endocrine and metabolic disorders
Secondary Aldosteronism
Introduction
Secondary aldosteronism is increased adrenal production of aldosterone in response to nonpituitary, extra-adrenal stimuli such as renal hypoperfusion. Symptoms are similar to those of primary aldosteronism. Diagnosis includes measurement of plasma aldosterone levels and plasma renin activity. Treatment involves correcting the cause. (See also Overview of Adrenal Function .) Aldosterone is the most potent mineralocorticoid produced by the adrenals. It causes sodium retention and potassium loss. In the kidneys, aldosterone causes transfer of sodium from the lumen of the distal tubule into the tubular cells in exchange for potassium and hydrogen. The same effect occurs in salivary glands, sweat glands, cells of the intestinal mucosa, and in exchanges between intracellular fluid (ICF) and extracellular fluid (ECF). Aldosterone secretion is regulated by the Primary Aldosteronism and, to a lesser extent, by adrenocorticotropic hormone (ACTH). Renin, a proteolytic enzyme, is stored in the juxtaglomerular cells of the kidneys. Reduction in blood volume and flow in the afferent renal arterioles or Secondary aldosteronism is caused by reduced renal blood flow, which stimulates the Primary Aldosteronism with resultant hypersecretion of aldosterone. Causes of reduced renal blood flow include Obstructive renal artery disease (eg, atheroma, stenosis) Renal vasoconstriction (as occurs in accelerated hypertension) Edematous disorders (eg, Heart Failure (HF) , Secretion may be normal in heart failure, but hepatic blood flow and aldosterone metabolism are reduced, so circulating levels of the hormone are high. 