Role of hyperkalemia in the metabolic acidosis of isolated hypoaldosteronism.
We studied the relative importance of hyperkalemia and mineralocorticoid deficiency in the metabolic acidosis of a patient with proved isolated hyporeninemic hypoaldosteronism and moderate kidney failure. The hyperkalemia and acidosis were severe in relation to the slight azotemia. Despite the systemic acidosis and urinary pH of 4.9, urinary ammonium excretion was distinctly blunted. Correction of the hyperkalemia by potassium-sodium exchange resin alone resolved the acidosis and restored the previously diminished urinary ammonium excretion to normal. Administration of mineralocorticoids only partially corrected the hyperkalemia and the acidosis. Hyperkalemia by itself, rather than hypoaldosteronism per se, caused the acidosis in this patient. Hyperkalemia apparently suppresses urinary ammonium excretion and thus interferes with urinary acidification.
D000138:Acidosis / Q000188:drug therapy / Q000209:etiology* / Q000652:urine; D000450:Aldosterone / Q000172:deficiency*; D000641:Ammonia / Q000652:urine; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006947:Hyperkalemia / Q000150:complications* / Q000188:drug therapy; D007475:Ion Exchange Resins / Q000627:therapeutic use; D007668:Kidney / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000150:complications; D008297:Male; D008875:Middle Aged; D008901:Mineralocorticoids / Q000627:therapeutic use; D011188:Potassium / Q000652:urine; D012083:Renin / Q000097:blood
D007475:Ion Exchange Resins; D008901:Mineralocorticoids; D000450:Aldosterone; D000641:Ammonia; D012083:Renin; D011188:Potassium