Literature DB >> 30016775

Clinicopathological Characteristics, Role of Immunosuppressive Therapy and Progression in IgA Nephropathy with Hyperuricemia.

Yiping Ruan1,2, Fuyuan Hong1,2, Jiabin Wu1,2, Miao Lin1,2, Chen Wang3, Fayang Lian4, Fang Cao1,2, Guokai Yang1,2, Meizhu Gao1,2.   

Abstract

BACKGROUND/AIMS: The aim of the study was to investigate clinicopathological characteristics, the role of immunosuppressive therapy and renal outcome in IgA nephropathy (IgAN) patients with hyperuricemia.
METHODS: 206 biopsy-proven primary IgAN patients were included between January 2010 and December 2015, and divided into two groups: patients without hyperuricemia (n=122), and patients with hyperuricemia (n=84). The clinicopathological features, response, renal outcome and safety were recorded. In univariate and multivariate models, hyperuricemia-associated pathological factors were analyzed.
RESULTS: The patients with hyperuricemia presented higher systolic blood pressure, worse kidney function and more severe time-averaged proteinuria. Proportions of glomerulosclerosis, segmental glomerulosclerosis, tubular atrophy/interstitial fibrosis, lymphocytes and monocytes infiltration were higher, while the proportion of segmental adhesion was lower 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. For hyperuricemic patients, the response rate to therapy and renal survival rate were significantly higher in patients that received RAS blockade in combination with immunosuppressive therapy. After RAS blockade treatment, renal survival in the patients with hyperuricemia was worse compared with the patients without hyperuricemia.
CONCLUSION: Hyperuricemic IgAN patients presented more severe clinical features. Tubulointerstitial injury could be a pathological feature closely related to hyperuricemia in IgAN. Immunosuppressive therapy and RAS blockade could reduce proteinuria and improve renal outcome in IgAN patients with hyperuricemia.
© 2018 The Author(s). Published by S. Karger AG, Basel.

Entities:  

Keywords:  Characteristics; Hyperuricemia; IgA nephropathy; Outcome; Therapy

Mesh:

Substances:

Year:  2018        PMID: 30016775     DOI: 10.1159/000491809

Source DB:  PubMed          Journal:  Kidney Blood Press Res        ISSN: 1420-4096            Impact factor:   2.687


  5 in total

1.  Hyperuricemia aggravates the progression of IgA nephropathy.

Authors:  Yin-Hong Geng; Zhe Zhang; Jun-Jun Zhang; Bo Huang; Zui-Shuang Guo; Xu-Tong Wang; Lin-Qi Zhang; Song-Xia Quan; Rui-Min Hu; Ya-Fei Liu
Journal:  Int Urol Nephrol       Date:  2022-01-24       Impact factor: 2.266

2.  The role of hypertriglyceridemia and treatment patterns in the progression of IgA nephropathy with a high proportion of global glomerulosclerosis.

Authors:  Jiayi Wang; Lingyan He; Wenzhe Yan; Xiaofei Peng; Liyu He; Danyi Yang; Hong Liu; Youming Peng
Journal:  Int Urol Nephrol       Date:  2020-01-18       Impact factor: 2.370

3.  Hyperuricemia and hypertriglyceridemia indicate tubular atrophy/interstitial fibrosis in patients with IgA nephropathy and membranous nephropathy.

Authors:  Bingman Liu; Liangyu Zhao; Qingqing Yang; Dongqing Zha; Xiaoyun Si
Journal:  Int Urol Nephrol       Date:  2021-04-24       Impact factor: 2.370

4.  Clinicopathological characteristics and outcomes of anti-neutrophil cytoplasmic autoantibody-related renal vasculitis with hyperuricemia: a retrospective case-control study.

Authors:  Ruiqiang Wang; Dongyue An; Yunqi Wu; Pupu Ma; Yuanyuan Guo; Lin Tang
Journal:  Sci Rep       Date:  2021-01-21       Impact factor: 4.379

5.  Is hyperuricemia an independent prognostic factor for IgA nephropathy: a systematic review and meta-analysis of observational cohort studies.

Authors:  Kang Zhang; Long Tang; Shang-Shang Jiang; Yue-Fen Wang; Yuan Meng; Meng-di Wang; Fang-Qiang Cui; Zhen Cai; Wen-Jing Zhao
Journal:  Ren Fail       Date:  2022-12       Impact factor: 2.606

  5 in total

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