Chronic Kidney Disease — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr Robert Williams, 69 years old. [1]

Presenting complaint: Routine renal clinic review. He reports increasing fatigue and breathlessness on exertion over the past 3 months, and his wife has noticed his ankles are swollen. He has also noticed pruritus. He denies chest pain, orthopnoea, or paroxysmal nocturnal dyspnoea. He has not noticed any change in his urine output or colour. [1]

Past history:

• Type 2 diabetes for 24 years (HbA1c 64 mmol/mol) — complications: diabetic nephropathy, peripheral neuropathy, background retinopathy
• Hypertension for 30 years
• Ischaemic heart disease — NSTEMI 6 years ago, DES to LAD; stable angina on exertion
• Dyslipidaemia
• Benign prostatic hypertrophy
• Former smoker (40 pack-years, ceased 8 years ago) [1]

Current medications:

• Metformin 1g BD
• Gliclazide 80mg BD
• Perindopril 10mg daily
• Amlodipine 10mg daily
• Frusemide 40mg daily
• Atorvastatin 80mg daily
• Aspirin 100mg daily
• Metoprolol 50mg BD
• Tamsulosin 400 micrograms daily [1]

Social history: Retired schoolteacher, lives with his wife, independent in activities of daily living. Drinks 2 standard drinks on weekends. [1]

Examination findings (trainee elicits):

• Alert, orientated, no distress. BMI 31.
• BP 150/92 seated (standardised, automated), 142/88 standing. HR 72 regular.
• Cardiovascular: JVP elevated 3 cm, apex beat displaced to the 6th intercostal space mid-axillary line (LVH/dilatation), dual heart sounds, soft systolic murmur at the apex (functional MR), no rub.
• Respiratory: fine inspiratory crackles at both lung bases, cleared on coughing.
• Abdomen: soft, non-tender, no organomegaly, no palpable masses or graft, no bruits. Bladder not distended.
• Peripheral: pitting oedema to mid-shin bilaterally. Reduced vibration sense and light touch in both feet (diabetic neuropathy). No AV fistula. No transplant scar.
• Fundoscopy: diabetic retinopathy with microaneurysms and hard exudates.
• Skin: excoriation marks on forearms and back (uraemic pruritus), sallow complexion. [1]

Investigations:

• Creatinine 195 micromol/L, eGFR 30 mL/min/1.73 m² (baseline 42 eighteen months ago)
• Urea 18.2, Na 138, K 5.5, bicarbonate 20 mmol/L
• Hb 94 g/L, MCV 86 fL, ferritin 38 micrograms/L, TSAT 13%
• Ca 2.28, PO4 1.8, PTH 22 pmol/L (ref 1.6-6.9), 25-OH vitamin D 30 nmol/L
• HbA1c 64 mmol/mol, total cholesterol 4.2, LDL 2.1
• Urine ACR 80 mg/mmol
• ECG: sinus rhythm, LVH by voltage criteria, non-specific ST-T changes
• Echo (12 months ago): LVEF 50%, concentric LVH, mild functional MR, no pericardial effusion
• Renal ultrasound: kidneys 9.5 cm (right) and 9.8 cm (left), increased echogenicity, no hydronephrosis [1]

Candidate's structured presentation (model)

Opening statement: [1]

"Mr Williams is a 69-year-old retired schoolteacher with a 24-year history of type 2 diabetes, a 30-year history of hypertension, and ischaemic heart disease, who presents with progressive fatigue, exertional breathlessness, ankle swelling, and pruritus, on a background of stage 3b chronic kidney disease from diabetic nephropathy. [1]

His main problems are:

1. Progressive diabetic CKD, stage 3b — eGFR has fallen from 42 to 30 over 18 months; G3b with A3 albuminuria (ACR 80), placing him in the very-high-risk category
2. Suboptimal blood pressure at 150 over 90 — well above the SPRINT target
3. Renal anaemia with absolute iron deficiency (Hb 94, ferritin 38, TSAT 13 percent)
4. CKD-MBD — secondary hyperparathyroidism (PTH 22) with elevated phosphate
5. Mild metabolic acidosis (bicarbonate 20) and hyperkalaemia (potassium 5.5)
6. Volume overload — elevated JVP, basal crackles, peripheral oedema, consistent with cardiorenal overlap
7. High cardiovascular risk — prior NSTEMI, LVH, diabetes, CKD
8. Polypharmacy — nine medications requiring reconciliation and sick-day education [1]

His dominant threat is cardiovascular disease, not kidney failure — I will manage him as a cardiorenal-metabolic patient with a four-pillar approach to his CKD, targeted complication management, and proactive dialysis and transplant planning." [1]

Investigation summary: [1]

"His eGFR has declined from 42 to 30 over 18 months — a clear progression trajectory. The ACR of 80 mg per mmol places him at very high risk on the KDIGO heat map. His small echogenic kidneys with a long diabetes history and retinopathy support diabetic nephropathy as the cause; biopsy is not indicated. His potassium of 5.5 and bicarbonate of 20 reflect reduced kidney function and need active management to permit continuation of his disease-modifying therapy. His anaemia is driven by iron deficiency and EPO deficiency. His CKD-MBD panel shows early secondary hyperparathyroidism. The echo shows concentric LVH and preserved ejection fraction — the cardiorenal syndrome with volume overload." [1]

Management plan: [1]

1. Progression-slowing therapy — the four pillars:

   • Continue perindopril 10 mg for albuminuria. Address his hyperkalaemia (below) to permit finerenone addition.
   • Add an SGLT2 inhibitor — dapagliflozin 10 mg or empagliflozin 10 mg daily. His eGFR of 30 is above the initiation threshold of 20. This is the highest-impact single intervention. Teach sick-day rules.
   • Add finerenone 10 mg daily once his potassium is controlled (below 4.8). FIDELIO-DKD supports this for diabetic albuminuric CKD on top of ACEi. [1]

2. Blood pressure to the SPRINT target (systolic less than 120 standardised):

   • Up-titrate frusemide to 80 mg (helps oedema, potassium, and BP).
   • Add chlorthalidone 12.5 mg or indapamide 1.5 mg if still above target (sequential nephron blockade).
   • Continue metoprolol and amlodipine. Monitor for postural hypotension given his age. [1]

3. Anaemia — iron first:

   • IV ferric carboxymaltose now to correct absolute iron deficiency (ferritin and TSAT well below target).
   • Recheck Hb in 4 weeks; if still under 100 after iron repletion, start an ESA (darbepoetin or Mircera) targeting Hb 100-110 g/L. Never target above 115 (TREAT stroke risk). [1]

4. CKD-MBD:

   • Increase cholecalciferol for vitamin D deficiency (25-OH vitamin D 30 nmol/L is insufficient).
   • Dietary phosphate counselling. Add a non-calcium phosphate binder (sevelamer) for his elevated phosphate — avoid calcium-based binders given his vascular risk and LVH.
   • If PTH continues to rise despite phosphate and vitamin D optimisation, consider calcitriol or a vitamin D analogue. [1]

5. Metabolic acidosis and hyperkalaemia:

   • Start oral sodium bicarbonate 600 mg TDS, titrate to bicarbonate 22-26 mmol/L (also lowers potassium).
   • Diuretic up-titration (kaliuretic). Dietary potassium and phosphate counselling.
   • If potassium remains above 5.5 despite these, add a potassium binder (patiromer or sodium zirconium cyclosilicate) to permit finerenone and continued ACEi. [1]

6. Cardiovascular protection:

   • Continue atorvastatin 80 mg, aspirin, metoprolol.
   • SGLT2 inhibitor (added above) provides cardiovascular protection in addition to renal benefit.
   • Optimise glycaemia: reduce metformin to 500 mg BD (eGFR under 45), stop gliclazide (hypoglycaemia risk), target HbA1c 53-58 mmol/mol. Consider a GLP-1 receptor agonist (semaglutide) for residual CV risk and weight.
   • Address his volume overload — the diuretic up-titration will help; if refractory, assess for cardiorenal syndrome. [1]

7. Dialysis and transplant planning:

   • Calculate his 2-year and 5-year Kidney Failure Risk Equation score (high given eGFR 30, ACR 80, and the 18-month decline).
   • Refer for dialysis modality education now (home-first).
   • Initiate transplant workup now — pre-emptive living-donor transplant is the goal; discuss with family.
   • Refer for vascular surgical assessment at eGFR 15-20 (AVF needs 6-12 months to mature); protect the non-dominant arm from cannulae from today. [1]

8. Communication and safety:

   • Written sick-day rules: hold ACEi, SGLT2i, diuretics, metformin during any acute illness; resume when recovered.
   • Permanent NSAID avoidance (including over-the-counter).
   • Vaccinations: influenza, COVID-19, pneumococcal, hepatitis B (check titres), herpes zoster.
   • Advance care planning discussion — appropriate at this stage. [1]

Examiner discussion questions

Q: "His eGFR fell from 42 to 30 in 18 months. Is this expected progression, or should you look for a superimposed acute process?" [1]

"This is faster than expected for pure diabetic CKD progression — a fall of 12 points in 18 months warrants excluding an acute-on-chronic contributor. I would ask about recent illness, volume depletion, new medications (especially NSAIDs, contrast, or new antihypertensives), urinary symptoms suggesting obstruction, and his adherence to sick-day rules. I would check a bladder scan to exclude obstruction (relevant given his BPH), review his medication list for nephrotoxins, and reassess his volume status. If there is a clear precipitant, I would treat it and recheck. If the decline continues despite addressing reversible factors, I would proceed on the basis of progressive CKD. The key is not to assume every decline in a known CKD patient is 'just progression' — acute-on-chronic episodes are common and often partly reversible." [1]

Q: "He is on metformin at eGFR 30. What is your concern?" [1]

"Metformin accumulates in CKD and risks lactic acidosis, particularly during intercurrent illness or hypoperfusion. The recommendations are: reduce the dose to 500 mg twice daily when eGFR falls below 45, and stop metformin when eGFR is below 30. His eGFR of 30 is right at that threshold. I would reduce his metformin to 500 mg twice daily now, teach him the sick-day rule to hold it during any acute illness, and plan to stop it when his eGFR falls below 30. I would replace the glycaemic control with the SGLT2 inhibitor I am adding (which is renoprotective independent of glucose) and consider a GLP-1 receptor agonist. I would not chase a tight HbA1c — a target of 53 to 58 mmol per mol balances glycaemic benefit against hypoglycaemia risk in CKD." [1]

Q: "When would you involve palliative care, and how do you decide between dialysis and conservative management?" [1]

"For Mr Williams, at eGFR 30 with preserved functional status, dialysis is clearly appropriate and I would plan for it. The conservative care discussion is most relevant for patients who are very elderly, frail, or have advanced comorbidity that dialysis will not meaningfully extend life — dementia, advanced heart failure with frequent hospitalisations, metastatic cancer, or severe functional dependence. I use prognostic tools: the Cohen 'surprise question' (would I be surprised if this patient died in the next 12 months?), functional scores, and the patient's own goals. For such patients I would offer a conservative care pathway explicitly — it is active symptom-focused care, not 'no care': diuretics for fluid, ESAs for symptomatic anaemia, symptom control for pruritus, nausea and pain, advance care planning, and renal palliative care involvement. The decision is always shared — I present both options honestly with their expected outcomes and quality of life implications, and support the patient and family in their choice. For Mr Williams specifically, I would hold this conversation as a parallel pathway now — establish his values and preferences — so that if his trajectory changes, the decision is not made in crisis." [1]

DCE Short Case — Dialysis Access Examination

Instruction

"Examine this patient's hands and arms. You have 7 minutes for examination and 8 minutes for discussion." [1]

Key signs the patient demonstrates (AVF model)

• Look: visible prominent cephalic vein on the left forearm, needle track marks in a rope-ladder distribution along the fistula, a curvilinear surgical scar at the left wrist (radiocephalic anastomosis)
• Feel: continuous thrill — both systolic and diastolic — over the anastomosis at the wrist, propagating up the cephalic vein
• Listen: continuous machinery bruit over the fistula
• Function: left hand warm, capillary refill 2 seconds, palpable radial pulse, no steal syndrome; no bounding pulse or wide pulse pressure to suggest high-output failure [1]

Presentation template

"I examined this patient's hands and arms. On the left forearm there is a prominent cephalic vein with needle track marks in a rope-ladder distribution and a curvilinear surgical scar at the wrist consistent with a radiocephalic arteriovenous fistula. On palpation there is a continuous thrill — both systolic and diastolic — over the anastomosis, the hallmark of a functioning fistula. On auscultation there is a continuous machinery bruit. The left hand is warm with normal capillary refill and a palpable radial pulse — no evidence of steal syndrome. There is no bounding pulse or wide pulse pressure to suggest high-output cardiac failure. [1]

In summary, this patient has a functioning left radiocephalic arteriovenous fistula for haemodialysis, with no complications. I would now complete my examination by examining the abdomen for a renal transplant, examining the skin for evidence of chronic kidney disease and immunosuppression, and assessing the cardiovascular system given the high cardiovascular risk in dialysis patients." [1]

Discussion

1. Summarise findings and conclusion: "The continuous thrill and machinery bruit confirm a functioning AVF. The needle tracks confirm it is in active use for haemodialysis. There are no complications — no steal syndrome, no high-output failure, no infection or aneurysm." [1]

2. What is the significance of a continuous versus systolic-only thrill? "A continuous thrill and bruit indicate normal laminar flow through the fistula throughout the cardiac cycle. A change to a systolic-only thrill or bruit, or a loss of the thrill entirely, suggests stenosis or thrombosis of the fistula — this is a vascular emergency that needs urgent review by the access surgeon or interventional radiology to salvage the fistula before it thromboses." [1]

3. What complications of an AVF should you assess for? "Steal syndrome — the fistula diverts arterial blood away from the hand, causing a cool, painful, pale hand with reduced pulses and potential digital ischaemia. High-output cardiac failure — a large fistula increases venous return and cardiac output, causing bounding pulses, wide pulse pressure, and eventually heart failure. Infection — cellulitis or tunnel infection at cannulation sites. Aneurysm or pseudoaneurysm — at repeated cannulation sites. Stenosis or thrombosis — suggested by loss of thrill or change in bruit character." [1]

4. Why is an AVF preferred over a tunnelled catheter? "An AVF has lower infection rates, longer patency, lower thrombosis, and lower mortality than a tunnelled central venous catheter. Catheters carry a substantial risk of bacteraemia, metastatic infection, and central venous stenosis. The 'fistula first' initiative and KDIGO guidelines prioritise AVF creation because catheter use at dialysis initiation is an independent predictor of mortality. This is why we plan AVF creation 6 to 12 months before the predicted dialysis start, so the patient never needs a catheter." [1]

5. How does this patient's dialysis access influence your cardiovascular assessment? "Dialysis patients, and those with AVFs, have very high cardiovascular risk. An AVF can itself contribute to high-output cardiac failure, especially a large upper-arm fistula. I would assess the JVP, listen for a gallop rhythm, check for signs of heart failure, and look at the ECG for ischaemia and the echo for LVH and ejection fraction. I would also examine for vascular disease elsewhere — carotid and abdominal bruits, peripheral pulses — because the same atherosclerotic process affects the whole vascular tree." [1]