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Impaired Renal Tubular Potassium Secretion in Systemic Lupus Erythematosus

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.; and ZALMAN S. AGUS, M.D.
[+] Article and Author Information

Grant support: by a research grant from the National Heart and Lung Institute, HL-0034, and by a training grant from the National Institute of Arthritis, Metabolism, and Digestive Diseases, AM 05634. Dr. Agus is a Clinical Investigator of the Veterans Administration.

▸Requests for reprints should be addressed to Zalman S. Agus, M.D.; Renal-Electrolyte Section, 860 Gates Pavilion, Hospital of the University of Pennsylvania, 3400 Spruce St.; Philadelphia, PA 19104.


Philadelphia, Pennsylvania, and Baltimore, Maryland


Ann Intern Med. 1977;86(3):268-271. doi:10.7326/0003-4819-86-3-268
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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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