Dos Santos Mariane, Veronese Francisco Veríssimo, Moresco Rafael Noal
Laboratory of Clinical Biochemistry, Department of Clinical and Toxicological Analysis, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil; Graduate Program in Pharmaceutical Sciences, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.
Division of Nephrology, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil.
Clin Chim Acta. 2020 Sep;508:197-205. doi: 10.1016/j.cca.2020.05.034. Epub 2020 May 16.
Systemic lupus erythematosus (SLE) is an autoimmune disease that affects multiple organs; lupus nephritis (LN) is one of the most severe complications of SLE. In the kidneys, an intense inflammatory reaction affects the glomeruli and tubular interstitium. Uric acid has been considered a key molecule in the pathogenesis of some conditions such as metabolic syndrome, hypertension, and kidney disease as it is produced by injured cells and promotes immune-inflammatory responses. In this regard, high serum uric acid concentrations may be involved in the activation of some inflammatory pathways, associated with kidney damage in SLE. Therefore, the purpose of this article was to review the main physiological mechanisms and clinical data on the association between serum uric acid and kidney damage in SLE. Scientific evidence indicates that hyperuricemia has the potential to be an adjuvant in the development and progression of kidney manifestations in SLE. Uric acid may promote the activation of inflammatory pathways and the formation and deposition of autoantibodies in kidneys, leading to a reduction of glomerular filtration rate. Other potential mechanisms of this association include the presence of polymorphisms in the urate transporters, metabolic syndrome, use of some medications, and other situations associated with a reduced renal excretion of uric acid.
系统性红斑狼疮（SLE）是一种影响多个器官的自身免疫性疾病；狼疮性肾炎（LN）是SLE最严重的并发症之一。在肾脏中，强烈的炎症反应会影响肾小球和肾小管间质。尿酸被认为是某些疾病（如代谢综合征、高血压和肾脏疾病）发病机制中的关键分子，因为它由受损细胞产生并促进免疫炎症反应。在这方面，高血清尿酸浓度可能参与了一些炎症途径的激活，这与SLE中的肾脏损伤有关。因此，本文的目的是综述血清尿酸与SLE肾脏损伤之间关联的主要生理机制和临床数据。科学证据表明，高尿酸血症有可能成为SLE肾脏表现发生和进展的辅助因素。尿酸可能促进炎症途径的激活以及肾脏中自身抗体的形成和沉积，导致肾小球滤过率降低。这种关联的其他潜在机制包括尿酸转运体多态性的存在、代谢综合征、某些药物的使用以及其他与尿酸肾脏排泄减少相关的情况。
