Hyperuricemia, the kidneys, and the spectrum of associated diseases: a narrative review

Abstract

Hyperuricemia (elevated serum uric acid) is prevalent, and an important mediator of gout, an increasingly common condition. In addition, hyperuricemia is associated with metabolic syndrome, diabetes, hypertension, and kidney and cardiovascular diseases. Although it remains controversial whether hyperuricemia is a causal factor for kidney disease, the kidneys play a major role in the regulation of serum uric acid levels. Approximately two-thirds of the uric acid produced in humans is excreted by the kidneys. The handling of urate in the renal proximal tubule is extensive, as uric acid undergoes filtration, reabsorption, and secretion. Variations in renal urate handling have been shown to influence the risk of gout. In observational studies, hyperuricemia has been shown to predict kidney disease onset and progression, with a variety of mechanisms implicated. Because of this close association between hyperuricemia and kidney disease, and due to limited studies on the topic, it is important to conduct future studies on the treatment of hyperuricemia to slow kidney disease progression and improve cardiovascular survival in patients with chronic kidney disease. Furthermore, it is important to monitor for gout in patients with kidney disease and to follow the guidelines for treatment of hyperuricemia in this group of patients. This narrative review provides an in-depth discussion of the link between serum uric acid levels, renal handling of uric acid, and diseases associated with dysfunction in uric acid homeostasis.

Keywords:

• Gout
• Hyperuricemia
• Kidney
• Renal insufficiency
• Uric acid
• Urate

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Declaration of funding

Editorial assistance was funded by AstraZeneca.

Declaration of financial/other relationships

D.I.J. has disclosed that she has no significant relationships with or financial interests in any commercial companies related to this study or article.

CMRO peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Acknowledgments

D.I.J. wishes to thank Meredith Rogers MS CMPP of The Lockwood Group for providing writing and editorial assistance funded by AstraZeneca. D.I.J. did not receive any honoraria for this publication.