INTRODUCTION: The renal vascular injury and consequent tubular/interstitial damage are account for the poor outcome of chronic kidney disease. In this study, we try to investigate if Endostatin, a potent inhibitor of angiogenesis, is associated with the tubular/interstitial damage, which is predictive for the prognosis, in patients with IgA Nephropathy (IgAN).

METHODS: Serum endostatin level was detected using commercial ELISA kits in 180 primary IgAN patients and 41 healthy controls. Oxford Classification score was evaluated by two pathologists, respectively, to renal biopsy of every patient. The data of Endostatin expression in renal interstitium of IgAN patients was downloaded from the array GSE35489, which included discovery cohort and validation cohort. All of the data was analysed by spss22.0.

RESULTS: Serum endostatin level was significantly increased in IgAN patients compared with healthy controls (61.71(53.42, 85.72) vs 54.69(52.23,69.03)ng/ml,p=0.032), as its expression in the renal interstitium in the mRNA array GSE35489 (IgAN vs HC: discovery cohort 7.78±0.36 vs 7.30±0.25, p=0.005; validation cohort 7.61±0.32 vs 7.18±0.17,p=0.003). IgAN patients were divided into two group according to the median data(61.71ng/ml), tubular/interstitial damage was more severe in the high serum endostatin group than the low serum endostatin group (T0/T1/T2: 41(45.55%)/15(16.67%)/34(37.78%) vs 58(64.45%)/10 (11.11%) /22(24.44%), p=0.039), Furthermore, patients with higher serum endostatin had a tendency of more arteriolar injury in the renal interstitium (68(75.56%) vs 56 (62.22%) , p=0.053)) and more endothelial cell proliferation in the glomerular (E1: 29(32.22%) vs 19(21.11%), p=0.092); Besides, we also found elevated serum endostatin was associated with serum creatinine (115(77,207) vs 82.50(63, 117) μmol/l, p=0.001) and serum BUN (7.39(5.18,11.45) vs 6.20(4.10, 8.60) μmol/l, p=0.024), as well as sex (male:59(65.56%) vs 45(50%), p=0.035)

CONCLUSIONS: Our study found elevated endostatin expression was associated with the tubular/interstitial damage in IgAN patients, as well as the more severe clinical states, which indicated its potential pathogenic role in IgAN.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://dbpia.nl.go.kr/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

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