Free water excretion due to suppressed vasopressin and stimulated aldosterone during sodium restriction in hypoaldosteronemic renal failure.
In two from 3 hyperkalemic patients with chronic glomerulonephritis associated with suppressed aldosterone production ("selective hypoaldosteronism") fractional free water excretion increased and urine osmolality decreased during sodium (Na) restriction. In one of the patients with severe renal concentrating defect in combination with partial vasopressin deficiency polyuria was paradoxically accentuated by lowered Na intake. Na restriction induced 1. a dramatic increase in plasma aldosterone levels, 2. a decrease in glomerular filtration rate associated with a marked disturbance in the glomerulotubular balance resembling to the effects of volume expansion, and 3. a decrease in urinary arginine vasopressin excretion. Paradoxical enhancement of water excretion was explained by increased delivery of filtrate into the distal nephron, increased abstraction of Na from the tubular fluid together with insufficient water permeability of the collecting tubules and lowered vasopressin production.
D000293:Adolescent; D000328:Adult; D000450:Aldosterone / Q000097:blood / Q000172:deficiency*; D001127:Arginine Vasopressin / Q000097:blood / Q000652:urine; D001834:Body Water / Q000378:metabolism*; D002908:Chronic Disease; D004039:Diet, Sodium-Restricted; D005919:Glomerular Filtration Rate; D005921:Glomerulonephritis / Q000378:metabolism*; D006801:Humans; D008297:Male; D011188:Potassium / Q000097:blood
D001127:Arginine Vasopressin; D000450:Aldosterone; D011188:Potassium