Uric acid and inflammation in kidney disease
Asymptomatic hyperuricemia is frequently observed in patients with kidney disease. Although a substantial number of epidemiologic studies have suggested that an elevated uric acid level plays a causative role in the development and progression of kidney disease, whether hyperuricemia is simply a res...
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Veröffentlicht in: | American journal of physiology. Renal physiology 2020-06, Vol.318 (6), p.F1327-F1340 |
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container_title | American journal of physiology. Renal physiology |
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creator | Jung, Su Woong Kim, Su-Mi Kim, Yang Gyun Lee, Sang-Ho Moon, Ju-Young |
description | Asymptomatic hyperuricemia is frequently observed in patients with kidney disease. Although a substantial number of epidemiologic studies have suggested that an elevated uric acid level plays a causative role in the development and progression of kidney disease, whether hyperuricemia is simply a result of decreased renal excretion of uric acid or is a contributor to kidney disease remains a matter of debate. Over the last two decades, multiple experimental studies have expanded the knowledge of the biological effects of uric acid beyond its role in gout. In particular, uric acid induces immune system activation and alters the characteristics of resident kidney cells, such as tubular epithelial cells, endothelial cells, and vascular smooth muscle cells, toward a proinflammatory and profibrotic state. These findings have led to an increased awareness of uric acid as a potential and modifiable risk factor in kidney disease. Here, we discuss the effects of uric acid on the immune system and subsequently review the effects of uric acid on the kidneys mainly in the context of inflammation. |
doi_str_mv | 10.1152/ajprenal.00272.2019 |
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Although a substantial number of epidemiologic studies have suggested that an elevated uric acid level plays a causative role in the development and progression of kidney disease, whether hyperuricemia is simply a result of decreased renal excretion of uric acid or is a contributor to kidney disease remains a matter of debate. Over the last two decades, multiple experimental studies have expanded the knowledge of the biological effects of uric acid beyond its role in gout. In particular, uric acid induces immune system activation and alters the characteristics of resident kidney cells, such as tubular epithelial cells, endothelial cells, and vascular smooth muscle cells, toward a proinflammatory and profibrotic state. These findings have led to an increased awareness of uric acid as a potential and modifiable risk factor in kidney disease. 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These findings have led to an increased awareness of uric acid as a potential and modifiable risk factor in kidney disease. Here, we discuss the effects of uric acid on the immune system and subsequently review the effects of uric acid on the kidneys mainly in the context of inflammation.</description><subject>Endothelial cells</subject><subject>Epidemiology</subject><subject>Epithelial cells</subject><subject>Gout</subject><subject>Hyperuricemia</subject><subject>Immune system</subject><subject>Inflammation</subject><subject>Kidney diseases</subject><subject>Kidney stones</subject><subject>Renal function</subject><subject>Risk factors</subject><subject>Smooth muscle</subject><subject>Uric acid</subject><issn>1931-857X</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNpdkE1LAzEQhoMotlZ_gSALXjy4ayZJs8lRil9Q8GLBW0izs5C6HzXpHvrvTW3rwdPMyzzvHB5CroEWAFP2YFfrgJ1tCkpZyQpGQZ-QcbqwHISUp2nXHHI1LT9H5CLGFaUUgME5GXHGGOdAx-R-EbzLrPNVZrsq813d2La1G993KWRfvupwm1U-oo14Sc5q20S8OswJWTw_fcxe8_n7y9vscZ47IcQmx5KXWte6RAtaWQkIiFKCQEmpFEuuSkiRs0paxNoxVTulJWNA7VKC4xNyt_-7Dv33gHFjWh8dNo3tsB-iYVwJBVpMaUJv_6GrfgjJSqIElVKA4mWi-J5yoY8xYG3Wwbc2bA1Qs5NpjjLNr0yzk5laN4ffw7LF6q9ztMd_AEOObw8</recordid><startdate>20200601</startdate><enddate>20200601</enddate><creator>Jung, Su Woong</creator><creator>Kim, Su-Mi</creator><creator>Kim, Yang Gyun</creator><creator>Lee, Sang-Ho</creator><creator>Moon, Ju-Young</creator><general>American Physiological Society</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20200601</creationdate><title>Uric acid and inflammation in kidney disease</title><author>Jung, Su Woong ; Kim, Su-Mi ; Kim, Yang Gyun ; Lee, Sang-Ho ; Moon, Ju-Young</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-e73799f97ea198a61e1ee6614e60064b387166132d6aeefc28fc8962210ab61c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Endothelial cells</topic><topic>Epidemiology</topic><topic>Epithelial cells</topic><topic>Gout</topic><topic>Hyperuricemia</topic><topic>Immune system</topic><topic>Inflammation</topic><topic>Kidney diseases</topic><topic>Kidney stones</topic><topic>Renal function</topic><topic>Risk factors</topic><topic>Smooth muscle</topic><topic>Uric acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jung, Su Woong</creatorcontrib><creatorcontrib>Kim, Su-Mi</creatorcontrib><creatorcontrib>Kim, Yang Gyun</creatorcontrib><creatorcontrib>Lee, Sang-Ho</creatorcontrib><creatorcontrib>Moon, Ju-Young</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology. Renal physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jung, Su Woong</au><au>Kim, Su-Mi</au><au>Kim, Yang Gyun</au><au>Lee, Sang-Ho</au><au>Moon, Ju-Young</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Uric acid and inflammation in kidney disease</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol Renal Physiol</addtitle><date>2020-06-01</date><risdate>2020</risdate><volume>318</volume><issue>6</issue><spage>F1327</spage><epage>F1340</epage><pages>F1327-F1340</pages><issn>1931-857X</issn><eissn>1522-1466</eissn><abstract>Asymptomatic hyperuricemia is frequently observed in patients with kidney disease. Although a substantial number of epidemiologic studies have suggested that an elevated uric acid level plays a causative role in the development and progression of kidney disease, whether hyperuricemia is simply a result of decreased renal excretion of uric acid or is a contributor to kidney disease remains a matter of debate. Over the last two decades, multiple experimental studies have expanded the knowledge of the biological effects of uric acid beyond its role in gout. In particular, uric acid induces immune system activation and alters the characteristics of resident kidney cells, such as tubular epithelial cells, endothelial cells, and vascular smooth muscle cells, toward a proinflammatory and profibrotic state. These findings have led to an increased awareness of uric acid as a potential and modifiable risk factor in kidney disease. 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subjects | Endothelial cells Epidemiology Epithelial cells Gout Hyperuricemia Immune system Inflammation Kidney diseases Kidney stones Renal function Risk factors Smooth muscle Uric acid |
title | Uric acid and inflammation in kidney disease |
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