Routine heparin therapy inhibits adrenal aldosterone production.

While heparin-induced aldosterone deficiency has been sporadically reported, it is not known whether heparin always inhibits aldosterone production to a variable extent or if this is an idiosyncratic effect, nor is the mechanism underlying the phenomenon known. We have examined plasma aldosterone, PRA, and aldosterone to renin activity ratios in 20 patients before, during and after treatment with heparin. Aldosterone cell during heparin treatment from 73.5 +/- 20.5 to 36.8 +/- 11.2 pg/ml (P less than 0.05) and rose after its withdrawal to 94.8 +/- 37.1 p/ml (P less than 0.05). PRA rose with heparin treatment from 2.8 +/- 1.0 to 6.1 +/- 1.6 ng/ml . h (P less than 0.05) and fell to 2.4 +/- 0.5 ng/ml . h (P less than 0.05) when the drug was withdrawn. Aldosterone to renin activity ratios, which are indices of aldosterone responsiveness to angiotensin, fell from 59.5 +/- 1.7 to 25 +/- 14.9 (P less than 0.01) with heparin treatment and rose after withdrawal of the drug to 58.5 +/- 24.9 (P less than 0.01). There was a significant small fall in serum sodium levels with the introduction of heparin, but none of the patients developed clinical mineralocorticoid deficiency. Although heparin consistently perturbs aldosterone production in the glomerulosa cell, this effect is not clinically significant when normal adjustments can be made in the generation of angiotensin. However, where limitations in the renin-angiotensin-aldosterone axis exist, e.g. in diabetes mellitus, mineralocorticoid insufficiency may be precipitated by heparin.