Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-9-13
pubmed:abstractText
Many clinical observations suggest common mediators in the progression of kidney disease leading to eventual kidney failure. Among them, accumulating evidence emphasizes the role of chronic hypoxia in the tubulointerstitium in this role. When advanced, tubulointerstitial damage is associated with the loss of peritubular capillaries, impairing blood delivery. Associated interstitial fibrosis further impairs oxygen diffusion and supply to tubular and interstitial cells. This in turn exacerbates chronic hypoxia in this compartment, resulting in a vicious cycle. Both singly or together, glomerular injury and vasoconstriction of efferent arterioles due to an imbalance in vasoactive substances decrease post-glomerular peritubular capillary blood flow and contribute to chronic hypoxia in the tubulointerstitium. Anemia in kidney disease also plays a significant role in hypoxia of the kidney. Moreover, increased metabolic demand in tubular cells, as observed in glomerular hyperfiltration for example, can cause relative hypoxia. Importantly, these factors can affect the kidney before the appearance of significant pathological changes in the vasculature and predispose it to tubulointerstitial injury. Therapeutic approaches targeting chronic hypoxia in the kidney should be effective against a broad range of renal diseases. Recent studies have elucidated the mechanisms of hypoxia-induced transcription, giving hope for the development of novel therapeutic approaches against this final common pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
1660-2129
pubmed:author
pubmed:copyrightInfo
Copyright 2004 S. Karger AG, Basel
pubmed:issnType
Electronic
pubmed:volume
98
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
e8-12
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Hypoxia and tubulointerstitial injury: a final common pathway to end-stage renal failure.
pubmed:affiliation
Division of Nephrology and Endocrinology, University of Tokyo School of Medicine, Tokyo, Japan. mnangaku-tky@umin.ac.jp
pubmed:publicationType
Journal Article, Review