Diuretic-related hypokalaemia: the role of diuretics, potassium supplements, glucocorticoids and ?2-adrenoceptor agonists

Abstract

All 5,047 consecutive inpatients admitted to the Internal Medicine Division of a teaching hospital (Zieglerspital, Berne) between 1982 and 1985 were registered in accordance with the CHDM (Comprehensive Hospital Drug Monitoring) questionnaire of adverse drug reactions (ADRs). Of them, 2,439 were treated with at least one potassium losing diuretic. The hospital records of the patients were reviewed with particular regard to serum potassium levels, and on the basis of this evaluation, the patients were assigned to four different diuretic treatment groups, and the incidence of hypokalaemia related to diuretic treatment was estimated. The overall rate of occurrence of hypokalaemia was 21.1% at a serum potassium level < 3.5 mmol.l-1, and 3.8% < 3.0 mmol.l-1. Hypokalaemia of less than 3.5 mml.l-1 developed 24.9% (217/870) of patients treated with potassium losing diuretics alone; in 19.7% (101/513) treated with potassium losing diuretics in conjunction with potassium substitution, in 15.1% (66/438) treated with a combination of diuretics (potassium losing with potassium sparing), and in 20.0% (12/60) treated with combined diuretics and potassium substitution. Only the differences between the first and the two subsequent groups were statistically significant. The overall incidence of hypokalaemia below 3.0 + mmol.l-1 was significantly lower in the patients on combined diuretics without potassium substitution than in the patients on potassium losing diuretics with potassium substitution. Oral or parenteral administration of glucocorticoids (prednisone 5 to 2,000 mg/d) was a significant risk factor for hypokalaemic events. beta 2-Adrenoceptor agonists had not effect. The patient's age, sex, renal function and numbers of drugs received were evaluated in a multivariate analysis, in order to take into account their influence on the risk of developing hypokalaemia. The number of drugs above 12 (and, less importantly, female sex) was the main risk factor for this ADR. The comparison between hypokalaemia and hyperkalaemia in this group of inpatients showed the significance of reduced renal function in the occurrence of hyperkalaemia.

Effect of the SGLT2 Inhibitor Dapagliflozin on Potassium Levels in Patients with Type 2 Diabetes Mellitus: A Pooled Analysis

“…Clinicians should balance the opposing risks of avoiding hyperkalemia and causing hypokalemia, or vice versa. For example, potassium-sparing diuretics have been shown to prevent diuretic-induced hypokalemia but are associated with an increased risk of hyperkalemia [ 39 ]. Furthermore, combinations of drugs with an associated risk of hyperkalemia (e.g., ACE inhibitor, ARBs, potassium-sparing diuretics [ 15 – 17 ]) or hypokalemia (e.g., thiazides or loop diuretics [ 18 ]) may rapidly precipitate serious serum electrolyte abnormalities.…”

Potential drug–drug interactions in a medical intensive care unit of a university hospital

“…The most frequent DDI group of the present study was found between corticosteroids and diltiazem or furosemide (12.8%). Corticosteroids can induce the hypokalemic effect of loop diuretics (21). Monitoring of serum electrolytes, especially potassium levels of patients, is recommended or an alternative diuretic can be substituted in order to avoid hypokalemia and subsequent arrhythmias.…”

Strategies for Avoiding Typical Drug–Drug Interactions and Drug-Related Problems in Patients with Vascular Diseases

“…Amiodarone may increase the serum concentration of atorvastatin, and atorvastatin toxicities (e.g., myalgia, liver function test elevations, and rhabdomyolysis) are possible [40,41]. Lower starting and maintenance doses of atorvastatin in patients taking amiodarone must be used.…”

“…In a large study of drug monitoring in hospitals, the records of 2439 patients on potassium-wasting diuretic therapy were reviewed to identify other factors that affected serum potassium levels. Oral or parenteral prednisone therapy was a significant risk factor for the development of hypokalemia [41].…”