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6.1 mmol/l ) and renal impairment (serum creatinine Introduction 160 mmol/l, creatinine clearance 60 ml/min). Laboratory investigation established the diagnosis of hypoHyperkalaemia is a potentially life-threatening electroreninaemic hypoaldosteronism secondary to chronic lyte abnormality. In normal subjects it is rare because interstitial nephritis of unknown origin. A lowthe homeostatic mechanisms to maintain normokalaepotassium diet plus small doses of frusemide were mia are highly effective. In particular, the capacity of introduced and the patient was discharged. A few days renal potassium excretion is very high under normal later he developed a urinary tract infection due to E circumstances [1–4]. Consequently, hyperkalaemia is coli and co-trimoxazole in conventional doses (1600 mg practically always associated with impaired urinary of sulphamethoxazole+320 mg of trimethoprim) was potassium excretion [5], but in patients with acute or administered. Five days later the patient was referred chronic renal failure high potassium intake can to our hospital with profound muscle weakness, further contribute to the development of hyperkalaenausea, and constipation. Laboratory investigation on mia (Table 1). the patient’s admission showed severe hyperkalaemia We describe three cases of iatrogenic hyperkalaemia (serum potassium 7.8 mmol/l ) with ECG changes secondary to drug therapy. The cases illustrate the (peaked narrow T waves and a shortened QT interval ). wide spectrum of causes and preconditioning circumHyperkalaemia was accompanied by low potasstances. Based on these cases we discuss the appropriate sium excretion (urine potassium 19 mmol/l, FEK+ 9%, clinical management of this problem. TTKG 2.4). Additionally, a normal anion gap hyperchloraemic metabolic acidosis with an arterial pH of Case report 1 7.29, a pCO2 of 32 mmHg, a serum chloride level of 112 mmol/l, a serum bicarbonate of 15 mmol/l, a urine A 71-year-old man was admitted to our hospital anion gap of 23 mmol/l, and a urine pH of 5.1 was for evaluation of hyperkalaemia (serum potassium found. There was also evidence of a low urea excretion urea 7.2%) in the face of the serum urea levels Table 1. Causes of hyperkalaemia (6.6 mmol/l ). Co-trimoxazole was discontinued and hyperkalaemia was appropriately treated. Serum 1. Increased (oral/intravenous) potassium intake potassium levels were then stabilized at 5.5–6 mmol/l.

Continuing nephrological education. Iatrogenic hyperkalaemia-points to consider in diagnosis and management