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Urinary endothelin-1 as a marker of renal damage in sickle cell disease.

Abstract : BACKGROUND: Sickle cell disease (SCD) affects the kidney by acute mechanisms as well as by insidious renal medullary/papillary necrosis, resulting in tubular defects, which increase the risk of dehydration and subsequent sickle crisis. Hypoxia has been reported to stimulate endothelin-1 (ET-1) synthesis by endothelial cells and also in the renal tubule. METHODS: This case-control study measured ET-1 in urine as a marker of its renal synthesis in asymptomatic SCD patients. Baseline plasma and urinary ET-1 levels were measured and followed during a water deprivation study and a subsequent administration of desmopressin. RESULTS: Urine and plasma levels of ET-1 were elevated in patients with SCD, compared with carefully matched African-French and African controls, and urine ET-1 excretion was associated with a marked urine-concentrating defect. Moreover, urinary ET-1 output was correlated with microalbuminuria in SCD patients. CONCLUSIONS: ET-1 is known to antagonize the tubular effects of vasopressin and to promote renal scarring; increased renal production of ET-1 could produce nephrogenic diabetes insipidus and dehydration in SCD patients through a combination of fibrosis and functional resistance to vasopressin. This study provides a rationale for trials with endothelin receptor antagonists in sickle cell disease nephropathy.
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Contributor : Pierre-Louis Tharaux Connect in order to contact the contributor
Submitted on : Wednesday, May 3, 2006 - 1:09:29 PM
Last modification on : Tuesday, May 31, 2022 - 3:32:45 AM

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Pierre-Louis Tharaux, Robert Girot, Alain Kanfer. Urinary endothelin-1 as a marker of renal damage in sickle cell disease.. Nephrology Dialysis Transplantation, Oxford University Press, 2005, 20, pp.2408-13. ⟨10.1093/ndt/gfi111⟩. ⟨inserm-00000115⟩



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