Hyperreninemia and hyperaldosteronism in sickle cell anemia

M. C. Matustik, U. Carpentieri, C. Corn, Walter Meyer

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Fourteen patients with sickle cell anemia, ages 6 to 20 years, were studied while ingesting high- and low-sodium diets. Although none of the patients had excessive urinary loss of sodium, the majority had elevated plasma renin activities (PRA) and aldosterone secretion rates (ASR). The PRA was higher in patients over 10 years of age; ASR in patients receiving the high-sodium diet increased with age. Patients with sickle cell anemia appeared to compensate for urinary sodium loss between crises. The mechanism of this loss could be a defect in the function of either the distal tubule or the loop of Henle.

Original languageEnglish (US)
Pages (from-to)206-209
Number of pages4
JournalJournal of Pediatrics
Volume95
Issue number2
StatePublished - 1979

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Hyperaldosteronism
Sickle Cell Anemia
Sodium
Aldosterone
Renin
Loop of Henle
Sodium-Restricted Diet
Diet

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Cite this

Matustik, M. C., Carpentieri, U., Corn, C., & Meyer, W. (1979). Hyperreninemia and hyperaldosteronism in sickle cell anemia. Journal of Pediatrics, 95(2), 206-209.

Hyperreninemia and hyperaldosteronism in sickle cell anemia. / Matustik, M. C.; Carpentieri, U.; Corn, C.; Meyer, Walter.

In: Journal of Pediatrics, Vol. 95, No. 2, 1979, p. 206-209.

Research output: Contribution to journalArticle

Matustik, MC, Carpentieri, U, Corn, C & Meyer, W 1979, 'Hyperreninemia and hyperaldosteronism in sickle cell anemia', Journal of Pediatrics, vol. 95, no. 2, pp. 206-209.
Matustik MC, Carpentieri U, Corn C, Meyer W. Hyperreninemia and hyperaldosteronism in sickle cell anemia. Journal of Pediatrics. 1979;95(2):206-209.
Matustik, M. C. ; Carpentieri, U. ; Corn, C. ; Meyer, Walter. / Hyperreninemia and hyperaldosteronism in sickle cell anemia. In: Journal of Pediatrics. 1979 ; Vol. 95, No. 2. pp. 206-209.
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