Chronic Kidney Disease — Written Clinical Reasoning

SAQ 1 — Integrated CKD Management (20 marks, 30 minutes)

Prompt: Outline your integrated management plan for this patient, including progression-slowing therapy, complication management, cardiovascular risk reduction, and dialysis planning. Justify each decision with reference to evidence. [1]

Model Answer

Problem list (4 marks):

1. Progressive diabetic CKD stage 3b (G3b A3) — eGFR falling 9 points in 12 months; very high progression risk
2. Suboptimal blood pressure (146/88) and persistent albuminuria despite ACE inhibitor
3. Renal anaemia with absolute iron deficiency (Hb 98, ferritin 45, TSAT 15%)
4. Early CKD-MBD — secondary hyperparathyroidism (PTH 18), borderline phosphate
5. Mild metabolic acidosis (bicarbonate 21)
6. High cardiovascular risk — prior NSTEMI, LVH, diabetes, CKD (coronary risk equivalent)
7. Hyperkalaemia (K+ 5.3) — limiting further RAAS blockade
8. Polypharmacy (8 medications) and the need for sick-day education [1]

Step 1 — Progression-slowing therapy: the four-pillar approach (6 marks): [1]

Step 2 — Complication management (5 marks): [1]

• Anaemia: This is the classic "iron first" scenario. Give IV ferric carboxymaltose (single dose, e.g., 1 g or weight-based) to correct absolute iron deficiency BEFORE any ESA. Target ferritin greater than 100, TSAT greater than 20%. Recheck Hb in 4 weeks; if still under 100 g/L after iron repletion, start an ESA (darbepoetin or Mircera) targeting Hb 100-110 g/L — never target above 115 (TREAT stroke risk).
• CKD-MBD: His PTH is elevated with normal phosphate and calcium. Optimise 25-OH vitamin D (increase cholecalciferol). Dietary phosphate counselling. If PTH continues to rise, consider calcitriol or paricalcitol. Avoid calcium-based binders if phosphate rises — use sevelamer (his calcium is low-normal and he has LVH/vascular risk).
• Metabolic acidosis: Start oral sodium bicarbonate 600 mg TDS, titrate to bicarbonate 22-26 mmol/L. Watch volume/BP (sodium load) — adjust diuretics.
• Hyperkalaemia (K+ 5.3): Address with bicarbonate (corrects acidosis, lowers K+), up-titrate diuretics (kaliuretic), dietary counselling. If K+ remains above 5.5 despite these, consider a potassium binder (patiromer or sodium zirconium cyclosilicate) to permit finerenone and continued ACEi. The goal is to keep him on the disease-modifying drugs, not to stop them. [1]

Step 3 — Cardiovascular risk reduction (2 marks): [1]

He is a coronary risk equivalent. Continue atorvastatin 80 mg, aspirin, metoprolol. Optimise glycaemia: reduce metformin dose (eGFR under 45 — halve to 500 mg BD; consider stopping if eGFR falls further), stop gliclazide (hypoglycaemia risk with the SGLT2i on board), target HbA1c 53-58 mmol/mol (avoid over-tight control in CKD). The SGLT2 inhibitor also provides cardiovascular protection. Consider a GLP-1 receptor agonist (semaglutide) for residual CV risk and weight/glycaemic benefit. [1]

Step 4 — Dialysis and transplant planning (2 marks): [1]

Calculate his 2-year and 5-year Kidney Failure Risk Equation score (high given eGFR 33, ACR 85, and recent decline). Refer for dialysis modality education now (home-first, including PD and home HD). Initiate transplant workup now — pre-emptive living-donor transplant is the goal; discuss with family. Refer for vascular surgery at eGFR 15-20 (AVF needs 6-12 months to mature). Protect the non-dominant arm from cannulae from today. If KFRE suggests less than 2-year dialysis probability is high, move the access referral earlier. [1]

Step 5 — Communication and safety (1 mark): [1]

Provide written sick-day rules: hold ACEi, SGLT2i, diuretics, metformin during any acute illness with reduced intake, vomiting, diarrhoea, or fever; resume when recovered. Permanent NSAID avoidance (including over-the-counter). Vaccinations (influenza, COVID-19, pneumococcal, hepatitis B, herpes zoster). Document the integrated plan and share with GP. Address his understanding and goals (advance care planning is appropriate at this stage). [1]

SAQ 2 — Investigation Interpretation and Differential (10 marks, 20 minutes)

Prompt: A 58-year-old woman presents with eGFR 28 (previously 55, 6 months ago) and ACR 110 mg/mmol. Urine dipstick shows blood 2+, protein 3+. She has a 3-month history of fatigue, night sweats, and arthralgia. She takes no regular medications. Outline your investigation strategy and the differential you are actively excluding. [1]

Model Answer

This is rapidly progressive CKD with active urinary sediment and systemic features — I must exclude a treatable glomerular disease, particularly a rapidly progressive glomerulonephritis (RPGN) or vasculitis, before attributing this to a chronic process. [1]

Urgent investigations: [1]

1. Urine microscopy — look for dysmorphic red cells and red cell casts (glomerular bleeding), which would mandate urgent renal biopsy. The combination of haematuria, proteinuria, and rapid decline is a nephrology emergency until proven otherwise.
2. Immunological screen — ANA, anti-dsDNA (lupus nephritis), ANCA (MPO and PR3 — ANCA-associated vasculitis, especially given the constitutional symptoms), anti-GBM (Goodpasture's), complements C3 and C4 (low in lupus, post-infectious GN, cryoglobulinaemia).
3. Infectious and haematological screen — hepatitis B, C, and HIV (secondary glomerular disease and pre-transplant workup), serum electrophoresis and serum free light chains (myeloma cast nephropathy in any older adult with unexplained CKD), cryoglobulins.
4. Renal ultrasound — check kidney size and exclude obstruction. Small kidneys may preclude biopsy; normal-sized or enlarged kidneys support an acute or subacute process amenable to biopsy. Asymmetry suggests renovascular disease.
5. Renal biopsy — if active sediment, positive immunology, or no alternative diagnosis — urgently, within days, given the speed of decline. [1]

Differentials I am actively excluding:

• ANCA-associated vasculitis (new onset in 50s-60s, constitutional symptoms, RPGN) — would need urgent immunosuppression (cyclophosphamide or rituximab plus glucocorticoids) to save renal function.
• Lupus nephritis (arthralgia, fatigue, female sex) — ANA, anti-dsDNA, low complements.
• Anti-GBM disease (Goodpasture's) — haematuria, possible haemoptysis; check anti-GBM; may need plasma exchange.
• Myeloma cast nephropathy — anaemia, hypercalcaemia, bone pain; check free light chains.
• Cryoglobulinaemic GN — hepatitis C, palpable purpura, arthralgia.
• An acute-on-chronic process (volume depletion, nephrotoxin, obstruction superimposed on chronic CKD) — would be suggested by a bland sediment and normal kidneys. [1]

The principle: rapid decline with active sediment in a systemic patient is a nephrology emergency. Do not label this "chronic CKD progression" without excluding a treatable cause. Most of these conditions lose the chance of renal recovery within weeks of onset. [1]