Document Detail


Benfotiamine protects against peritoneal and kidney damage in peritoneal dialysis.
MedLine Citation:
PMID:  21511829     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Residual renal function and the integrity of the peritoneal membrane contribute to morbidity and mortality among patients treated with peritoneal dialysis. Glucose and its degradation products likely contribute to the deterioration of the remnant kidney and damage to the peritoneum. Benfotiamine decreases glucose-induced tissue damage, suggesting the potential for benefit in peritoneal dialysis. Here, in a model of peritoneal dialysis in uremic rats, treatment with benfotiamine decreased peritoneal fibrosis, markers of inflammation, and neovascularization, resulting in improved characteristics of peritoneal transport. Furthermore, rats treated with benfotiamine exhibited lower expression of advanced glycation endproducts and their receptor in the peritoneum and the kidney, reduced glomerular and tubulointerstitial damage, and less albuminuria. Increased activity of transketolase in tissue and blood contributed to the protective effects of benfotiamine. In primary human peritoneal mesothelial cells, the addition of benfotiamine led to enhanced transketolase activity and decreased expression of advanced glycation endproducts and their receptor. Taken together, these data suggest that benfotiamine protects the peritoneal membrane and remnant kidney in a rat model of peritoneal dialysis and uremia.
Authors:
Lars P Kihm; Sandra Müller-Krebs; Julia Klein; Gregory Ehrlich; Laura Mertes; Marie-Luise Gross; Antonysunil Adaikalakoteswari; Paul J Thornalley; Hans-Peter Hammes; Peter P Nawroth; Martin Zeier; Vedat Schwenger
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-04-21
Journal Detail:
Title:  Journal of the American Society of Nephrology : JASN     Volume:  22     ISSN:  1533-3450     ISO Abbreviation:  J. Am. Soc. Nephrol.     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-05-02     Completed Date:  2011-07-01     Revised Date:  2012-05-01    
Medline Journal Info:
Nlm Unique ID:  9013836     Medline TA:  J Am Soc Nephrol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  914-26     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 by the American Society of Nephrology
Affiliation:
Department of Nephrology, University of Heidelberg, Im Neuenheimer Feld 162, 69120 Heidelberg, Germany. lars.kihm@med.uni-heidelberg.de
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MeSH Terms
Descriptor/Qualifier:
Albuminuria / etiology
Animals
Fibrosis
Glycosylation End Products, Advanced / analysis
Kidney / metabolism,  pathology*
Male
Peritoneal Dialysis / adverse effects*
Peritoneum / blood supply,  metabolism,  pathology*
Rats
Rats, Sprague-Dawley
Reactive Oxygen Species / metabolism
Receptors, Immunologic / analysis
Thiamine / analogs & derivatives*,  pharmacology
Transketolase / metabolism
Uremia / therapy*
Vascular Endothelial Growth Factor A / analysis
Chemical
Reg. No./Substance:
0/Glycosylation End Products, Advanced; 0/Reactive Oxygen Species; 0/Receptors, Immunologic; 0/Vascular Endothelial Growth Factor A; 0/advanced glycosylation end-product receptor; 22457-89-2/benphothiamine; 59-43-8/Thiamine; EC 2.2.1.1/Transketolase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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