Abstract

Background and objectives: In kidney transplant recipients (KTR), hyperuricemia (HU) is a commonly-observed phenomenon, due to calcineurin inhibitors and reduced kidney graft function. Factors predicting HU, and its association with graft function, remains equivocal. Materials and Methods: We conducted a retrospective longitudinal study to assess factors associated with HU in KTR, and to determine risk factors associated with graft function, measured as glomerular filtration rate (GFR). Moreover, GFR > 60 mL/min/1.73 m2 was considered normal. HU was defined as a serum uric acid level of > 416 μmol/L (4.70 mg/dL) in men and >357 μmol/L (4.04 mg/dL) in women, or xanthine-oxidase inhibitor use. We built multiple logistic regression models to assess predictors of HU in KTR, as well as the association of demographic, clinical, and biochemical parameters of patients with normal GFR after a three-year follow-up. We investigated the effect modification of this association with HU. Results: There were 144 patients (mean age 46.6 ± 13.9), with 42.4% of them having HU. Predictors of HU in KTR were the presence of cystic diseases (OR = 9.68 (3.13; 29.9)), the use of diuretics (OR = 4.23 (1.51; 11.9)), and the male gender (OR = 2.45 (1.07; 5.56)). Being a younger age, of female gender, with a normal BMI, and the absence of diuretic medications increased the possibility of normal GFR. HU was the effect modifier of the association between demographic, clinical, and biochemical factors and a normal GFR. Conclusions: Factors associated with HU in KTR: Presence of cystic diseases, diuretic use, and male gender. HU was the effect modifier of the association of demographic, clinical, and biochemical factors to GFR.

Highlights

  • Hyperuricemia (HU) is associated with clinical consequences when saturating concentrations result in symptomatic urate or uric acid crystal deposition—gout, acute or chronic uric acid nephropathy, and urolithiasis [1], which makes it more complicated to assess the role of asymptomatic HU in the development and progression of chronic kidney disease; the main route for elimination of uric acid (UA) is via the kidneys

  • Groups with and without HU differed on dyslipidemia and the presence of cystic diseases, use of ACE inhibitors/angiotensin receptor blockers, and use of diuretics (Table 1)

  • Factors associated with HU in kidney transplant recipients (KTR) were presence of cystic diseases, use of diuretics, and male gender

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Summary

Introduction

Hyperuricemia (HU) is associated with clinical consequences when saturating concentrations result in symptomatic urate or uric acid crystal deposition—gout, acute or chronic uric acid nephropathy, and urolithiasis [1], which makes it more complicated to assess the role of asymptomatic HU in the development and progression of chronic kidney disease; the main route for elimination of uric acid (UA) is via the kidneys. The association of HU and chronic kidney disease remains unclear: Different studies investigating the Medicina 2020, 56, 95; doi:10.3390/medicina56030095 www.mdpi.com/journal/medicina. HU can induce oxidative stress and endothelial dysfunction, resulting in the development of systemic and glomerular hypertension; this can lead to reduced renal blood flow and gradual decline in kidney function [3,10].

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