RALPH A. DeFRONZO, M.D.; PHYLLIS AUGUST TAUFIELD, M.D.; HENRY BLACK, M.D.; PETER McPHEDRAN, M.D.; C. ROBERT COOKE, M.D.
Grant support: in part by U.S. Public Health Service Grant HL-03303.
▸Requests for reprints should be addressed to Ralph A. DeFronzo, M.D.; Yale University School of Medicine, 333 Cedar Street; New Haven, CT 06510.
DeFRONZO RA, TAUFIELD PA, BLACK H, McPHEDRAN P, COOKE CR. Impaired Renal Tubular Potassium Secretion in Sickle Cell Disease. Ann Intern Med. 1979;90:310-316. doi: 10.7326/0003-4819-90-3-310
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Published: Ann Intern Med. 1979;90(3):310-316.
We examined renal tubular function in six patients with sickle cell hemoglobin. All had normal inulin and para-aminohippurate clearances and impaired urinary concentrating and acidifying abilities. After intravenous potassium chloride administration, maximum excretion of potassium (UKV) was significantly lower in sickle cell patients than in control subjects, and the percentage of potassium load excreted in 5 h was markedly reduced. Urinary potassium excretion after sodium sulfate infusion was also markedly reduced in sickle cell patients compared to control subjects. After 40 mg of oral furosemide, UKV was also diminished in sickle cell patients. Plasma aldosterone response to ACTH and intravenous potassium was similar to that of control subjects. Plasma renin activity increased normally after volume contraction. We conclude that sickle cell patients have a defect in their ability to excrete an acute potassium load that cannot be attributed to abnormal renin or aldosterone secretion. Overall potassium homeostasis is maintained by extrarenal mechanisms during acute potassium loading.
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Hematology/Oncology, Red Cell Disorders.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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