Document Detail


Endothelin-1 in the kidney and urine of patients with glomerular disease and proteinuria.
MedLine Citation:
PMID:  12425483     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Endothelin-1 (ET-1) is a strong vasoconstrictive peptide that is involved in the pathogenesis of arterial hypertension. There is increasing evidence, based on studies in experimental animals, that endothelin-1 is produced by tubular epithelial cells in response to activation by filtered protein and is involved in the development of renal scarring. The aim of this study is to examine the distribution of ET-1 in the renal tissue of patients with heavy proteinuria and to estimate the changes in its urinary excretion after immunosuppressive therapy. PATIENTS AND METHODS: Twenty-four patients with severe proteinuria (7.5 +/- 6.5 g/24 h) due to different types of glomerular disease and normal renal function (creatinine clearance 91 +/- 14 ml/ min) were investigated. All patients underwent a renal biopsy and commenced on immunosuppressive therapy with corticosteroids and cyclosporin A. The localization of ET-1 in the renal tissue was examined by immunohistochemistry and compared to control renal tissue from 9 patients who underwent nephrectomies because of hypernephroma. In patients with proteinuria, endothelin-1 excretion in the urine at diagnosis was determined by radioimmunoassay and compared to that of 14 healthy subjects. A second measurement of urinary ET-1 excretion was performed after remission of proteinuria or 6 months after the initiation of treatment in patients with persistent nephrotic syndrome. RESULTS: ET-1 in renal tissue of patients and controls was localized within the cytoplasm of endothelial cells. In nephrotic patients, it was also localized within the cytoplasm of tubular epithelial cells. Urinary ET-1 levels were higher in nephrotic patients compared to healthy subjects (746 +/- 180 ng/24 h vs 410 +/- 112 ng/ml, p < 0.001). In 17 of 24 patients who showed remission of proteinuria with immunosuppressive therapy, the urinary ET-1 levels decreased (from 803 +/- 168 ng/24 h to 511 +/- 80 ng/24 h, p < 0.001) whereas in 7 patients with persistent proteinuria, urinary ET-1 excretion remained elevated. CONCLUSIONS: The increased urinary excretion of ET-1 in patients with severe proteinuria followed by a significant decrease after remission ofproteinuria with immunosuppressive treatment, along with its expression within tubular epithelial cells, suggests a possible relationship between proteinuria and renal ET-1 production.
Authors:
J G Vlachojannis; S Tsakas; C Petropoulou; D S Goumenos; S Alexandri
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Clinical nephrology     Volume:  58     ISSN:  0301-0430     ISO Abbreviation:  Clin. Nephrol.     Publication Date:  2002 Nov 
Date Detail:
Created Date:  2002-11-11     Completed Date:  2003-02-25     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  0364441     Medline TA:  Clin Nephrol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  337-43     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, Nephrology, University Hospital, Patras, Greece. johnvl@med.upatras.gr
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MeSH Terms
Descriptor/Qualifier:
Adult
Anti-Inflammatory Agents / therapeutic use
Cyclosporine / therapeutic use
Endothelin-1 / analysis*,  urine*
Female
Humans
Immunosuppressive Agents / therapeutic use
Kidney Diseases / drug therapy,  pathology*,  urine*
Kidney Glomerulus / drug effects,  pathology*
Male
Middle Aged
Prednisolone / therapeutic use*
Proteinuria / drug therapy,  pathology*,  urine*
Remission Induction
Severity of Illness Index
Chemical
Reg. No./Substance:
0/Anti-Inflammatory Agents; 0/Endothelin-1; 0/Immunosuppressive Agents; 50-24-8/Prednisolone; 59865-13-3/Cyclosporine

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