In a retrospective study from Japan, researchers report an association between asymptomatic hyperuricemia and decline in estimated glomerular filtration (eGFR) in patients with highly dysfunctional ATP-binding cassette subfamily G member 2 (ABCG2). “This new finding highlights the potential importance of ABCG2 in the pathogenesis of hyperuricemia-induced kidney injury,” the authors conclude.
Data from 1,885 Japanese adults seen for routine healthcare follow-up in 2007–17 were analyzed using linear mixed-effects models. All had eGFR ≥60 mL/min/1.73 m2 at baseline, and 311 patients had asymptomatic hyperuricemia with serum uric acid concentrations (SUAs) in the elevated range (>7.0 mg/dL).
“Asymptomatic hyperuricemia was negligibly associated with eGFR decline overall,” the authors report. “However, among those with eGFR 60-89 mL/min/1.73 m2 and ≤50% ABCG2 function, eGFR decline was associated with asymptomatic hyperuricemia (P = 0.03). ABCG2 was not associated with eGFR reductions when the SUA was <6.0 mg/dL. Among participants with SUA ≥6.0 mg/dL and eGFR 60-89 mL/min/1.73 m2, ≤50% ABCG2 function was associated with approximately 1.2-fold faster eGFR decline compared with fully functional ABCG2 (P = 0.02). Among the participants with SUA ≥6.0 mg/dL and eGFR 60-89 mL/min/1.73 m2, the adjusted eGFR slopes (given as mean ± standard error of the mean, in mL/min/1.73 m2 per year) were −0.946 ± 0.049, −1.040 ± 0.046, and −1.148 ± 0.069 for full, 75%, and ≤50% ABCG2 function, respectively.”