Urinary endothelin-1 as a marker of renal damage in sickle cell disease.
Nephrol Dial Transplant
; 20(11): 2408-13, 2005 Nov.
Article
in En
| MEDLINE
| ID: mdl-16144850
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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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Diabetes Insipidus, Nephrogenic
/
Endothelin-1
/
Albuminuria
/
Anemia, Sickle Cell
Type of study:
Etiology_studies
/
Observational_studies
/
Risk_factors_studies
Limits:
Adult
/
Female
/
Humans
/
Male
Language:
En
Journal:
Nephrol Dial Transplant
Journal subject:
NEFROLOGIA
/
TRANSPLANTE
Year:
2005
Document type:
Article
Affiliation country:
France