A known diabetic on oral hypoglycaemic agents attends for routine review; serum potassium is 5.7 mEq/L. Investigation and treatment

First — confirm the value and assess urgency simultaneously. Exclude pseudohyperkalaemia by repeating with a properly taken sample: causes are a tight or prolonged tourniquet, fist clenching, haemolysis, difficult venepuncture, delayed transport or prolonged storage, and marked thrombocytosis or leucocytosis. At the same time perform a 12-lead ECG — the presence of ECG change converts this from an outpatient problem into an emergency, and its absence permits an unhurried outpatient approach.

Understand why this particular patient is at risk — the geriatric-diabetic substrate. Renal excretion of potassium is significantly lower in the aged: there is reduced serum aldosterone and a reduced tubular response to aldosterone, together with increased H⁺/K⁺-ATPase activity (potassium reabsorption) in the intercalated cells of the aged collecting duct. Consequently elderly people are predisposed to hyperkalaemia, particularly when treated with NSAIDs, ACE inhibitors, beta blockers and/or potassium-sparing diuretics. In a diabetic, add type 4 renal tubular acidosis (hyporeninaemic hypoaldosteronism), diabetic nephropathy, and insulin deficiency, since insulin drives potassium into cells.

Take a targeted drug and diet history — the highest-yield step. Drugs: ACE inhibitors, ARBs, spironolactone or eplerenone, amiloride, beta blockers, NSAIDs, co-trimoxazole (trimethoprim acts like amiloride), heparin, digoxin, calcineurin inhibitors. Diet and over-the-counter items: "low-sodium" salt substitutes, which are potassium chloride — a very common and frequently missed cause in Indian practice — plus tender coconut water, banana, citrus, tomato, potato and dry fruits. Also ask about constipation (the colon is an important route of potassium excretion in CKD) and about traditional or ayurvedic preparations.

Investigate systematically. Repeat serum potassium on a clean sample; ECG; urea, creatinine and eGFR; sodium; serum bicarbonate — a normal anion gap acidosis with hyperkalaemia points to type 4 RTA; blood glucose and HbA1c; urine albumin–creatinine ratio; calcium and magnesium; full blood count and platelet count (for pseudohyperkalaemia); creatine kinase if rhabdomyolysis is possible; and 9 a.m. cortisol with a short Synacthen test if adrenal insufficiency is plausible. Where the cause remains unclear, a urine potassium or transtubular potassium gradient distinguishes impaired renal excretion from a transcellular shift.

Know the ECG sequence and its limitations. In order: tall peaked T waves → flattening and loss of P waves → PR prolongation → widening of the QRS → sine wave → ventricular fibrillation or asystole. Critically, ECG changes correlate poorly with the potassium level in chronic hyperkalaemia and may be entirely absent even at 6.5 mEq/L — so a normal ECG does not exclude danger, and a changing ECG demands action irrespective of the number.

Treat this level — 5.7 mEq/L, asymptomatic, no ECG change — as moderate chronic hyperkalaemia, not an emergency. This does not require calcium, insulin-dextrose or salbutamol. Do the following: (a) stop or reduce the culprit — NSAIDs first, then reassess the potassium-sparing diuretic, and eliminate salt substitutes; (b) dietary potassium restriction with dietitian input; (c) correct metabolic acidosis with oral sodium bicarbonate if bicarbonate is below 22 mEq/L; (d) improve glycaemic control; (e) add or increase a loop or thiazide diuretic if the patient is volume-replete; (f) treat constipation; (g) recheck potassium in 3–7 days. Reserve emergency treatment for K⁺ ≥6.5 mEq/L or any ECG change: 10% calcium gluconate 10 mL IV for membrane stabilisation (repeat as needed; it does not lower potassium), 10 units soluble insulin with 25% dextrose 50–100 mL, nebulised salbutamol 10–20 mg, sodium bicarbonate if acidotic, and dialysis if refractory or if renal failure is advanced.

Potassium binders now allow prognostically important RAS blockade to be continued — a change of doctrine directly relevant to this patient. The KDIGO 2024 CKD guideline states that in hyperkalaemia, potassium binders may help facilitate essential use of RAS inhibitors and mineralocorticoid receptor antagonists, that potassium binders should be considered before reducing the RAS inhibitor, and that RASi discontinuation should be the last resort. The modern agents are sodium zirconium cyclosilicate (SZC) and patiromer, both licensed for adults and both effective for chronic control and prevention of recurrence; the UK Kidney Association 2023 guideline broadened their use to moderate as well as severe hyperkalaemia and removed calcium resonium (sodium polystyrene sulphonate) from the acute algorithm because of weak evidence and the risk of colonic necrosis. For this diabetic patient, whose ACE inhibitor or ARB is renoprotective, the correct modern reasoning is therefore to remove the avoidable contributors first (NSAID, salt substitute, dietary potassium), then add a binder — and only then, if all else fails, reduce the RAS blocker.