal segmental glomerulosclerosis (FSGS): steroids for primary, but often resistant; consider calcineurin inhibitors. Anticoagulate if albumin <20 g/L due to thromboembolism risk.
- ANCA-Associated Vasculitis and RPGN: Rapidly progressive glomerulonephritis (RPGN) presents with haematuria, red cell casts, crescents on biopsy. Anti-GBM disease: plasma exchange, cyclophosphamide, steroids. ANCA vasculitis (granulomatosis with polyangiitis, microscopic polyangiitis): induction with cyclophosphamide or rituximab plus high-dose steroids; maintenance with azathioprine or rituximab. Check ANCA (c-ANCA/PR3 in GPA, p-ANCA/MPO in MPA).
- Electrolyte Emergencies: Hyperkalaemia: Life-threatening if K+ >6.5 mmol/L or ECG changes (peaked T waves, loss of P wave, widened QRS). Immediate: 10 mL 10% calcium gluconate IV over 2-3 min (cardioprotection). Then shift K+ intracellularly: 10 units Actrapid insulin + 50 mL 50% dextrose IV over 15 min; salbutamol 5 mg nebulised. Remove K+: calcium resonium 15 g oral/PR, or patiromer, or haemodialysis if severe/refractory.
- Metabolic Acidosis: AG and Non-AG: Calculate anion gap (AG = Na - [Cl + HCO3]; normal 8-12). High AG acidosis: MUDPILES (methanol, uraemia, DKA, propylene glycol, isoniazid, lactate, ethylene glycol, salicylates). Non-AG (hyperchloraemic) acidosis: renal tubular acidosis (RTA), diarrhoea, acetazolamide. RTA type 1 (distal): hypokalaemia, nephrocalcinosis, urine pH >5.5. RTA type 2 (proximal): hypokalaemia, Fanconi syndrome (glycosuria, phosphaturia, aminoaciduria). RTA type 4: hyperkalaemia, hypoaldosteronism (e.g., DM, ACEi).
- CKD-MBD and Anaemia Management: CKD-mineral bone disorder: monitor Ca, PO4, PTH, vitamin D. Treat hyperphosphataemia with dietary restriction and phosphate binders (calcium acetate, sevelamer, lanthanum). For secondary hyperparathyroidism, use active vitamin D (calcitriol) or cinacalcet. Renal anaemia: target Hb 100-120 g/L; give IV iron if ferritin <100 µg/L or TSAT <20%; start ESA (epoetin alfa or darbepoetin) if Hb <100 g/L after iron repletion.
- Renal Replacement Therapy Indications: AEIOU: Acidosis (pH <7.15), Electrolytes (K+ >6.5 refractory), Intoxications (lithium, methanol, ethylene glycol, salicylates), Overload (pulmonary oedema unresponsive to diuretics), Uraemia (pericarditis, encephalopathy, bleeding). Also consider when creatinine >800 µmol/L or eGFR <10 mL/min/1.73m² in CKD. Modalities: haemodialysis, peritoneal dialysis, or haemofiltration in ICU.
- Hereditary Renal Diseases: Autosomal dominant polycystic kidney disease (ADPKD): PKD1 or PKD2 mutation; presents with hypertension, haematuria, flank pain, recurrent UTIs; screen for berry aneurysms. Alport syndrome: X-linked COL4A5 mutation; sensorineural deafness, lenticonus, progressive CKD; no specific treatment, ACEi slows progression. Fabry disease: X-linked α-galactosidase A deficiency; acroparesthesias, angiokeratomas, corneal opacities, CKD; treat with agalsidase alfa/beta enzyme replacement.
Common Traps in Renal Medicine Questions
- Confusing prerenal AKI with ATN: prerenal has low urine Na (<20) and FENa <1%, while ATN has high urine Na (>40) and FENa >2%.
- Assuming all hyperkalaemia with ECG changes can wait for lab confirmation: give calcium gluconate immediately if ECG abnormal or K+ >6.5 mmol/L.
- Mistaking nephritic syndrome (haematuria, hypertension, oliguria, red cell casts) for nephrotic syndrome (heavy proteinuria, oedema, hypoalbuminaemia) — they have different management.
- Forgetting that ACEi/ARB can cause acute rise in creatinine (up to 30%) which is acceptable and not a reason to stop unless rise >50% or hyperkalaemia develops.
- Thinking that renal biopsy is contraindicated if single kidney or eGFR <30 — it is possible with careful planning (e.g., transjugular approach) but higher risk.
- Overlooking that in type 4 RTA (hyperkalaemic metabolic acidosis), the primary defect is hypoaldosteronism; treat with fludrocortisone if not volume-overloaded.
How to Revise Renal Medicine for the MRCP Part 1
Focus on acute scenarios: AKI with drug history (NSAIDs, ACEi, aminoglycosides), glomerulonephritis presenting with haematuria and proteinuria, and electrolyte crises. Practice interpreting ABG and renal function trends quickly. Questions often give a vignette with urine dipstick, serum creatinine, and potassium; you must decide next step (e.g., fluid challenge vs. stop nephrotoxin vs. biopsy vs. dialysis). Memorise key cut-offs: K+ >6.5 for emergency, creatinine rise criteria for AKI staging, eGFR thresholds for drug dosing (e.g., metformin stop at eGFR <30, DOACs adjust at <15-30). Revise drug nephrotoxicity: lithium (nephrogenic DI), tenofovir (Fanconi), cisplatin (ATN), calcineurin inhibitors (hypertension, hyperkalaemia). Use question banks with clinical reasoning; expect 2-3 questions on acid-base and 2-3 on glomerular disease per paper. Prioritise understanding pathophysiology over rare syndromes.
Practise it: MedLumen has 50 Renal Medicine questions for the MRCP Part 1, each with a full explanation and references.
Sample Practice Questions
A 68-year-old male presents with a 3-month history of progressive fatigue, anorexia, and pruritus. His past medical history includes hypertension and type 2 diabetes mellitus, both managed with oral medications. On examination, he is pale and has bilateral pitting oedema to the mid-shins. Blood pressure is 155/95 mmHg. Investigations reveal: Haemoglobin 9.2 g/dL, Urea 28 mmol/L (normal range 2.5-7.5 mmol/L), Creatinine 450 umol/L (normal range 60-110 umol/L), eGFR 12 mL/min/1.73m2. Urine dipstick shows 3+ protein. What is the most likely underlying diagnosis based on this presentation?
A 24-year-old woman presents with sudden onset flank pain, haematuria, and fever. She recently had a urinary tract infection treated with trimethoprim. On examination, she has a temperature of 39.1°C, tenderness in the right costovertebral angle, and appears unwell. Blood tests show an elevated white cell count and C-reactive protein. Urinalysis reveals leucocytes, erythrocytes, and nitrites. What is the most appropriate initial management step?
A 55-year-old man with a history of hypertension and hyperlipidaemia presents with recurrent episodes of gross haematuria and colicky flank pain, radiating to the groin. The episodes last several hours and are associated with nausea. He has no fever or dysuria. His blood pressure is 140/85 mmHg. Urinalysis during an episode shows numerous red blood cells. Serum creatinine is 90 umol/L. What is the most likely diagnosis?
A 35-year-old female is found to have an incidental finding of microalbuminuria (urine albumin-to-creatinine ratio 45 mg/g) on routine screening. She has no known medical history, takes no medications, and her blood pressure is 120/70 mmHg. Her fasting blood glucose is 5.2 mmol/L. She is asymptomatic. What is the most appropriate next step in her management?
A 72-year-old male with known prostatic hypertrophy presents with anuria for 12 hours. He has lower abdominal discomfort but denies dysuria or fever. On examination, a distended bladder is palpable suprapubically. His serum creatinine has risen from 100 umol/L to 250 umol/L since his last blood test a month ago. What is the most appropriate immediate management?
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Renal Medicine Questions for MRCP Part 1 — FAQ
How many Renal Medicine questions does MedLumen have for MRCP Part 1?
MedLumen currently has 50+ Renal Medicine practice questions for MRCP Part 1, each with a detailed explanation so you understand the reasoning behind every answer.
Are the Renal Medicine questions updated for the 2026 MRCP Part 1 syllabus?
Yes. Our Renal Medicine questions are mapped to the latest MRCP Part 1 blueprint and reviewed regularly so they stay aligned with the current 2026 syllabus.
Can I practise Renal Medicine questions for free?
You can preview sample Renal Medicine questions for free. A MedLumen subscription unlocks all 50+ Renal Medicine questions, full answer explanations, and performance analytics for MRCP Part 1.
How should I revise Renal Medicine for MRCP Part 1?
Practise Renal Medicine questions in timed blocks, read the explanation for every answer (right or wrong), and use MedLumen's analytics to revisit your weak areas until your accuracy is consistently high.