Abstract
The aim of the study was to investigate clinicopathological characteristics, the role of immunosuppression and renal outcome in IgA nephropathy (IgAN) patients with hyperuricemia. We included 206 biopsy-proven primary IgAN patients between 2010 and 2015. The clinicopathological features, response to therapy, renal outcome and safety were recorded and analyzed. In univariate and multivariate models, hyperuricemia-associated pathological factors were analyzed. The patients with hyperuricemia presented higher systolic blood pressure, worse kidney function and more severe time-averaged proteinuria. Glomerulosclerosis, segmental glomerulosclerosis, tubular atrophy/interstitial fibrosis and interstitial inflammation were worse in patients with hyperuricemia. By multivariate logistic regression analysis, only tubular atrophy/interstitial fibrosis (T1~2) (HR=3.969, 95% CI=1.439−10.945, P=0.008) was significantly associated with hyperuricemia, which was similar for IgAN patients with chronic kidney disease stage 1~2. For hyperuricemic patients, the response rate to therapy and renal survival rate were significantly higher in patients that received RAS blockade in combination with immunosuppression. Hyperuricemic IgAN patients presented more severe clinical characteristics. Tubulointerstitial injury could be a pathological feature closely related to hyperuricemia in IgAN. Immunosuppression could reduce proteinuria and improve renal outcome in IgAN patients with hyperuricemia.
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