Routine Heparin Therapy Inhibits Adrenal Aldosterone Production*

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Abstract
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 ratiosin 20 patients before, during and after treatment with heparin. Aldosterone fell during heparin treatment from 73.5 ± 20.5 to 36.8 ± 11.2 pg/ml (P < 0.05) and rose after its withdrawal to 94.8 ± 37.1 pg/ml (P < 0.05). PRA rose with heparin treatment from 2.8 ± 1.0 to 6.1 ± 1.6 ng/ml-h (P < 0.05) and fell to 2.4 ± 0.5 ng/ml-h (P < 0.05) when the drug was withdrawn. Aldosterone to renin activity ratios, which are indices of aldosterone responsiveness to angiotensin, fell from 59.5 ± 17.1 to 25 ± 14.9 (P < 0.01) with heparin treatment and rose after withdrawal of the drug to 58.5 ± 24.9 (P < 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.

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