Hypokalaemia and diuretics: an analysis of publications.

Abstract

Summary and conclusionsPublished data have been used to define the characteristics of the fall in serum potassium concentration after taking diuretics and the efficacy of the various treatments given to prevent or correct it. The average fall is less after the usual doses of frusemide (about 0 3 mmol/l) than after the usual doses of thiazides (about 0 6 mmol/l) and is little influenced by the dose or duration of treatment. The fall with a given drug is the same in heart failure and hypertension, but the initial serum potassium concentration is higher in heart failure, so that the final value is lower in hypertension. In standard doses potassium supplements are less effective than potassium-retaining diuretics in correcting the hypokalaemia.The relation between the average serum potassium value and the frequency of low values (hypokalaemia) is such that very low values after taking diuretics are unusual in patients with hypertension or heart failure. Hypokalaemia would almost disappear as an important complication of diuretic treatment if it was defined as a value less than 3-0 mmol/l rather than as a value less than 3 5 mmol/l.

Thiazide Diuretics, Potassium, and the Development of Diabetes

“…14 The maximal potassium-depleting effect does not seem to be drug dependent or related to the total duration of exposure to the drug. 13,[15][16][17] However, there seems to be a dose-dependent effect regardless of thiazide diuretic used. Some reports suggest that doses of 12.5 to 25 mg daily of hydrochlorothiazide or chlorthalidone may produce less hypokalemia than doses of Ն50 mg daily.…”

“…13 It is estimated that Յ50% of patients receiving thiazide-type diuretics develop hypokalemia (defined as a serum Kϩ Ͻ3.5 mmol/L). 14 The maximal potassium-depleting effect does not seem to be drug dependent or related to the total duration of exposure to the drug.…”

Thiazide-Induced Dysglycemia

“…65 However, the effect of K ϩ -sparing diuretics on serum K ϩ values is dose dependent and, therefore, poorly predictable, with patients becoming normokalemic, remaining hypokalemic, or possibly developing hyperkalemia.…”

Thiazide‐induced hypokalaemia; prevalence higher in women.

“…The type (Anderson et al, 1971) and dose of diuretic, the concurrent use of ,-adrenoceptor blockers (Hettiarachchi et al, 1977), or methyldopa (Colwill et al, 1964), and the presence of heart failure (Morgan & Davidson, 1980) are known to influence this variability, but the response of an individual patient to diuretics remains largely unpredictable .…”