Impaired renal tubular potassium secretion in sickle cell disease

R. A. DeFronzo, P. A. Taufield, H. Black, P. McPhedran, C. R. Cooke

Research output: Contribution to journalArticlepeer-review

67 Scopus citations

Abstract

The authors examined tubular function in six patients with sickle cell hemoglobin. All had normal inulin and paraaminohippurate clearances and impaired urinary concentrating and acidifying abilities. After intravenous potassium chloride administration, maximum excretion of potassium (U(k)V) 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, U(k)V 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. The authors 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.

Original languageEnglish (US)
Pages (from-to)310-316
Number of pages7
JournalUnknown Journal
Volume90
Issue number3
DOIs
StatePublished - 1979
Externally publishedYes

ASJC Scopus subject areas

  • Internal Medicine

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