Chronic Kidney Disease Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mrs Patel is a 67-year-old woman with a 20-year history of type 2 diabetes, hypertension for 25 years, and ischaemic heart disease — a prior NSTEMI 5 years ago with a drug-eluting stent to her left anterior descending artery. She presents to the renal clinic for ongoing management of stage 3b chronic kidney disease from diabetic nephropathy. [1]

Her eGFR has declined from 42 to 32 mL per minute over the past 18 months. Her current urine albumin-to-creatinine ratio is 75 mg per mmol, placing her in the very-high-risk category on the KDIGO heat map — G3b with A3 albuminuria. Her most recent HbA1c is 60 mmol per mol. [1]

She is currently on metformin 1 gram twice daily, gliclazide 80 mg twice daily, perindopril 10 mg, amlodipine 10 mg, frusemide 40 mg, atorvastatin 80 mg, aspirin 100 mg, and metoprolol 50 mg twice daily. [1]

On examination her blood pressure is 148 over 90 by standardised measurement, heart rate 74, she has peripheral oedema to mid-shin, and her fundoscopy shows diabetic retinopathy. Her bloods show creatinine 180, potassium 5.4, bicarbonate 20, haemoglobin 96 grams per litre, ferritin 40, transferrin saturation 14 percent, calcium 2.28, phosphate 1.7, parathyroid hormone 19, and 25-hydroxyvitamin D of 32 nanomoles per litre. [1]

Her main problems are:

1. Progressive diabetic CKD, stage 3b, G3b A3 — very high progression and cardiovascular risk
2. Suboptimal blood pressure at 148 over 90 — well above target
3. Renal anaemia with absolute iron deficiency
4. Early CKD-MBD with secondary hyperparathyroidism
5. Mild metabolic acidosis and hyperkalaemia
6. High cardiovascular risk — CKD is a coronary risk equivalent
7. Polypharmacy requiring careful reconciliation and sick-day education [1]

I would manage her with a four-pillar approach to slow progression, treat her complications to target, intensify cardiovascular protection, and begin dialysis and transplant planning." [1]

Examiner probing questions and model answers

Q1: "What is the single most important new medication you would start today, and why?" [1]

"I would start an SGLT2 inhibitor — either dapagliflozin 10 mg or empagliflozin 10 mg daily. This is the single highest-impact intervention for her. DAPA-CKD showed a 39 percent reduction in the composite of sustained eGFR decline, kidney failure, or renal or cardiovascular death. EMPA-KIDNEY extended this benefit across all causes of CKD including non-diabetic disease. Her eGFR of 32 is well above the threshold of 20 for initiation. The SGLT2 inhibitor works independently of its glucose-lowering effect — it restores tubuloglomerular feedback, lowers intraglomerular pressure, and reduces albuminuria. I would also counsel her on sick-day rules: hold it during acute illness, surgery, or fasting to avoid euglycaemic ketoacidosis and volume depletion, and resume when recovered." [1]

Q2: "Her potassium is 5.4 on perindopril. How does this change your management, and would you stop the ACE inhibitor?" [1]

"I would NOT stop the perindopril — it is renoprotective and her albuminuria is the marker that most needs it. Instead, I would address the hyperkalaemia with a stepwise approach to allow me to continue and even intensify RAAS blockade. First, correct her metabolic acidosis with oral sodium bicarbonate, titrated to a bicarbonate of 22 to 26 — this itself lowers potassium. Second, optimise her diuretics: up-titrate frusemide to 80 mg and consider adding a thiazide-like diuretic — the combination is kaliuretic. Third, dietary potassium counselling with a dietitian. Fourth, if her potassium remains above 5.5 despite these measures, I would add a gastrointestinal potassium binder such as patiromer or sodium zirconium cyclosilicate to permit the addition of finerenone and continued ACE inhibition. The goal is to keep her on the disease-modifying drugs, not to stop them." [1]

Q3: "Would you add finerenone? What is the evidence?" [1]

"Yes. Finerenone is a non-steroidal mineralocorticoid receptor antagonist that adds renoprotection on top of maximum-tolerated ACE inhibition in patients with type 2 diabetes and albuminuric CKD. FIDELIO-DKD showed an 18 percent reduction in the composite of kidney failure, sustained eGFR decline, or renal death, and a 14 percent reduction in cardiovascular events. She meets the criteria — she has type 2 diabetes, albuminuric CKD, is already on perindopril, her eGFR is above 25, and if I address her potassium she will be under the 4.8 threshold for starting. I would start finerenone 10 mg daily and recheck potassium at 4 weeks and after each dose change. I would NOT combine finerenone with spironolactone — that would cause additive hyperkalaemia. Crucially, I would manage her potassium first so I can safely start finerenone." [1]

Q4: "Her haemoglobin is 96 with ferritin 40 and TSAT 14 percent. Walk me through your anaemia management." [1]

"She has absolute iron deficiency — that is the first thing I must correct, before any erythropoiesis-stimulating agent. Iron deficiency in CKD is common from reduced absorption (hepcidin blocks gut uptake), chronic inflammation, and blood loss. I would give her intravenous iron — ferric carboxymaltose as a single dose — because oral iron is poorly absorbed and poorly tolerated in CKD. I would target a ferritin above 100 micrograms per litre and a transferrin saturation above 20 percent. I would recheck her haemoglobin in 4 weeks. If it remains under 100 grams per litre after iron repletion, I would then start an ESA such as darbepoetin or methoxy polyethylene glycol-epoetin beta (Mircera), targeting a haemoglobin of 100 to 110 grams per litre. I would never target above 115 — the TREAT trial showed that targeting higher haemoglobin with darbepoetin in diabetic CKD doubled the risk of stroke without improving outcomes. So the answer is iron first, then ESA to a conservative target." [1]

Q5: "Her blood pressure is 148 over 90 despite perindopril 10 and amlodipine 10. What is your target and how will you reach it?" [1]

"My target is a standardised systolic blood pressure of less than 120 mmHg, per the KDIGO 2021 update informed by SPRINT. SPRINT showed a 25 percent reduction in cardiovascular events and 27 percent reduction in all-cause mortality with intensive control in a non-diabetic high-risk population including a CKD subgroup — and her CKD and prior NSTEMI place her squarely in that high-risk group. She is currently at 148, so I have significant work to do. I would first up-titrate her frusemide to 80 mg — this also helps her oedema and potassium. If she is still above target, I would add chlorthalidone 12.5 mg or indapamide 1.5 mg (sequential nephron blockade with the loop diuretic). I would consider a beta-blocker adjustment if her heart rate supports it. I would monitor closely for postural hypotension given her age — the SPRINT target is by standardised automated office measurement, which reads lower than routine manual measurement, and I would individualise if she becomes symptomatic. The ACE inhibitor stays — it is renoprotective for her albuminuria." [1]

Q6: "When would you start planning for dialysis, and how?" [1]

"I would start planning now, at eGFR 32, because she has progressive disease and a high Kidney Failure Risk Equation score. The KFRE — the 4-variable model of age, sex, eGFR, and albuminuria — would give me her 2-year and 5-year probability of kidney failure, and I would use that to time the steps. The timeline runs backwards from the predicted need: an arteriovenous fistula needs 6 to 12 months to mature and a proportion fail and need revision, so if her KFRE suggests dialysis within 18 to 24 months, I would refer for vascular surgical assessment and vein mapping at eGFR 15 to 20, sooner if she is declining fast. Right now, I would: one, refer her for dialysis modality education — home-first, including peritoneal dialysis and home haemodialysis; two, initiate transplant workup now, because pre-emptive living-donor transplant offers the best outcomes; three, protect her non-dominant arm from cannulae and blood pressure cuffs from today. I would also have the conservative care discussion framed positively — it is a parallel pathway, not a failure, and for some patients it is the right choice." [1]

Q7: "She is on metformin 1 gram twice daily at eGFR 32. What do you do with her diabetes medications?" [1]

"I would reduce her metformin dose to 500 mg twice daily, because the eGFR is now below 45 where dose reduction is recommended — metformin accumulates in CKD and risks lactic acidosis, particularly during intercurrent illness. I would stop gliclazide — it risks hypoglycaemia and the SGLT2 inhibitor I am adding will help her glycaemia. I would target an HbA1c of 53 to 58 mmol per mol — not over-tight, because hypoglycaemia is dangerous in CKD (reduced insulin clearance, altered drug pharmacokinetics) and the cardiovascular and renal benefits of good but not aggressive control outweigh tight glycaemia. If she needs additional glycaemic control, I would add a GLP-1 receptor agonist such as semaglutide — it has independent cardiovascular benefit and is safe in CKD. I would teach her the sick-day rules for metformin and the SGLT2 inhibitor." [1]

Q8: "What is her prognosis, and how would you communicate it?" [1]

"Her biggest threat is cardiovascular disease, not kidney failure — a stage 3b patient is more likely to die of an MI than reach dialysis, especially with her prior NSTEMI and LVH. So my management is explicitly cardiovascular-risk reduction as much as kidney protection: statin, BP to SPRINT target, SGLT2 inhibitor (cardio-renal-protective), glycaemia, aspirin. I would communicate this honestly — that her kidneys are at risk and we are working to slow progression, but that her heart is the more immediate concern, and that the same medications (SGLT2 inhibitor, BP control, statin) protect both. I would use the Kidney Failure Risk Equation to give her a concrete number for her kidney progression risk, which is more useful than an abstract 'stage.' I would discuss the plan with her family, provide written information and sick-day rules, and ensure her GP is informed at every step." [1]

Short Case Discussion

Scenario: "Examine this patient's hands and arms"

Candidate presentation (model): [1]

"I examined this patient's hands and arms. On the left forearm there is a prominent cephalic vein with visible needle track marks in a buttonhole 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, which is the hallmark of a functioning fistula. On auscultation there is a continuous machinery bruit over the fistula. The hand is warm with normal capillary refill of 2 seconds, a palpable radial pulse, and no evidence of steal syndrome. The right arm is normal. [1]

In summary, this patient has a functioning left radiocephalic arteriovenous fistula for haemodialysis, with no complications. I would also examine the abdomen for a transplant, the skin for evidence of chronic kidney disease, and would ask about dialysis-related complications including access infections, hepatitis status, and cardiovascular disease." [1]

Examiner: "What complications of an AV fistula should you look for?" [1]

"The key complications are: one, steal syndrome — where the fistula diverts blood away from the hand, causing a cool, painful hand with reduced pulses and, in severe cases, digital ischaemia. Two, high-output cardiac failure — a large fistula can cause a bounding pulse, wide pulse pressure, and eventually heart failure from chronic volume overload on the heart. Three, infection — cellulitis around the needle sites or a tunnel infection. Four, aneurysm or pseudoaneurysm formation at cannulation sites. Five, stenosis or thrombosis — loss of the thrill or bruit, or a change from continuous to systolic-only, suggests a problem and needs urgent vascular review. I assess for all of these when I examine a fistula." [1]

Examiner: "If this patient had an iliac fossa scar instead, what would you be looking for?" [1]

"That would suggest a renal transplant. I would palpate the graft — a transplanted kidney lies in the iliac fossa and is often ballottable. I would listen for a bruit over the graft, which may indicate transplant renal artery stenosis or just normal turbulent flow. I would look for signs of immunosuppression: a cushingoid appearance from glucocorticoids, gingival hypertrophy from calcineurin inhibitors such as cyclosporin or tacrolimus, tremor, hirsutism, and most importantly skin cancers — transplant recipients have a dramatically increased risk of non-melanoma skin cancers from chronic immunosuppression, and a full skin examination is essential. I would also check the blood pressure (transplant patients are often hypertensive), look for post-transplant diabetes, and ask about rejection episodes, infection prophylaxis, and graft function." [1]

Examiner: "What general signs would suggest chronic kidney disease in a patient you have not yet examined for access?" [1]

"I would look for pallor of the skin and conjunctivae from anaemia, scratch marks and excoriations from uraemic pruritus, a sallow yellow-grey pigmentation of advanced CKD, a uraemic frost (rare, a white powdery deposit on the skin from very high urea), nail changes including half-and-half nails (Lindsay nails — proximal white, distal brown-red), peripheral and sacral oedema from volume overload, asterixis from uraemic encephalopathy, a pericardial rub from uraemic pericarditis, and evidence of vascular disease including aortic bruits and reduced pulses. In a long case I would also look for evidence of the underlying cause — diabetic retinopathy, tophi, signs of autoimmune disease, signs of polycystic kidney disease such as palpable ballotable flank masses." [1]