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| 2007 JASN IMPACT FACTOR 7.111 | HOME AUTHOR INFO EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP | |||
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*
Division of Nephrology, Université
Catholique de Louvain Medical School, Brussels, Belgium
Department of Pathology, Université
Catholique de Louvain Medical School, Brussels, Belgium
Division of Cell Biology, Commissariat à
l'Energie Atomique, Saclay, France
§
Institute of Medical Science and Department of Internal Medicine, Tokai
University School of Medicine, Kanagawa, Japan
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Division of Nephrology, Centre Hospitalier de Luxembourg,
Luxembourg.
Correspondence to Dr. Olivier Devuyst, Division of Nephrology, Université Catholique de Louvain, 10 Avenue Hippocrate, B-1200 Brussels, Belgium. Phone: +32 2 764 1855; Fax: +32 2 764 2836; E-mail: devuyst{at}nefr.ucl.ac.be
Abstract. Long-term peritoneal dialysis (PD) is associated with alterations in peritoneal permeability and loss of ultrafiltration. These changes originate from increased peritoneal surface area, but the morphologic and molecular mechanisms involved remain unknown. The hypothesis that modifications of activity and/or expression of nitric oxide synthase (NOS) isozymes might play a role in these modifications, via enhanced local production of nitric oxide, was tested in this study. NOS activities were measured by the L-citrulline assay in peritoneal biopsies from seven control subjects, eight uremic patients immediately before the onset of PD, and 13 uremic patients on short-term (<18 mo, n = 6) or long-term (>18 mo, n = 7) PD. Peritoneal NOS activity is increased fivefold in long-term PD patients compared with control subjects. In uremic patients, NOS activity is positively correlated with the duration of PD. Increased NOS activity is mediated solely by Ca2+-dependent NOS and, as shown by immunoblotting, an upregulation of endothelial NOS. The biologic relevance of increased NOS in long-term PD was demonstrated by enhanced nitrotyrosine immunoreactivity and a significant increase in vascular density and endothelial area in the peritoneum. Immunoblotting and immunostaining studies demonstrated an upregulation of vascular endothelial growth factor (VEGF) mostly along the endothelium lining peritoneal blood vessels in long-term PD patients. In the latter, VEGF colocalized with the advanced glycation end product pentosidine deposits. These data provide a morphologic (angiogenesis and increased endothelial area) and molecular (enhanced NOS activity and endothelial NOS upregulation) basis for explaining the permeability changes observed in long-term PD. They also support the implication of local advanced glycation end product deposits and liberation of VEGF in that process.
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