Hyperkalemia heparins

Heparin-induced hypoaldosteronism is well documented, both in patients treated with standard heparin, even at low doses, and in patients treated with low molecular weight heparin (477,478). The most important mechanism of aldosterone inhibition appears to be a reduction in both the number and affinity of angiotensin II receptors in the zona glomerulosa (477). A direct effect of heparin on aldosterone synthesis, with inhibition of conversion of corticosterone to 18-hydroxycorticosterone, has also been suggested. This effect is believed to be responsible for the hyperkalemia that can occur in heparin-treated patients with impaired renal function and particularly in patients on chronic hemodialysis (479), or with diabetes mellitus, or who are taking other potentially hyperkalemic drugs. 

Oster JR, Singer I, Fishman LM. Heparin-induced aldosterone suppression and hyperkalemia. Am J Med 1995 98(6) 575-86. 

Hottelart C, Achard JM, Moriniere P, Zoghbi F, Dieval J, Fournier A. Heparin-induced hyperkalemia in chronic hemodialysis patients comparison of low molecular weight and unfractionated heparin. Artif Organs... 

Hyperkalemia due to a decrease in aldosterone secretion is rarely found in patients with normal renal function, but it is relatively common in those with CHF and in the elderly. Hyperkalemia is more frequent in patients with renal impairment, diabetes, and in those receiving either K+ or potassium K+-sparing diuretics, heparin or non-steroidal anti-inflammatory drugs (NSAIDs). 

Hyperkalemia is an occasional complication of heparin therapy. It has been attributed to hypoaldosteronism, and fludrocortisone has been used to treat it (12). It has been suggested that marked hyperkalemia is only likely to occur in the presence of other factors that alter potassium balance (13). 

Sherman DS, Kass CL, Fish DN. Fludrocortisone for the treatment of heparin-induced hyperkalemia. Ann Pharmacother 2000 34(5) 606-10. 

Koren-Michowitz M, Avni B, Michowitz Y, Moravski G, Efrati S, Golik A. Early onset of hyperkalemia in patients treated with low molecular weight heparin a prospective study. Pharmacoepidemiol Drug Saf 2004 13(5) 299-302. 

Two forms of heparin-induced thrombocytopenia (HIT) have been observed. The first (HIT I) is a transient, mild, and benign thrombocytopenia seen soon after initiation of heparin therapy (normally within 2 days) and is felt to be due to inherent plateletaggregating properties of heparin. A second, more severe form of HIT (HIT II) is typically seen later and is immune-mediated. The incidence of HIT II is estimated at 3-5%. The onset is generally 3-14 days after initiation of heparin therapy but may occur sooner with repeat exposure. HIT II may occur with any dose and type of heparin, but the frequency is highest with continuous intravenous infusions of unfractionated heparin. HIT with subsequent thrombosis is a feared complication. These thrombi can form in the venous or arterial circulation. Thrombotic complications include necrotic skin lesions, myocardial infarction, stroke, and gangrene. Hyperkalemia may be seen with heparin therapy due to aldosterone synthesis inhibition. 

Heparin is known to inhibit aldosterone synthesis. This is not considered clinically significant. However the effects on aldosterone may lead to hyperkalemia and metabolic abnormalities with long term therapy. 

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