Urate Transporters in the Kidney: What Clinicians Need to Know
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Chung, Sungjin | - |
dc.contributor.author | Kim, Gheun-Ho | - |
dc.date.accessioned | 2022-07-06T17:16:57Z | - |
dc.date.available | 2022-07-06T17:16:57Z | - |
dc.date.created | 2021-08-25 | - |
dc.date.issued | 2021-06 | - |
dc.identifier.issn | 1738-5997 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/141719 | - |
dc.description.abstract | Urate is produced in the liver by the degradation of purines from the diet and nucleotide turnover and excreted by the kidney and gut. The kidney is the major route of urate removal and has a pivotal role in the regulation of urate homeostasis. Approximately 10% of the glomerular filtered urate is excreted in the urine, and the remainder is reabsorbed by the proximal tubule. However, the transport of urate in the proximal tubule is bidirectional: reabsorption and secretion. Thus, an increase in reabsorption or a decrease in secretion may induce hyperuricemia. In contrast, a decrease in reabsorption or an increase in secretion may result in hyperuricosuria. In the proximal tubule, urate reabsorption is mainly mediated by apical URAT1 (SLC22A12) and basolateral GLUT9 (SLC2A9) transporter. OAT4 (SLC22A11) also acts in urate reabsorption in the apical membrane, and its polymorphism is associated with the risk of hyperuricemia. Renal hypouricemia is caused by SLC22A12 or SLC2A9 loss-of-function mutations, and it may be complicated by exercise-induced acute kidney injury. URAT1 and GLUT9 are also drug targets for uricosuric agents. Sodium-glucose cotransporter inhibitors may induce hyperuricosuria by inhibiting GLUT9b located in the apical plasma membrane. Urate secretion is mediated by basolateral OAT1 (SLC22A6) and OAT3 (SLC22A8) and apical ATP-binding cassette super-family G member 2 (ABCG2), NPT1 (SLC17A1), and NPT4 (SLC17A3) transporter in the proximal tubule. NPT1 and NPT4 may be key players in renal urate secretion in humans, and deletion of SLC22A6 and SLC22A8 in mice leads to decreased urate excretion. Dysfunctional variants of ABCG2 inhibit urate secretion from the gut and kidney and may cause gout. In summary, the net result of urate transport in the proximal tubule is determined by the dominance of transporters between reabsorption (URAT1, OAT4, and GLUT9) and secretion (ABCG2, NPT1, NPT4, OAT1, and OAT3). | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | 전해질고혈압연구회 | - |
dc.title | Urate Transporters in the Kidney: What Clinicians Need to Know | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Gheun-Ho | - |
dc.identifier.doi | 10.5049/EBP.2021.19.1.1 | - |
dc.identifier.scopusid | 2-s2.0-85114828424 | - |
dc.identifier.bibliographicCitation | Electrolytes & Blood Pressure, v.19, no.1, pp.1 - 9 | - |
dc.relation.isPartOf | Electrolytes & Blood Pressure | - |
dc.citation.title | Electrolytes & Blood Pressure | - |
dc.citation.volume | 19 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 1 | - |
dc.citation.endPage | 9 | - |
dc.type.rims | ART | - |
dc.identifier.kciid | ART002732979 | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
dc.subject.keywordPlus | breast cancer resistance protein | - |
dc.subject.keywordPlus | organic anion transporter 1 | - |
dc.subject.keywordPlus | organic anion transporter 3 | - |
dc.subject.keywordPlus | organic anion transporter 4 | - |
dc.subject.keywordPlus | protein slc2a9 | - |
dc.subject.keywordPlus | slc17a3 protein | - |
dc.subject.keywordPlus | sodium glucose cotransporter inhibitor | - |
dc.subject.keywordPlus | sodium phosphate cotransporter 1 | - |
dc.subject.keywordPlus | unclassified drug | - |
dc.subject.keywordPlus | urate | - |
dc.subject.keywordPlus | urate transporter | - |
dc.subject.keywordPlus | uricosuric agent | - |
dc.subject.keywordPlus | acute kidney failure | - |
dc.subject.keywordPlus | apical membrane | - |
dc.subject.keywordPlus | clinician | - |
dc.subject.keywordPlus | drug targeting | - |
dc.subject.keywordPlus | gene deletion | - |
dc.subject.keywordPlus | homeostasis | - |
dc.subject.keywordPlus | human | - |
dc.subject.keywordPlus | hyperuricemia | - |
dc.subject.keywordPlus | hypouricemia | - |
dc.subject.keywordPlus | intestine | - |
dc.subject.keywordPlus | kidney proximal tubule | - |
dc.subject.keywordPlus | kidney tubule absorption | - |
dc.subject.keywordPlus | loss of function mutation | - |
dc.subject.keywordPlus | regulatory mechanism | - |
dc.subject.keywordPlus | Review | - |
dc.subject.keywordPlus | risk | - |
dc.subject.keywordPlus | uric acid urine level | - |
dc.subject.keywordPlus | urinary excretion | - |
dc.subject.keywordAuthor | Gout | - |
dc.subject.keywordAuthor | Hyperuricosuria | - |
dc.subject.keywordAuthor | Hypouricemia | - |
dc.subject.keywordAuthor | Proximal tubule | - |
dc.subject.keywordAuthor | Uric acid transport | - |
dc.identifier.url | https://enbpr.org/DOIx.php?id=10.5049/EBP.2021.19.1.1 | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
222, Wangsimni-ro, Seongdong-gu, Seoul, 04763, Korea+82-2-2220-1365
COPYRIGHT © 2021 HANYANG UNIVERSITY.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.