Diabetic Kidney Disease — Written Clinical Reasoning

SAQ 1 — Integrated Diabetic Kidney Disease Management (20 marks, 30 minutes)

Prompt: Outline your integrated management plan for this patient, addressing each problem with evidence-based therapy and a clear rationale. Address the decision points where the examiner will probe. [1]

Model Answer

Problem list (4 marks):

1. Progressive diabetic kidney disease — CKD G3b A3, eGFR falling 14 points in 14 months (rapid decline), very high progression risk
2. Suboptimal blood pressure (148/90) and persistent macroalbuminuria despite ACE inhibitor
3. Suboptimal glycaemic control (HbA1c 68 mmol/mol) — contributing to progression
4. Renal anaemia with iron deficiency (Hb 101, ferritin 52, TSAT 17%)
5. Early CKD-MBD — secondary hyperparathyroidism (PTH 16), vitamin D deficiency (25-OH D 32)
6. Mild metabolic acidosis (bicarbonate 21)
7. High cardiovascular risk — prior NSTEMI, diabetes, CKD (coronary risk equivalent), obesity
8. Polypharmacy (8 medications) and sick-day medication risk [1]

Step 1 — Confirm this is DKD and assess for atypical features (2 marks): [1]

The clinical picture is classic diabetic kidney disease: long-standing T2DM with retinopathy, progressive macroalbuminuria, bland urine (no haematuria reported), and a typical trajectory. Retinopathy is the strongest correlate of classic DKD and its presence here strongly supports the clinical diagnosis — renal biopsy is NOT indicated unless atypical features emerge (haematuria, active sediment, rapid decline beyond expectation, or signs of systemic disease). I would document the rate of eGFR decline and apply the Kidney Failure Risk Equation (Tangri) to quantify his 2- and 5-year risk of kidney failure — with eGFR 32, ACR 92 and a steep decline, his risk is high and dialysis planning must begin. [1]

Step 2 — Progression-slowing therapy: the four-pillar approach (6 marks): [1]

Step 3 — Complication management (4 marks): [1]

• Anaemia: Iron first. Give IV ferric carboxymaltose (weight-based, e.g. 1 g) to correct 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) targeting Hb 100 to 115 g/L — never above 115 (TREAT showed harm: stroke, thromboembolism).
• CKD-MBD: Optimise 25-OH vitamin D — increase cholecalciferol to 1000 to 2000 units daily. Dietary phosphate counselling. If PTH continues to rise, consider calcitriol or paricalcitol. Use a non-calcium phosphate binder (sevelamer) if phosphate rises — avoid calcium-based binders given his vascular disease.
• Metabolic acidosis: Start oral sodium bicarbonate 600 mg TDS, titrate to bicarbonate 22 to 26 mmol/L. Correcting acidosis slows progression and reduces muscle wasting. Watch the sodium load — adjust diuretics.
• Hyperkalaemia (K+ 5.1): Bicarbonate corrects acidosis and lowers potassium; uptitrate loop diuretic (kaliuretic). 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 4 — Cardiovascular risk reduction and glycaemic strategy (2 marks): [1]

He is a coronary risk equivalent and cardiovascular disease is his dominant mortality risk. Continue atorvastatin 80 mg (high-intensity; atorvastatin is hepatically cleared so safe in CKD), aspirin, metoprolol. Adjust glycaemic therapy for his eGFR 32: reduce metformin to 500 mg BD (eGFR less than 45 — halve the dose; stop below 30), stop gliclazide (hypoglycaemia risk in CKD; sulfonylurea clearance falls), add a GLP-1 receptor agonist (semaglutide weekly) for residual cardiovascular protection, weight loss and additional albuminuria reduction. Target HbA1c 53 to 58 mmol/mol — avoid over-tight control (ACCORD harm in older high-risk patients). The SGLT2 inhibitor also provides cardiovascular protection. [1]

Step 5 — Dialysis and transplant planning (1 mark): [1]

His Kidney Failure Risk Equation risk is high given eGFR 32, ACR 92 and the steep decline. Refer now for dialysis modality education (home-first — PD and home HD). Initiate transplant workup now — pre-emptive living-donor transplant is the best survival option; discuss with family. Refer for vascular surgery at eGFR 15 to 20 (AVF needs 6 to 12 months to mature). Protect the non-dominant arm from cannulae from today. Offer a conservative care pathway discussion if he is unlikely to benefit. [1]

Step 6 — 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 for 24 to 48 hours. Permanent NSAID avoidance (including over-the-counter). Vaccinations (influenza, COVID-19, pneumococcal, hepatitis B, herpes zoster). Document and share the integrated plan with the GP. Address his understanding and goals. Smoking cessation if applicable. The Steno-2 model [6] is the evidence that this integrated approach halves cardiovascular events over the long term.

SAQ 2 — Atypical Presentation and Biopsy Decision-Making (10 marks, 20 minutes)

Prompt: A 47-year-old man with type 1 diabetes for 30 years presents with new-onset peripheral oedema. His eGFR is 41 mL/min/1.73 m² (down from 76 six months ago) and his ACR is 310 mg/mmol (nephrotic-range). He has no diabetic retinopathy on recent dilated fundoscopy. Urine microscopy shows dysmorphic red blood cells and red cell casts. He is on no antihypertensives. Outline your investigation strategy, the differentials you are actively excluding, and your management priorities. [1]

Model Answer

This presentation is atypical for classic diabetic kidney disease and mandates a renal biopsy to exclude a superimposed or alternative glomerulonephritis. The principle: classic DKD is a clinical diagnosis, but atypical features demand tissue. [1]

The atypical features I am acting on (3 marks):

1. Rapid eGFR decline (76 to 41 in 6 months) — far steeper than DKD progression
2. Active urinary sediment (dysmorphic red cells, red cell casts) — DKD has bland urine; this is glomerular bleeding
3. Absence of retinopathy in long-standing T1DM with nephrotic-range proteinuria — strongly against classic DKD (in T1DM, retinopathy coexists with classic DKD in over 90% of cases)
4. Nephrotic-range proteinuria (ACR 310 mg/mmol) without the typical slow DKD trajectory [1]

These features together suggest a superimposed or alternative glomerulonephritis — IgA nephropathy, membranous nephropathy, FSGS, ANCA-associated vasculitis, lupus nephritis, anti-GBM disease, or amyloidosis. Each is treatable and would be mismanaged as DKD. [1]

Urgent investigations (4 marks): [1]

1. Urine microscopy (already abnormal — confirms glomerular bleeding) — quantifies the activity
2. Immunological screen — ANA, anti-dsDNA (lupus), ANCA (MPO and PR3 — ANCA-associated vasculitis), 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 adult with unexplained CKD), cryoglobulins
4. Renal ultrasound — check kidney size, exclude obstruction; normal-sized kidneys support an acute/subacute process amenable to biopsy
5. Renal biopsy — urgently, within days, given the speed of decline and the active sediment; this is the definitive investigation [1]

Differentials I am actively excluding (2 marks):

• ANCA-associated vasculitis (new onset in 40s to 60s, constitutional symptoms, RPGN) — would need urgent immunosuppression (cyclophosphamide or rituximab plus glucocorticoids) to save renal function
• IgA nephropathy (most common primary GN; can present with haematuria and proteinuria)
• Membranous nephropathy (nephrotic-range proteinuria; check anti-PLA2R antibodies)
• Lupus nephritis (check ANA, anti-dsDNA, complements)
• Anti-GBM disease (Goodpasture's) — check anti-GBM; may need plasma exchange
• Amyloidosis (chronic inflammatory history; nephrotic-range proteinuria) [1]

Management priorities (1 mark): [1]

The immediate priority is to secure a tissue diagnosis rapidly. While awaiting biopsy, control his blood pressure (start an ACE inhibitor — first-line for proteinuria and hypertension), manage his oedema (loop diuretic), and assess for complications. Do NOT empirically start immunosuppression before biopsy, because the biopsy result determines the regimen (ANCA vasculitis and lupus nephritis need different immunosuppressive protocols). The nephrotic syndrome also mandates assessment for venous thromboembolism risk (consider prophylactic anticoagulation if serum albumin is very low). [1]

The principle: rapid decline with active sediment in a patient without the classic DKD phenotype is a nephrology emergency. Most of these conditions lose the chance of renal recovery within weeks of onset. Atypical DKD is not DKD until tissue confirms it. [1]