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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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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