The Association between Serum Uric Acid and Renal Damage: The Takahata Study - New Insights

Hyperuricemia is a risk factor for causing end-stage kidney disease and cardiovascular disease in the general population; however, several aspects, such as the site of kidney damaged by hyperuricemia and the threshold levels of serum uric acid for the development of renal damage, have not been fully clarified.

To examine these aspects, we analyzed data from the Takahata study, a community-based cohort study involving participants of an annual health check-up, and used urinary albumin creatinine ratio (UACR) and urinary β2-microglobulin creatinine ratio (UBCR) in spot urine as indices of glomerular and tubular damage respectively. In cross-sectional analysis, increased serum uric acid levels were accompanied by higher UACR values and lower UBCR values. Multivariate analysis revealed that albuminuria (UACR ≥30 mg/g), but not elevated UBCR, was independently associated with increased uric acid (≥7 mg/dL for males, ≥6 mg/dL for females). In longitudinal analysis, uric acid at baseline was an independent factor for a 1-year increase in the UACR. Cox-proportional hazard model analysis with adjustment for possible confounders including age, renal function, and comorbidities revealed that hyperuricemia was an independent risk factor for all-cause and cardiovascular mortality in females. Key Messages: Our results revealed that elevated uric acid is an independent risk factor for glomerular damage, but not tubular damage, and that the risk for renal damage and mortality might be increased at the high-normal range of uric acid in the community-based population.