Dear Editor:

Introduction

Chlorthalidone is a thiazide diuretic. Among its adverse effects is ypopotassaemia.1

Clinical case study

74 year old female suffering arterial hypertension for the last 20 years. Continuing treatment with chlorthalidone 50mg/24h for 20 years, with the addition a few months previously of omeprazole 20mg/24h and alprazolam 0.25mg/24h.

The patient presented with a potassium level of K 2.4mEq/l and pH 7.49 following a knee arthroplasty. Chlorthalidone was withdrawn and oral potassium was administered, normalising the potassium serum and pH. In an analysis of the past four years, the potassium levels were around 3.22mEq/l.

Physical examination was normal. Haemogram, routine biochemistry, cortisol, aldosterone, rennin, TSH and PTH, magnesium and chlorine were normal. In a 24 hour urine test, calcium, sodium and potassium of 53mmol/24h (normal: 20-125) were normal. Urological ultrasound normal.

After normalising the potassium and pH, the intake was withdrawn. Three days after having withdrawn the supply, the potassium was 3.45mEq/l and the pH was 7.49, which normalised after reintroducing the supply. One week later the potassium supply was withdrawn with levels of K 3.45 and pH 7.49; it was decided to continue treatment indefinitely and maintain subsequent follow-ups. The patient required potassium input for ten months, until it was definitively withdrawn.

Discussion

Among the severe adverse effects of chlorthalidone are hypopotassaemia and alkalosis.

Chlorthalidone and thiazide diuretics act primarily in the distal renal tubule, inhibiting the reabsorption of NaCl and increasing the reabsorption of Ca. The increase in Na and water in the cortical collecting tubule, or an increased flow rate, cause an increase in the secretion and excretion of K and H. Where hypopotassaemia is severe, an exchange of intracellular K and extracellular H takes place, bringing about alkalosis. Hypopotassaemia also causes the renal reabsorption of bicarbonate to increase. When plasma concentration exceeds the reabsorption capacity at proximal tubule level, it brings about bicarbonaturia; since Na is normally exchanged with K and H in the distal tubule, if this diminishes, the elimination of H increases, also producing alkalosis. When hypopotassaemia is severe, less than 2mEq/l, this impedes the tubular reabsorption of Cl, causing alkalosis to persist. In the case described, hypopotassaemia and alkalosis are probably secondary to a lasting renal tubular alteration associated with over twenty years of treatment with chlorthalidone, since treatment with potassium could be withdrawn after ten months.

Hypopotassaemia can be present in hiperaldosteronism and renninproducing tumours, Bartter¿s syndrome2 and Gitelman¿s syndrome.3