| Literature DB >> 32223309 |
Lashodya V Dissanayake1, Denisha R Spires1, Oleg Palygin1, Alexander Staruschenko1,2.
Abstract
Recently, research has redirected its interests in uric acid (UA) from gout, an inflammatory disease in joints, to groups of closely interrelated pathologies associated with cardiovascular and kidney dysfunction. Many epidemiological, clinical, and experimental studies have shown that UA may play a role in the pathophysiology of the cardiorenal syndrome continuum; however, it is still unclear if it is a risk factor or a causal role. Hyperuricemia has been well studied in the past two decades, revealing mechanistic insights into UA homeostasis. Likewise, some epidemiological and experimental evidence suggests that hypouricemia can lead to cardiorenal pathologies. The goal of this review is to highlight why studying both hyperuricemia and hypouricemia is warranted as well as to summarize the relevance of UA to kidney function.Entities:
Keywords: hyperuricemia; hypouricemia; uric acid; xanthine dehydrogenase; xanthine oxidase; xanthine oxidoreductase
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Year: 2020 PMID: 32223309 PMCID: PMC7294331 DOI: 10.1152/ajprenal.00066.2020
Source DB: PubMed Journal: Am J Physiol Renal Physiol ISSN: 1522-1466