Drug-Induced Hyperkalemia
A 66-year-old man with type 2 diabetes, hypertension, and heart failure takes lisinopril, furosemide, and insulin. Heparin and warfarin were started for deep vein thrombosis. He now has worsening leg edema. Potassium is 6.5 mmol/L, creatinine 168 µmol/L, activated partial thromboplastin time prolonged, and prothrombin time normal. Which medication should be stopped?
- A.Warfarin
- B.Furosemide
- C.LisinoprilCorrect
- D.Insulin
Explanation
The single dangerous abnormality is a potassium of 6.5 mmol/L, and the drug most responsible is the angiotensin-converting enzyme inhibitor. ACE inhibitors block angiotensin II generation and therefore reduce adrenal aldosterone release, decreasing distal tubular potassium secretion; the effect is amplified by diabetic hyporeninaemic hypoaldosteronism, by chronic kidney disease with a creatinine of 168 µmol/L, and by heart failure with reduced renal perfusion. Withholding lisinopril, together with acute measures such as intravenous calcium gluconate for membrane stabilization if electrocardiographic changes are present, insulin with dextrose, and a potassium binder, is the correct action. The coagulation profile is entirely expected and reassuring rather than alarming: heparin prolongs the activated partial thromboplastin time, and warfarin has not yet had time to prolong the prothrombin time because factor VII depletion takes several days, so overlap therapy is proceeding normally and warfarin should continue. Furosemide is a potassium-wasting loop diuretic that is helping to lower potassium and is also treating the oedema, so stopping it would worsen both problems. Insulin drives potassium intracellularly and is essential in a diabetic patient, making it the last drug to withdraw. After the acute episode, the ACE inhibitor may often be cautiously reintroduced at a lower dose with a potassium binder, because it remains prognostically important in heart failure and diabetic kidney disease.
Why each option
- A.
- Warfarin is appropriate for deep vein thrombosis; a normal prothrombin time this early simply reflects that its effect has not yet developed.
- B.
- Furosemide promotes kaliuresis and is lowering potassium while treating the oedema; stopping it would be counterproductive.
- C.
- Correct. The ACE inhibitor suppresses aldosterone and is the main driver of hyperkalemia in a diabetic patient with impaired renal function.
- D.
- Insulin shifts potassium into cells and is essential therapy; it is protective rather than causative here.
Reference: KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease
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