RALPH A. DeFRONZO, M.D.; C. ROBERT COOKE, M.D., F.A.C.P.; MARTIN GOLDBERG, M.D., F.A.C.P.; MALCOLM COX, M.D.; ALLEN R. MYERS, M.D., F.A.C.P.; ZALMAN S. AGUS, M.D.
DeFRONZO RA, COOKE CR, GOLDBERG M, COX M, MYERS AR, AGUS ZS. Impaired Renal Tubular Potassium Secretion in Systemic Lupus Erythematosus. Ann Intern Med. 1977;86:268-271. doi: 10.7326/0003-4819-86-3-268
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Published: Ann Intern Med. 1977;86(3):268-271.
Two patients with long-standing systemic lupus erythematosus were found to have persistent hyperkalemia. The hyperkalemia could not be explained by renal insufficiency, oliguria, diminished distal sodium delivery, acidemia, or hemolysis. After sodium depletion, urinary aldosterone excretion and plasma aldosterone concentration rose appropriately. No increase in urinary potassium excretion or decrease in serum potassium concentration was noted after fludrocortisone acetate, furosemide, or acetazolamide plus sodium bicarbonate. We conclude that these patients have a primary defect in renal tubular potassium secretion that may be related to an immune complex interstitial nephritis.
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Lupus Erythematosus, Nephrology, Rheumatology.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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