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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

The role of uric acid in inflammasome-mediated kidney injury

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Braga, Tarcio Teodoro [1, 2] ; Foresto-Neto, Orestes [3, 4] ; Saraiva Camara, Niels Olsen [3, 4]
Total Authors: 3
[1] Univ Fed Parana, Dept Basic Pathol, Curitiba, PR - Brazil
[2] Carlos Chagas Inst Fiocruz Parana, Curitiba, Parana - Brazil
[3] Univ Fed Sao Paulo, Nephrol Div, Sao Paulo, SP - Brazil
[4] Univ Sao Paulo, Inst Biomed Sci 4, Dept Immunol, Sao Paulo, SP - Brazil
Total Affiliations: 4
Document type: Review article
Source: CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION; v. 29, n. 4, p. 423-431, JUL 2020.
Web of Science Citations: 2

Purpose of review Uric acid is produced after purine nucleotide degradation, upon xanthine oxidase catalytic action. In the evolutionary process, humans lost uricase, an enzyme that converts uric acid into allantoin, resulting in increased serum uric acid levels that may vary according to dietary ingestion, pathological conditions, and other factors. Despite the controversy over the inflammatory role of uric acid in its soluble form, crystals of uric acid are able to activate the NLRP3 inflammasome in different tissues. Uric acid, therefore, triggers hyperuricemic-related disease such as gout, metabolic syndrome, and kidney injuries. The present review provides an overview on the role of uric acid in the inflammasome-mediated kidney damage. Recent findings Hyperuricemia is present in 20-35% of patients with chronic kidney disease. However, whether this increased circulating uric acid is a risk factor or just a biomarker of renal and cardiovascular injuries has become a topic of intense discussion. Despite these conflicting views, several studies support the idea that hyperuricemia is indeed a cause of progression of kidney disease, with a putative role for soluble uric acid in activating renal NLRP3 inflammasome, in reprograming renal and immune cell metabolism and, therefore, in promoting kidney inflammation/injury. Summary Therapies aiming to decrease uric acid levels prevent renal NLRP3 inflammasome activation and exert renoprotective effects in experimental kidney diseases. However, further clinical studies are needed to investigate whether reduced circulating uric acid can also inhibit the inflammasome and be beneficial in human conditions. (AU)

FAPESP's process: 18/08479-7 - Multi-user equipment approved in grant 17/05264-7: analisador de fluxo extracelular Seahorse XFe96
Grantee:Niels Olsen Saraiva Câmara
Support type: Multi-user Equipment Program
FAPESP's process: 19/02893-9 - The hypoxia-inducible factor 1 alpha (HIF-1 alpha) and the metabolism of tubular epithelial cells and podocytes in the development and progression of experimental kidney disease
Grantee:Orestes Foresto Neto
Support type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 17/05264-7 - Cell metabolism, microbiota and immune system: new paradigms in renal diseases physiopathology
Grantee:Niels Olsen Saraiva Câmara
Support type: Research Projects - Thematic Grants