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Serum Uric Acid Levels and Kidney Transplant Outcomes: Cause, Consequence, or Confounded?

Uric acid is an end product of purine metabolism by the liver, intestines, and other tissues (including muscle and kidneys). It was first discovered in 1776 in a bladder calculus. The association of uric acid with human diseases beyond kidney stones was initially described in patients with gouty arthritis, but has since extended to other conditions such as hypertension, cardiovascular disease, cerebrovascular disease, metabolic syndrome, preeclampsia, and kidney disease. Several mechanisms have been proposed to explain the linkage between uric acid and various disease states, but central to these explanations has been uric acid’s potential role in endothelial dysfunction (by nitric oxide depletion), vascular smooth muscle proliferation, inflammation, oxidative stress, and activation of the renin-angiotensin system. The relationship between serum uric acid (SUA) concentration and chronic kidney disease (CKD) has been explored in several studies. Recently, Li et al conducted an umbrella review, which systematically collected and evaluated evidence from multiple sources, to examine the impact of SUA on various health outcomes, including CKD. Although the results from studies assessing renal end points were variable, convincing evidence for a causal role of SUA was noted only for gout and nephrolithiasis, whereas suggestive evidence was present for CKD. Moreover, several small randomized controlled trials of allopurinol therapy in patients with CKD have suggested that xanthine oxidase inhibition and/or lowering of SUA concentrations may reduce renal disease progression and/or improve measures of kidney function. In this issue of AJKD, Kalil et al used data from the Folic Acid for Vascular Outcome Reduction in Transplantation (FAVORIT) trial to conduct an observational cohort study examining the potential association between baseline SUA concentrations and various health outcomes after kidney transplantation. The authors hypothesized that SUA may be linked to cardiovascular, mortality, and renal end points in