Diabetic Kidney Disease — Viva Defence

Long Case Viva Defence

The scenario

A 66-year-old retired truck driver with type 2 diabetes for 19 years, hypertension, ischaemic heart disease (NSTEMI 5 years ago), diabetic retinopathy (laser-treated) and peripheral neuropathy presents to the renal clinic with progressive nephropathy. eGFR has fallen from 46 to 32 over 14 months; ACR 92 mg/mmol. He is on perindopril 10 mg, amlodipine 10 mg, metformin 1g BD, gliclazide 80 mg BD, atorvastatin 80 mg, aspirin, metoprolol. Not on an SGLT2 inhibitor or finerenone. Blood pressure 148/90, HbA1c 68 mmol/mol, BMI 33. [1]

Opening statement (SASPOP)

"This is a 66-year-old retired truck driver with 19 years of type 2 diabetes, presenting to the renal clinic with progressive diabetic kidney disease. He has established diabetic end-organ damage including laser-treated retinopathy and peripheral neuropathy, and significant cardiovascular comorbidity with a prior NSTEMI. His main problems are a rapidly progressive nephropathy with macroalbuminuria, suboptimal blood pressure and glycaemic control, and high cardiovascular risk — together making him a classic cardiorenal-metabolic long case. My priorities are to confirm the diagnosis, slow his renal progression with evidence-based therapy, manage his CKD complications, reduce his cardiovascular risk, and prepare for kidney replacement therapy." [1]

Problem list (numbered, prioritised)

1. Progressive diabetic kidney disease — CKD G3b A3, eGFR falling 14 points in 14 months
2. Suboptimal blood pressure (148/90) and persistent macroalbuminuria despite ACE inhibitor
3. Suboptimal glycaemic control (HbA1c 68 mmol/mol) with inappropriate agents for his eGFR
4. High cardiovascular risk — prior NSTEMI, diabetes, CKD, obesity
5. CKD complications emerging — anaemia, CKD-MBD, metabolic acidosis, hyperkalaemia
6. Polypharmacy and sick-day medication risk
7. The need to plan for kidney replacement therapy [1]

Integrated management plan

Pillar 1 — SGLT2 inhibitor: "I would add dapagliflozin 10 mg daily. He is well above the eGFR 20 threshold. This is the single most impactful intervention to slow his renal progression and reduce cardiovascular events, independent of glycaemia, via restoration of tubuloglomerular feedback. CREDENCE, DAPA-CKD and EMPA-KIDNEY underpin this. I would counsel him on genital mycotic infection, volume depletion, and provide written sick-day rules to hold it during illness." [1]

Pillar 2 — RAAS blockade optimised: "I would continue perindopril 10 mg daily — already at maximal dose. I would not add an ARB (dual blockade is harmful — ONTARGET), nor a direct renin inhibitor (aliskiren — ALTITUDE harm). I would address his hyperkalaemia to permit finerenone." [1]

Pillar 3 — Finerenone: "I would add finerenone 10 mg daily once his potassium is controlled. FIDELIO-DKD showed an 18% relative risk reduction in the renal composite and 14% in cardiovascular events when added to maximal RAAS blockade in T2DM CKD with albuminuria. I would recheck potassium at 4 weeks and not combine with spironolactone or eplerenone." [1]

Pillar 4 — Blood pressure and glycaemia: "I would uptitrate his frusemide to 80 mg (helps potassium and oedema) and add indapamide to reach a target below 130/80. For glycaemia, I would halve his metformin to 500 mg BD (eGFR less than 45), stop gliclazide (hypoglycaemia risk), and add weekly semaglutide — a GLP-1 receptor agonist with cardiovascular benefit, weight loss, and additional albuminuria reduction. His HbA1c target would be 53 to 58 mmol/mol — avoiding over-tight control given the ACCORD harm signal." [1]

Pillar 5 — Complications and KRT planning: "I would correct his iron deficiency with IV iron (before any ESA), optimise his vitamin D, treat his metabolic acidosis with sodium bicarbonate, and manage his hyperkalaemia with bicarbonate and diuretic. I would calculate his Kidney Failure Risk Equation — it will be high — and begin dialysis modality education and pre-emptive transplant workup now. The Steno-2 evidence [7] underpins why I am treating all of this together rather than one target at a time."

Probing questions the examiner would ask

Q: How does an SGLT2 inhibitor protect the kidney — and why continue it when the eGFR falls and it no longer lowers glucose? [1]

A: "An SGLT2 inhibitor blocks sodium-glucose cotransport in the proximal tubule, delivering more sodium to the macula densa. This restores tubuloglomerular feedback — the afferent arteriole constricts, lowering intraglomerular pressure and single-nephron GFR. This reduces albuminuria and glomerular injury independent of the systemic glucose-lowering effect. As eGFR falls, the glucose-lowering effect diminishes (less glucose to block), but the intraglomerular pressure effect persists. CREDENCE, DAPA-CKD and EMPA-KIDNEY enrolled patients down to eGFR 20 and 25, and the renoprotection persisted. So I continue it down to eGFR 20, and do not stop it solely because the HbA1c has not moved — that is exactly the wrong reason." [1]

Q: Why choose one of ACEi or ARB — never combine — and what do RENAAL and IDNT actually show? [1]

A: "RENAAL randomised 1,513 patients with T2DM and nephropathy to losartan or placebo, showing a 16% relative risk reduction in the primary composite (doubling creatinine, ESKD or death), a 28% reduction in ESKD, and a 35% reduction in proteinuria — independent of blood pressure [6]. IDNT randomised 1,715 patients to irbesartan, amlodipine or placebo, showing a 20% reduction in the primary composite versus placebo and 23% versus amlodipine — again independent of blood pressure. These established ARBs as first-line. ACE inhibitors have equivalent supporting data (the ADVANCE combination, microalbuminuric trials). I choose one class — because combining ACEi and ARB (ONTARGET) increases AKI, hyperkalaemia and harm, and adding aliskiren to either (ALTITUDE) does the same. The antiproteinuric effect is dose-dependent, so I titrate to the maximally tolerated dose of a single agent."

Q: When would you biopsy this patient? [1]

A: "Not now — his presentation is classic DKD: long-standing T2DM with retinopathy, macroalbuminuria, bland urine, and a typical though steep trajectory. I would biopsy if any atypical feature emerged — haematuria with dysmorphic red cells or red cell casts, a sudden acceleration of decline, nephrotic-range proteinuria without retinopathy, or signs of systemic disease (arthralgia, rash, constitutional symptoms). The principle: classic DKD is a clinical diagnosis; atypical features mandate biopsy to exclude a treatable glomerulonephritis. Treating an ANCA vasculitis or membranous nephropathy as if it were DKD would be a serious error." [1]

Q: What is the role of finerenone and how does it differ from spironolactone? [1]

A: "Finerenone is a non-steroidal mineralocorticoid receptor antagonist. It blocks the profibrotic and proinflammatory effects of aldosterone at the mineralocorticoid receptor, but its bulky non-steroidal structure gives it more selective receptor binding and a lower risk of hyperkalaemia and gynaecomastia than spironolactone. FIDELIO-DKD [5] showed an 18% relative risk reduction in the renal composite and 14% in cardiovascular events when added to maximal RAAS blockade in T2DM CKD with albuminuria. The mean potassium rise was 0.2 to 0.5 mmol/L, with hyperkalaemia-related discontinuation around 2.3% versus 0.9% placebo. I would not use spironolactone in this setting — the steroidal MRAs carry a much higher hyperkalaemia risk in CKD on top of ACEi and lack DKD-specific outcome data."

Q: He has cardiovascular disease as his dominant mortality risk. How does your management address this? [1]

A: "Cardiovascular disease kills more DKD patients than kidney failure does — he is a coronary risk equivalent. My integrated plan addresses this directly: the SGLT2 inhibitor reduces cardiovascular death and heart failure hospitalisation (DAPA-CKD, EMPA-KIDNEY), the GLP-1 receptor agonist reduces major adverse cardiovascular events, the high-intensity statin lowers LDL, the antiplatelet and beta-blocker are continued, and the blood pressure target below 130/80 is itself cardiovascular risk reduction. The Steno-2 multifactorial model [7] showed that this integrated approach halves cardiovascular events over the long term. Single-pill thinking fails in DKD."

Q: How would you prepare him for kidney replacement therapy? [1]

A: "I would calculate his 2- and 5-year Kidney Failure Risk Equation score — given eGFR 32, ACR 92 and a steep decline, it will be high. I would begin dialysis modality education now, with a home-first preference (PD or home HD), and initiate transplant workup immediately — pre-emptive living-donor transplant is the best survival option and I would discuss this with him and his family. I would protect the non-dominant arm from cannulae from today, and refer for vascular surgery at eGFR 15 to 20 to allow 6 to 12 months for AVF maturation. I would also offer a conservative care pathway discussion if he is frail or highly comorbid — but he is not, and his priorities are likely dialysis-free survival." [1]

Q: What sick-day rule education would you give him? [1]

A: "Written instructions to temporarily hold his ACE inhibitor, SGLT2 inhibitor, diuretics and metformin during any illness with vomiting, diarrhoea, fever or reduced oral intake — and to resume them once he is eating and drinking normally for 24 to 48 hours. He should avoid NSAIDs permanently, including over-the-counter. He should present early for assessment if he cannot keep medications down, has ongoing illness beyond 48 hours, or feels lightheaded. This is a core safety intervention in CKD and prevents the common scenario of AKI on chronic DKD." [1]

Communication and shared decision-making

"I would frame DKD as a chronic, modifiable disease: we cannot cure it, but we can substantially slow it, and most patients die with their kidneys rather than of them, if we control cardiovascular risk. I would explain the SGLT2 inhibitor in patient terms — that it protects his kidneys through a different mechanism than controlling his sugar, and he will keep taking it even if his sugar improves. I would individualise his glycaemic target with him — weighing tight control against hypoglycaemia risk at his age. I would discuss dialysis and transplant early so planning is not crisis-driven. And I would acknowledge his medication burden and align the plan with what matters to him — staying independent, avoiding dialysis, and managing his diabetes without hypoglycaemia." [1]

Short Case Discussion — Examination in the Diabetic Patient

Instruction: "Examine this patient with diabetes." [1]

Systematic examination routine

1. End of bed — body habitus (obesity, Cushingoid features), insulin injection sites, dialysis alertness band, mobility aids
2. Hands — arterial venous fistula (thrill, bruit, scar, radio-radial delay, steal signs), peripheral neuropathy (glove-and-stocking sensory loss), diabetic cheiroarthropathy (limited joint mobility), trigger finger, Dupuytren contracture
3. Pulse and blood pressure — lying and standing (autonomic neuropathy produces a postural drop), atrial fibrillation, peripheral vascular disease (radio-femoral delay, absent pulses)
4. Face — xanthelasma, anaemia (conjunctival pallor), glossy tongue (atrophic glossitis), gum hypertrophy (cyclosporin if post-transplant)
5. Eyes — visual acuity, cataracts, fundoscopy for retinopathy (background: microaneurysms, dot-blot haemorrhages, hard exudates; pre-proliferative: cotton-wool spots, IRMAs, venous beading; proliferative: neovascularisation, vitreous haemorrhage; laser scars; macular oedema)
6. Neck — JVP (volume status), carotid bruits, thyroid (goitre)
7. Chest — heart (sustained displaced apex of LVH, S4 gallop, murmurs of calcific AS, S3 of heart failure), lungs (pulmonary oedema, effusion)
8. Abdomen — renal transplant (iliac fossa, scar, bruit), arteriovenous fistula, peritoneal dialysis catheter, hepatomegaly (NAFLD), abdominal obesity, aortic bruit, bladder
9. Legs — peripheral pulses (femoral, popliteal, posterior tibial, dorsalis pedis), foot examination (ulcers, callus, Charcot deformity, infection, pressure areas), peripheral oedema, neuropathy (10 g monofilament, vibration sense, proprioception)
10. Skin — diabetic dermopathy (shin spots), necrobiosis lipoidica diabeticorum, acanthosis nigricans (insulin resistance), injection-site lipohypertrophy [1]

Presentation template

"I have performed a focused examination of this patient with type 2 diabetes. The key findings are evidence of extensive end-organ damage: background-to-pre-proliferative diabetic retinopathy with laser scars on fundoscopy, a symmetrical distal peripheral neuropathy with loss of the 10 g monofilament, absent posterior tibial pulses with dry skin suggestive of peripheral vascular disease, and a bruitable arteriovenous fistula at the left radiocephalic region indicating preparation for haemodialysis. There is no peripheral oedema or clinical evidence of heart failure. These findings, in combination with a long history of type 2 diabetes, are consistent with advanced diabetic kidney disease with multisystem involvement and a planned renal replacement therapy pathway." [1]

Discussion questions

Q: What is the significance of finding retinopathy in a patient with suspected diabetic kidney disease? [1]

A: "In type 1 diabetes, retinopathy coexists with classic diabetic kidney disease in over 90% of cases — its presence strongly supports the clinical diagnosis of DKD and reduces the need for renal biopsy. In type 2 diabetes the association is weaker but still supportive. The absence of retinopathy in long-standing T1DM with proteinuria is a red flag for an alternative or superimposed glomerular disease and is an indication for renal biopsy." [1]

Q: How would you examine for autonomic neuropathy, and why does it matter in DKD? [1]

A: "I would check for a postural drop in blood pressure (a fall of greater than 20 mmHg systolic or 10 mmHg diastolic on standing after 3 minutes), assess for gastroparesis (early satiety, postprandial vomiting, erratic glycaemic control), erectile dysfunction, and sweating abnormalities. Autonomic neuropathy matters in DKD because the postural drop limits how aggressively I can lower blood pressure, gastroparesis complicates medication absorption and glycaemic control, and the combination worsens quality of life and prognosis." [1]

Q: What does an arteriovenous fistula tell you? [1]

A: "An AVF indicates preparation for haemodialysis — it is created 6 to 12 months before anticipated need to allow maturation. I would examine its quality — a palpable thrill and audible bruit throughout the cardiac cycle indicate a functioning fistula; absent thrill suggests thrombosis. I would check for signs of steal (cool hand, reduced radial pulse on fistula compression, digital ischaemia) and high-output cardiac failure (a large fistula can contribute). I would never take blood pressure or cannulate the fistula arm." [1]