Affiliation:
1. Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin
2. Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin
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.
Funder
HHS | NIH | National Heart, Lung, and Blood Institute
U.S. Department of Veterans Affairs
Publisher
American Physiological Society
Cited by
20 articles.
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