Advanced Renal Clinic: Recurrent Hyperkalaemia

Correct answer: Give intravenous calcium to stabilize the myocardium, together with insulin–glucose to shift potassium intracellularly, while arranging definitive potassium removal.

Hyperkalaemia with ECG changes is an emergency. Intravenous calcium is given first when there are ECG manifestations because it antagonizes the cardiac membrane effects of potassium; it does not lower the serum potassium. Insulin with glucose provides a rapid intracellular shift, while the team simultaneously addresses potassium removal and the cause, including acidosis, medication contributors, renal function, and the need for urgent dialysis if refractory or clinically indicated.

Losartan should not be labelled as permanently contraindicated solely because of one episode. RAAS blockade is often kidney- and cardioprotective, so the longer-term decision is individualized after emergency treatment, repeated potassium monitoring, dietary and medication review, correction of reversible contributors, and consideration of a potassium binder. Oral bicarbonate, loop diuretic monotherapy, or a delayed potassium binder is insufficient as sole treatment when ECG changes are present.

Correct answer: Reintroduce or continue kidney-protective therapy with close potassium/creatinine monitoring, dietary and medication review, and consider a licensed potassium binder if recurrent hyperkalaemia limits RAAS therapy.

Once the immediate emergency has resolved, the clinical objective is not simply to avoid potassium at all costs. RAAS inhibition is valuable in albuminuric CKD, and SGLT2 inhibition can provide kidney and cardiovascular protection when appropriate. The decision should be individualized, with repeat potassium and creatinine measurements, review of NSAIDs and other contributors, dietary counselling, correction of metabolic acidosis when appropriate, and use of a potassium binder when recurrent hyperkalaemia threatens continuation of RAAS therapy.

Dual ACE inhibitor/ARB therapy is not recommended because it increases adverse events without improving outcomes. Permanent withdrawal after one episode and unmonitored continuation both ignore the need for structured follow-up.

Correct answer: Stop ibuprofen and the potassium-containing salt substitute, review all medicines and diet, repeat potassium promptly, and assess bicarbonate and renal function.

Non-steroidal anti-inflammatory drugs can reduce renal potassium excretion and worsen kidney perfusion, particularly in people with CKD who are also receiving renin–angiotensin system blockade. Potassium-containing salt substitutes are a common overlooked source. The correct clinical response is a structured medication and dietary review, prompt repeat testing using appropriate sampling, and reassessment of renal function and acid–base status.

A single recurrent result does not establish primary hyperaldosteronism, which more typically causes hypertension with hypokalaemia. Immediate dialysis is not justified solely by this stable outpatient value without assessment of severity, symptoms, ECG findings, response to medical treatment, and overall clinical context.

Correct answer: Continue the individualized kidney-protective plan, review volume status and medicines, repeat creatinine and potassium soon, and investigate further if the decline is progressive or exceeds the expected early change.

A modest early fall in eGFR can occur after haemodynamic changes from RAAS or SGLT2 therapy and does not automatically represent structural nephrotoxicity. The correct response is active surveillance: confirm volume status, review concurrent medicines, repeat kidney function and potassium at an appropriate interval, and assess for other causes if the decline is larger than expected, progressive, or accompanied by symptoms or urinary abnormalities.

Therapy should not be stopped reflexively, but neither should a sustained decline be ignored. Dual renin–angiotensin blockade is inappropriate, and an eGFR of 21 alone does not mandate dialysis or access placement without broader kidney-failure planning and patient-centred discussion.