Hyperuricemia and deterioration of renal function in autosomal dominant polycystic kidney disease
1 Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea
2 Research Coordination Center for Rare Diseases, Seoul National University Hospital, Seoul, Korea
3 Transplantation Research Institute, Seoul National University Medical Research Center, Seoul, Korea
4 Department of Medicine, Program of Immunology, The Graduate School, Seoul National University, Seoul, Korea
5 Department of Radiology, Seoul National University College of Medicine, Seoul, Korea
6 Kidney Research Institute, Medical Research Center, Seoul National University College of Medicine, Seoul, Korea
7 Department of Pediatrics and Adolescent Medicine, Seoul National University College of Medicine, Seoul, Korea
8 Department of Internal Medicine, Ewha Womans University School of Medicine, Ewha Medical Research Center, Seoul, Korea
9 Transplantation Center, Seoul National University Hospital, Seoul, Korea
10 Department of Internal Medicine, Eulji General Hospital, Eulji University, 14 Hangeulbiseong-ro, Nowon-gu, Seoul 139-872, Korea
11 Department of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-Ro Jongno-Gu, Seoul 110-744, Korea
BMC Nephrology 2014, 15:63 doi:10.1186/1471-2369-15-63Published: 16 April 2014
The role of hyperuricemia in disease progression of autosomal dominant polycystic kidney disease (ADPKD) has not been defined well. We investigated the association of serum uric acid (sUA) with renal function and the effect of hypouricemic treatment on the rate of renal function decline.
This is a single-center, retrospective, observational cohort study. A total of 365 patients with ADPKD who had estimated glomerular filtration rate (eGFR) ≥ 15 mL/min/1.73 m2 and who were followed up for > 1 year were included in our analysis. Hyperuricemia was defined by a sUA level of ≥ 7.0 mg/dL in male and ≥ 6.0 mg/dL in female or when hypouricemic medications were prescribed.
Hyperuricemia was associated with reduced initial eGFR, independent of age, sex, hypertension, albuminuria, and total kidney volume. During a median follow-up period of over 6 years, patients with hyperuricemia showed a faster annual decline in eGFR (−6.3% per year vs. −0.9% per year, p = 0.008). However, after adjusting for age, sex, hypertension and initial eGFR, sUA was no longer associated with either annual eGFR decline or the development of ESRD. Among 53 patients who received hypouricemic treatment, the annual eGFR decline appeared to be attenuated after hypouricemic treatment (pretreatment vs. posttreatment: −5.3 ± 8. 2 vs. 0.2 ± 6.2 mL/min/1.73 m2 per year, p = 0.001 by Wilcoxon signed-rank test).
Although hyperuricemia was associated with reduced eGFR, it was not an independent factor for renal progression in ADPKD. However, the correction of hyperuricemia may attenuate renal function decline in some patients with mild renal insufficiency.