Hyponatremia and hyperkalemia in adrenal insufficiency
- David B Mount, MD
David B Mount, MD
- Assistant Professor of Medicine
- Harvard Medical School
- Section Editors
- Richard H Sterns, MD
Richard H Sterns, MD
- Section Editor — Fluid and Electrolytes
- Professor of Medicine
- University of Rochester School of Medicine and Dentistry
- André Lacroix, MD
André Lacroix, MD
- Section Editor — Adrenal Disease
- Professor of Medicine
- University of Montreal, Quebec, Canada
The electrolyte disturbances in primary adrenal insufficiency are due to diminished secretion of cortisol and aldosterone. A major function of aldosterone is to increase urinary potassium secretion. As a result, hypoaldosteronism can be associated with hyperkalemia and mild metabolic acidosis [1,2]. Sodium wasting is a variable feature of this disorder. It is not prominent in adults with isolated hypoaldosteronism, probably because aldosterone secretion is only modestly reduced. (See "Etiology, diagnosis, and treatment of hypoaldosteronism (type 4 RTA)".)
Although aldosterone normally enhances sodium reabsorption, other sodium-retaining factors (such as angiotensin II and norepinephrine) are able to compensate for the decreased availability of aldosterone . However, patients with primary adrenal insufficiency may have severe hypoaldosteronism, leading to salt wasting and possibly hypotension and adrenal crisis. (See "Clinical manifestations of adrenal insufficiency in adults".)
Other causes of hyponatremia and hyperkalemia, as well as the evaluation of patients with hyponatremia or hyperkalemia, are discussed elsewhere. (See "Causes of hyponatremia in adults" and "Causes and evaluation of hyperkalemia in adults" and "Evaluation of adults with hyponatremia".)
HYPONATREMIA AND HYPERKALEMIA
Hyponatremia and hyperkalemia are the two major electrolyte abnormalities of primary adrenal insufficiency. Hyponatremia is mediated by increased release of antidiuretic hormone (ADH) which results in water retention and a reduction in the plasma sodium concentration [3,4]. Both cortisol and aldosterone deficiency contribute to this problem:
●The hypersecretion of ADH seen in cortisol deficiency may be due in part to the reductions in systemic blood pressure and cardiac output induced (via an unknown mechanism) by the lack of cortisol. However, a more important mechanism may be that cortisol deficiency results in increased hypothalamic secretion of corticotropin releasing hormone (CRH), an ADH secretagogue [5-8]. Cortisol feeds back negatively on CRH and ACTH, an inhibitory effect that is removed with adrenal insufficiency [5,9]. In addition, cortisol appears to directly suppress ADH secretion [10-12]. Thus, ADH levels increase when plasma cortisol levels are low.
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