Abstract
BackgroundIn patients with chronic kidney disease (CKD) hyperuricemia is common. Evidence that hyperuricemia might also play a causal role in vascular disease, hypertension and progression of CKD is accumulating. Therefore, we studied the association between baseline uric acid (UA) levels and the rate of decline in renal function and time until start of dialysis in pre-dialysis patients.MethodsData from the PREPARE-2 study were used. The PREPARE-2 study is an observational prospective cohort study including incident pre-dialysis patients with CKD stages IV-V in the years between 2004 and 2011. Patients were followed for a median of 14.9 months until start of dialysis, kidney transplantation, death, or censoring. Main outcomes were the change in the rate of decline in renal function (measured as estimated glomerular filtration rate (eGFR)) estimated using linear mixed models, and time until start of dialysis estimated using Cox proportional hazards models.ResultsIn this analysis 131 patients were included with a baseline UA level (mean (standard deviation (SD)) of 8.0 (1.79) mg/dl) and a mean decline in renal function of -1.61 (95% confidence interval (CI), -2.01; -1.22) ml/min/1.73 m2/year. The change in decline in GFR associated with a unit increase in UA at baseline was -0.14 (95% CI -0.61;0.33, p = 0.55) ml/min/1.73 m2/year. Adjusted for demography, comorbidities, diet, body mass index (BMI), blood pressure, lipids, proteinuria, diuretic and/or allopurinol usage the change in decline in eGFR did not change. The hazard ratio (HR) for starting dialysis for each mg/dl increase in UA at baseline was 1.08 (95% CI, 0.94;1.24, p = 0.27). After adjustment for the same confounders the HR became significant at 1.26 (95% CI, 1.06;1.49, p = 0.01), indicating an earlier start of dialysis with higher levels of UA.ConclusionAlthough high UA levels are not associated with an accelerated decline in renal function, a high serum UA level in incident pre-dialysis patient is a risk factor for an earlier start of dialysis.
Highlights
IntroductionEvidence that hyperuricemia might play a causal role in vascular disease, hypertension and progression of chronic kidney disease (CKD) is accumulating
In patients with chronic kidney disease (CKD) hyperuricemia is common
Uric acid and decline in renal function Previous animal studies have shown that uric acid (UA) can lead to glomerular hypertension, elevated renal vascular resistance, reduced renal blood flow [26,27,28], activation of renin-angiotensin system (RAS), arteriolosclerosis, glomerular hypertrophy, glomerulosclerosis, and interstitial disease [29,30] by inducing oxidative stress and endothelial dysfunction indicating that UA could contribute to renal damage
Summary
Evidence that hyperuricemia might play a causal role in vascular disease, hypertension and progression of CKD is accumulating. Hyperuricemia is common in patients with chronic kidney disease (CKD) and evidence that hyperuricemia may play a causal role in hypertension, vascular disease and progression of CKD is accumulating [1,2,3,4,5,6,7,8,9]. The association between UA and decline in renal function has been investigated in several studies which included healthy individuals [12,13], patients with CKD stages I-II [14,15], patients with diabetes [6], and patients on peritoneal dialysis [16] Evidence about this association in patients with advanced CKD (stages IV-V) is scarce, and the effect on time until start of dialysis has not been addressed . We hypothesize that UA in these patients is associated with accelerated decline in renal function and an earlier start of dialysis
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