The Role of Uric Acid in Kidney Fibrosis: Experimental Evidences for the Causal Relationship

Hyperuricemia is a common finding in chronic kidney disease due to decreased uric acid clearance. The role of uric acid as a risk factor for chronic kidney disease has been largely debated, and recent studies suggested a role of uric acid in the causation and progression of kidney fibrosis, a final...

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Main Authors: Il Young Kim, Dong Won Lee, Soo Bong Lee, Ihm Soo Kwak
Format: Article
Language:English
Published: Hindawi Limited 2014-01-01
Series:BioMed Research International
Online Access:http://dx.doi.org/10.1155/2014/638732
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spelling doaj-532376b63e38457c819258448e9741512020-11-24T20:50:55ZengHindawi LimitedBioMed Research International2314-61332314-61412014-01-01201410.1155/2014/638732638732The Role of Uric Acid in Kidney Fibrosis: Experimental Evidences for the Causal RelationshipIl Young Kim0Dong Won Lee1Soo Bong Lee2Ihm Soo Kwak3Division of Nephrology, Department of Internal Medicine, Pusan National University School of Medicine, Yangsan 626-770, Republic of KoreaDivision of Nephrology, Department of Internal Medicine, Pusan National University School of Medicine, Yangsan 626-770, Republic of KoreaDivision of Nephrology, Department of Internal Medicine, Pusan National University School of Medicine, Yangsan 626-770, Republic of KoreaDivision of Nephrology, Department of Internal Medicine, Pusan National University School of Medicine, Yangsan 626-770, Republic of KoreaHyperuricemia is a common finding in chronic kidney disease due to decreased uric acid clearance. The role of uric acid as a risk factor for chronic kidney disease has been largely debated, and recent studies suggested a role of uric acid in the causation and progression of kidney fibrosis, a final common pathway in chronic kidney disease. Uric acid and xanthine oxidase may contribute to kidney fibrosis mainly by inducing inflammation, endothelial dysfunction, oxidative stress, and activation of the renin-angiotensin system. Besides, hyperuricemia induces alterations in renal hemodynamics via afferent arteriolopathy and contributes to the onset and progression of kidney fibrosis. Xanthine oxidase inhibitors may prevent kidney damage via lowering uric acid and/or inhibiting xanthine oxidase. However, there is still no sufficient evidence from interventional clinical researches supporting the causal relationship between uric acid and kidney fibrosis. The effect and role of xanthine oxidase inhibitors in preventing kidney fibrosis and chronic kidney disease progression must be further explored by performing future large scale clinical trials.http://dx.doi.org/10.1155/2014/638732
collection DOAJ
language English
format Article
sources DOAJ
author Il Young Kim
Dong Won Lee
Soo Bong Lee
Ihm Soo Kwak
spellingShingle Il Young Kim
Dong Won Lee
Soo Bong Lee
Ihm Soo Kwak
The Role of Uric Acid in Kidney Fibrosis: Experimental Evidences for the Causal Relationship
BioMed Research International
author_facet Il Young Kim
Dong Won Lee
Soo Bong Lee
Ihm Soo Kwak
author_sort Il Young Kim
title The Role of Uric Acid in Kidney Fibrosis: Experimental Evidences for the Causal Relationship
title_short The Role of Uric Acid in Kidney Fibrosis: Experimental Evidences for the Causal Relationship
title_full The Role of Uric Acid in Kidney Fibrosis: Experimental Evidences for the Causal Relationship
title_fullStr The Role of Uric Acid in Kidney Fibrosis: Experimental Evidences for the Causal Relationship
title_full_unstemmed The Role of Uric Acid in Kidney Fibrosis: Experimental Evidences for the Causal Relationship
title_sort role of uric acid in kidney fibrosis: experimental evidences for the causal relationship
publisher Hindawi Limited
series BioMed Research International
issn 2314-6133
2314-6141
publishDate 2014-01-01
description Hyperuricemia is a common finding in chronic kidney disease due to decreased uric acid clearance. The role of uric acid as a risk factor for chronic kidney disease has been largely debated, and recent studies suggested a role of uric acid in the causation and progression of kidney fibrosis, a final common pathway in chronic kidney disease. Uric acid and xanthine oxidase may contribute to kidney fibrosis mainly by inducing inflammation, endothelial dysfunction, oxidative stress, and activation of the renin-angiotensin system. Besides, hyperuricemia induces alterations in renal hemodynamics via afferent arteriolopathy and contributes to the onset and progression of kidney fibrosis. Xanthine oxidase inhibitors may prevent kidney damage via lowering uric acid and/or inhibiting xanthine oxidase. However, there is still no sufficient evidence from interventional clinical researches supporting the causal relationship between uric acid and kidney fibrosis. The effect and role of xanthine oxidase inhibitors in preventing kidney fibrosis and chronic kidney disease progression must be further explored by performing future large scale clinical trials.
url http://dx.doi.org/10.1155/2014/638732
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