Diabetic Kidney Disease — Clinical Case

DCE Long Case

Patient profile

Mr R is a 64-year-old retired schoolteacher with type 2 diabetes for 17 years, referred to the renal clinic by his GP for progressive CKD. [1]

Presenting concern: A routine blood test 2 weeks ago showed creatinine 188 micromol/L (eGFR 33), up from 142 (eGFR 48) twelve months ago. His GP also found a urinary ACR of 88 mg/mmol. He feels well but reports new ankle swelling toward the end of the day, early satiety, and occasional orthostatic lightheadedness. [1]

Past medical history:

• Type 2 diabetes (17 years) — HbA1c 69 mmol/mol; complicated by proliferative diabetic retinopathy (panretinal photocoagulation 3 years ago), distal symmetrical peripheral neuropathy, and autonomic neuropathy (gastroparesis, orthostatic hypotension)
• Hypertension (20 years)
• Ischaemic heart disease — NSTEMI 6 years ago, DES to LAD and circumflex; stable angina on mild exertion
• Dyslipidaemia
• Obesity (BMI 34)
• Gout
• Benign prostatic hypertrophy [1]

Medications: metformin 1g BD, gliclazide 80 mg BD, perindopril 10 mg daily, amlodipine 10 mg daily, frusemide 40 mg daily, atorvastatin 80 mg, aspirin 100 mg, metoprolol 50 mg BD, pantoprazole 20 mg, allopurinol 300 mg, tamsulosin 400 micrograms. [1]

Social: Lives with his wife, independent in activities of daily living. Ex-smoker (stopped 6 years ago at the time of his NSTEMI, 40 pack-years). Rare alcohol. Two adult children. [1]

Examination:

• Blood pressure 150/92 seated, 128/82 standing (postural drop); HR 72; BMI 34
• Cardiovascular: sustained displaced apex (LVH), no murmur, S4 present, JVP 3 cm, no gallop
• Respiratory: clear, oxygen saturation 97% on room air
• Abdomen: soft, no organomegaly, no masses, no renal bruit; bladder not palpable
• Lower limbs: pitting oedema to mid-shin bilaterally; peripheral pulses present but diminished distally; loss of 10 g monofilament sensation to the ankles bilaterally
• Fundoscopy: panretinal laser scars, no active neovascularisation
• Hands: no AVF, no joint deformity [1]

Investigations:

• Creatinine 188, eGFR 33 (CKD-EPI 2021), confirmed on repeat; trend 48 to 38 to 33 over 14 months
• ACR 88 mg/mmol (A3), confirmed on two further samples
• Urine microscopy: no haematuria, no casts, no cells (bland)
• HbA1c 69 mmol/mol
• K+ 5.0, bicarbonate 21, urea 12.4
• Hb 104 g/L, MCV 88, ferritin 48 micrograms/L, TSAT 16%, B12 and folate normal
• Ca 2.30, PO4 1.4, PTH 14 pmol/L (ref 1.6 to 6.9), 25-OH vitamin D 30 nmol/L
• Lipids: total cholesterol 3.8, LDL 1.9, HDL 1.0, triglycerides 2.1
• Renal ultrasound: normal-sized kidneys (10.8 cm right, 10.5 cm left), no hydronephrosis, no stones, no cysts
• ECG: sinus rhythm, LVH by voltage criteria, non-specific ST-T changes, old anterior T-wave inversions
• Echo (recent): LVH with preserved ejection fraction (60%), grade 1 diastolic dysfunction [1]

Candidate's opening statement (SASPOP)

"This is Mr R, a 64-year-old retired schoolteacher with 17 years of type 2 diabetes, presenting to the renal clinic with progressive diabetic kidney disease. He has extensive diabetes end-organ damage including laser-treated proliferative retinopathy, distal peripheral and autonomic 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, emerging CKD complications, and high cardiovascular risk. My priorities are to confirm the diagnosis, slow his renal progression with evidence-based therapy, manage his complications, reduce his cardiovascular risk, and begin planning for kidney replacement therapy." [1]

Structured problem list (numbered, prioritised)

1. Progressive diabetic kidney disease — CKD G3b A3; eGFR falling 15 points in 14 months; confirmed macroalbuminuria; high Kidney Failure Risk Equation score anticipated
2. Suboptimal blood pressure control (150/92 seated) with a postural drop limiting aggressive targets; persistent macroalbuminuria despite ACE inhibitor
3. Suboptimal glycaemic control (HbA1c 69 mmol/mol) on inappropriate agents for his eGFR (metformin 1g BD exceeds the dose-adjustment threshold; gliclazide carries hypoglycaemia risk in CKD)
4. High cardiovascular risk — prior NSTEMI, diabetes, CKD, obesity, ex-smoker; he is a coronary risk equivalent
5. Emerging CKD complications — iron-deficiency anaemia (Hb 104, ferritin 48, TSAT 16%), early secondary hyperparathyroidism (PTH 14), vitamin D deficiency, mild metabolic acidosis (bicarbonate 21), borderline hyperkalaemia (K 5.0)
6. Diabetic autonomic and peripheral neuropathy — orthostatic hypotension limits BP targets; gastroparesis affects medication absorption; foot ulcer risk
7. Polypharmacy and sick-day medication risk — 11 medications; metformin, ACEi, SGLT2i (when added) and diuretics all carry AKI risk during illness
8. Gout — allopurinol 300 mg (appropriate; consider whether dose needs adjustment) [1]

Integrated management plan

Step 1 — Confirm the diagnosis and exclude atypical disease (discussion): [1]

His presentation is classic diabetic kidney disease: long-standing T2DM with retinopathy, progressive macroalbuminuria, bland urine, and a typical though steep trajectory on ultrasound with normal-sized kidneys. Renal biopsy is NOT indicated unless atypical features emerge (haematuria with dysmorphic red cells or casts, sudden acceleration beyond expectation, nephrotic-range proteinuria without retinopathy, or systemic features). I would document the rate of decline and apply the Kidney Failure Risk Equation — with eGFR 33, ACR 88 and the steep decline, his 2- and 5-year risk of kidney failure is high, and dialysis planning must begin now. [1]

Step 2 — Progression-slowing therapy: [1]

Step 3 — Glycaemic strategy: [1]

Halve metformin to 500 mg BD (eGFR less than 45 requires dose reduction; stop below 30). Stop gliclazide (hypoglycaemia risk in CKD; sulfonylurea clearance falls). Add a GLP-1 receptor agonist (weekly semaglutide) for cardiovascular protection, weight loss, and additional albuminuria reduction. Target HbA1c 53 to 58 mmol/mol — avoiding over-tight control (ACCORD harm in older high-risk patients). The SGLT2 inhibitor will modestly lower HbA1c as a bonus. [1]

Step 4 — Complication management: [1]

• Anaemia: IV iron first (ferric carboxymaltose, weight-based) 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 targeting Hb 100 to 115 g/L (never above 115 — TREAT stroke risk).
• CKD-MBD: Increase cholecalciferol to 1000 to 2000 units daily to replete 25-OH vitamin D. Dietary phosphate counselling. If PTH continues to rise, consider calcitriol or paricalcitol. Use a non-calcium phosphate binder (sevelamer) if phosphate rises.
• Metabolic acidosis: Oral sodium bicarbonate 600 mg TDS, titrate to bicarbonate 22 to 26 mmol/L. Watch the sodium load — adjust diuretics. Correcting acidosis slows progression.
• Hyperkalaemia: Bicarbonate and uptitrated loop diuretic will help; if potassium remains above 5.5, consider a potassium binder (patiromer or sodium zirconium cyclosilicate) to permit finerenone and continued ACEi. [1]

Step 5 — Cardiovascular risk reduction: [1]

Continue atorvastatin 80 mg (high-intensity; hepatically cleared, safe in CKD), aspirin, metoprolol. The SGLT2 inhibitor and GLP-1 receptor agonist both reduce cardiovascular events. Address his obesity with the GLP-1 agonist and lifestyle counselling. Smoking cessation already achieved. Consider coronary re-assessment if his exertional angina worsens. The Steno-2 model [6] is the evidence that this integrated approach halves cardiovascular events over the long term.

Step 6 — Kidney replacement therapy planning: [1]

Calculate his Kidney Failure Risk Equation — high. Begin dialysis modality education now (home-first: PD or home HD), initiate pre-emptive transplant workup, and discuss with him and his family the option of a living donor. Protect the non-dominant arm from cannulae from today. Refer for vascular surgery at eGFR 15 to 20 (AVF maturation takes 6 to 12 months). Offer a conservative care pathway discussion if he becomes frail — but at present he is a dialysis and transplant candidate. [1]

Step 7 — Communication and safety: [1]

Provide written sick-day rules (hold ACEi, SGLT2i, diuretics, metformin during illness; permanent NSAID avoidance). Arrange vaccinations (influenza, COVID-19, pneumococcal, hepatitis B, herpes zoster). Refer to a diabetes educator, dietitian and podiatrist (foot surveillance given his neuropathy and vascular disease). Document and share the plan with his GP. Address his understanding and goals — staying independent, avoiding dialysis, avoiding hypoglycaemia. [1]

Probing questions the examiner would ask

Q: What is his 2-year Kidney Failure Risk Equation score likely to show, and how does it change your management? [1]

A: "The KFRE uses age, sex, eGFR and ACR (4-variable) to estimate 2- and 5-year risk of kidney failure. With eGFR 33, ACR 88 mg/mmol and his age, his 2-year risk is likely above 10 to 20% and 5-year risk substantially higher. A high score prompts early dialysis and transplant planning — not waiting for eGFR to fall below 20. It also motivates maximal progression-slowing therapy. The KFRE is the modern tool for triaging CKD referral intensity." [1]

Q: Why is he not on an SGLT2 inhibitor already, and what counselling will you give? [1]

A: "He should have been started on an SGLT2 inhibitor years ago when his DKD was first identified. Starting now is overdue. Counselling covers: genital mycotic infection (hygiene, prompt treatment), volume depletion (especially with his frusemide and autonomic neuropathy — monitor, uptitrate fluids in hot weather), euglycaemic DKA (rare, present with malaise, nausea, abdominal pain — check ketones), and sick-day rules to hold it during illness. He should not stop it without discussing with me." [1]

Q: How would you address his orthostatic hypotension when controlling his blood pressure? [1]

A: "This is a genuine constraint. His autonomic neuropathy means aggressive BP lowering will worsen his postural symptoms and fall risk. I would accept a seated target closer to 140/90 if his standing pressure drops below 110 systolic or is symptomatic. I would favour medications that do not worsen the postural drop (avoid alpha-blockers like his tamsulosin if possible, avoid pure vasodilators). I would ensure he is not volume-overloaded (which can paradoxically worsen postural drops via baroreceptor dysfunction) and not volume-depleted. The SGLT2 inhibitor can contribute to volume depletion initially — I would uptitrate frusemide cautiously and review in 2 weeks. Midodrine is an option if postural symptoms are disabling but is rarely needed if I balance his volume status carefully." [1]

Q: He has gastroparesis. How does this affect your medication strategy? [1]

A: "Gastroparesis causes erratic drug absorption — particularly of oral hypoglycaemics, leading to unpredictable glucose levels. It favours non-oral routes where possible: a weekly subcutaneous GLP-1 receptor agonist (semaglutide) bypasses absorption variability, and SGLT2i absorption is less affected by gastroparesis than oral agents that depend on rapid absorption (like sulfonylureas — another reason to stop gliclazide). For symptomatic gastroparesis, metoclopramide (caution: tardive dyskinesia, limit duration), domperidone (QT prolongation), or erythromycin (if not on a QT-prolonging agent) are options. Dietary modifications (small frequent low-fat low-fibre meals) help. Gastroparesis is also a reason to favour insulin (subcutaneous, predictable) over oral agents if his glycaemia remains uncontrolled." [1]

Q: When would you initiate dialysis, and what modality would you favour? [1]

A: "I would initiate dialysis when he becomes symptomatic from uraemia (anorexia, nausea, lethargy, pruritus), when volume overload becomes refractory to escalating diuretics, or when eGFR approaches 10. I would not initiate dialysis on a number alone if he is asymptomatic. Given his obesity, autonomic neuropathy and hand-limited access considerations, I would present both modalities: peritoneal dialysis (home-based, gentler haemodynamics, no vascular access needs initially, but requires intact peritoneum and manual dexterity or a carer for automated PD) and haemodialysis (in-centre or home, requires AVF maturation, haemodynamic swings that his autonomic neuropathy may not tolerate well). I would favour a home-first approach where feasible. Pre-emptive living-donor transplant is the best option if a donor comes forward — it doubles graft survival versus deceased donor and is associated with better patient survival than staying on dialysis." [1]

Communication and shared decision-making

"I would frame DKD for Mr R 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 plain terms: 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 at his age and with his autonomic neuropathy (which blunts hypoglycaemia awareness). I would discuss dialysis and transplant early so the plan is not crisis-driven, and offer a conservative care pathway if he becomes frail. I would address his medication burden — 11 medications — and explore deprescribing where appropriate. And I would align the plan with what matters to him — staying independent, avoiding dialysis, and managing his diabetes without hypoglycaemia." [1]

DCE Short Case — Focused Examination of the Diabetic Patient

Instruction

"Examine this patient's abdomen and peripheral systems. He has type 2 diabetes." [1]

Systematic examination routine

1. End of bed — observe body habitus, mobility, dialysis alertness band, oxygen
2. Hands — examine for arteriovenous fistula (palpate thrill, listen for bruit, assess radio-radial delay, check for steal); peripheral neuropathy (10 g monofilament, vibration with 128 Hz tuning fork, proprioception); diabetic cheiroarthropathy; trigger finger; Dupuytren contracture
3. Pulse and blood pressure — radial pulse (rate, rhythm), lying and standing blood pressure for postural drop (autonomic neuropathy); radio-femoral delay (coarctation or aortic disease)
4. Face — xanthelasma, conjunctival pallor (anaemia), glossy tongue, parotid enlargement (alcohol, diabetes), gum hypertrophy (cyclosporin if transplant)
5. Eyes — visual acuity, cataracts, fundoscopy for diabetic retinopathy (microaneurysms, dot-blot haemorrhages, hard exudates, cotton-wool spots, venous beading, IRMAs, neovascularisation, vitreous haemorrhage, laser scars, macular oedema); hypertensive changes (AV nipping, silver wiring)
6. Neck — JVP (volume status), carotid bruits, thyroid (goitre)
7. Chest — heart (displaced sustained apex of LVH, S4 gallop, murmurs of calcific AS, S3 of heart failure), lungs (pulmonary oedema, pleural effusion)
8. Abdomen — inspect for scars (transplant, PD catheter, AVF, vascular surgery), palpate for masses (transplant in iliac fossa, polycystic kidneys, enlarged bladder from BPH), hepatomegaly (NAFLD), listen for bruits (renal artery, aortic); assess for ascites
9. Legs — peripheral pulses (femoral, popliteal, posterior tibial, dorsalis pedis), pitting oedema, foot examination (ulcers between toes and on pressure points, callus, Charcot deformity, infection, nail care), peripheral neuropathy testing
10. Skin — diabetic dermopathy (shin spots), necrobiosis lipoidica diabeticorum (yellow-brown plaques on shins), acanthosis nigricans (insulin resistance), injection-site lipohypertrophy [1]

Key physical signs the patient demonstrates (for this case)

• Proliferative diabetic retinopathy with panretinal laser scars — evidence of microvascular end-organ damage and strong support for the diagnosis of DKD
• Distal symmetrical peripheral neuropathy — loss of 10 g monofilament sensation to the ankles, loss of vibration sense
• Orthostatic hypotension — postural drop exceeding 20 mmHg systolic, indicating autonomic neuropathy
• Sustained displaced apex — left ventricular hypertrophy from chronic hypertension
• Pitting peripheral oedema to mid-shin — volume overload from CKD and nephrotic-range proteinuria
• Diminished peripheral pulses — peripheral vascular disease
• BMI 34 — obesity contributing to insulin resistance [1]

Presentation template

"I have examined this 64-year-old man with type 2 diabetes. The key findings are evidence of extensive multisystem diabetic end-organ damage: panretinal laser scars from treated proliferative retinopathy on fundoscopy, a distal symmetrical peripheral neuropathy with loss of the 10 g monofilament to the ankles, a significant postural blood pressure drop indicating autonomic neuropathy, a sustained displaced apex consistent with left ventricular hypertrophy, and pitting peripheral oedema to mid-shin consistent with volume overload from his nephropathy. There is no arteriovenous fistula or transplant, and no clinical evidence of heart failure. These findings, combined with his long history of type 2 diabetes and a progressive decline in kidney function, are consistent with advanced diabetic kidney disease in a multisystem diabetic patient." [1]

Discussion questions

Q: What is the significance of the laser scars? [1]

A: "Panretinal photocoagulation scars indicate treated proliferative diabetic retinopathy. In a patient with nephropathy, retinopathy strongly supports a diagnosis of classic diabetic kidney disease — the microvascular complications of diabetes tend to track together. The presence of retinopathy reduces the need for renal biopsy; the absence of retinopathy in long-standing type 1 diabetes with proteinuria would be a red flag for an alternative glomerular disease." [1]

Q: How would you investigate his foot ulcer risk? [1]

A: "Annual foot risk assessment using the 10 g monofilament, vibration perception threshold (128 Hz tuning fork or neurothesiometer), palpation of pulses, inspection for deformity, callus and previous ulceration. He is at high risk given his neuropathy and peripheral vascular disease. He needs podiatry, daily foot inspection, well-fitting footwear, prompt treatment of any ulcer or infection, and consideration of vascular imaging if claudication or rest pain develops. A foot ulcer in a diabetic with CKD is a medical emergency given infection and amputation risk." [1]

Q: Why does his autonomic neuropathy matter for his kidney management? [1]

A: "Autonomic neuropathy produces an orthostatic drop in blood pressure that limits how aggressively I can lower his BP — a key target in slowing DKD progression. It also causes gastroparesis, which complicates drug absorption and glycaemic control, and blunts the counter-regulatory response to hypoglycaemia, making him less aware of low sugars. It also contributes to erectile dysfunction and sweating abnormalities that affect quality of life. The combination of autonomic and peripheral neuropathy with CKD and vascular disease places him at very high risk of foot disease and falls." [1]

Q: What is the significance of his LVH? [1]

A: "Left ventricular hypertrophy reflects long-standing hypertension and the pressure and volume overload of CKD. It is an independent predictor of cardiovascular mortality. It drives my aggressive (but posturally constrained) blood pressure management and underlines the importance of the SGLT2 inhibitor, which reduces heart failure hospitalisation independent of glycaemia. The S4 gallop reflects a stiff, non-compliant ventricle from diastolic dysfunction — he is at risk of heart failure with preserved ejection fraction, and volume management is a careful balance." [1]

Q: How would you address his gout in CKD? [1]

A: "Continue allopurinol 300 mg daily — it is appropriate and does not need dose reduction to this eGFR in a stable patient (modern practice is to continue rather than withhold; the Crystallisation of dose concerns are historical). Avoid NSAIDs permanently — they precipitate AKI in CKD. For an acute flare, use colchicine (dose-adjusted to 500 micrograms BD in CKD) or oral or intra-articular glucocorticoids. Avoid long-term glucocorticoids given his diabetes and cardiovascular risk. The SGLT2 inhibitor modestly lowers serum urate as a bonus." [1]