The adrenal cortex and the kidney

The adrenal cortex regulates renal function in a number of important ways; indeed, normal renal function cannot be understood without recognition of such regulation. Well-recognized examples of such regulation are the control of body fluid tonicity through regulation of urinary solute concentration-a function controlled “primarily” by vasopressin, but secondarily and importantly by the adrenal cortex-and control of body sodium-a function controlled primarily by renal tubular sodium reabsorption but regulated by sodium-retaining steroids.The kidney can regulate adrenal function by changing reabsorption of sodium and secretion of potassium, and also by release of renin. The primary target of such regulation is the secretion of aldosterone, which may be influenced by body fluid volume, potassium ion and angiotensin II.Because of these interrelationships, the pathophysiology of certain disease states may be described as aberrations in feedback loops between adrenal cortex and kidney. In this paper we will consider this “system” in some detail, and attempt to explain four disorders as examples of errors in control.In the form of “primary” aldosteronism resulting from hyperplasia of all adrenal cortical tissue, overproduction of aldosterone persists in the absence of all known stimulatory factors. In renovascular hypertension, angiotensin and aldosterone production may persist despite systemic hypertension. In the non-salt-losing form of the adrenogenital syndrome of congenital adrenal hyperplasia without treatment, failure of feedback inhibition by Cortisol may result in overproduction of adrenocorticotropic hormone (ACTH) which, in turn, may lead to overproduction of progesterone. Progesterone may cause sodium loss and overproduction of renin and aldosterone while blocking their effects. In the syndrome of juxtaglomerular hyperplasia with normal blood pressure, overproduction of renin may result from unresponsiveness of blood vessels leading to a lack of feedback inhibition by pressure rise. Under certain circumstances sodium loss can potentiate both the overproduction and the unresponsiveness. Excessive renin leads to aldosteronism and potassium loss