title: The prevalence of immunologic injury in renal allograft recipients with de novo proteinuria.
abstract: Post-transplant proteinuria is a common complication after renal transplantation; it is associated with reduced graft and recipient survival. However, the prevalence of histological causes has been reported with considerable variation. A clinico-pathological re-evaluation of post-transplant proteinuria is necessary, especially after dismissal of the term "chronic allograft nephropathy," which had been considered to be an important cause of proteinuria. Moreover, urinary protein can promote interstitial inflammation in native kidney, whether this occurs in renal allograft remains unknown. Factors that affect the graft outcome in patients with proteinuria also remain unclear. Here we collected 98 cases of renal allograft recipients who developed proteinuria after transplant, histological features were characterized using Banff scoring system. Cox proportional hazard regression models were used for graft survival predictors. We found that transplant glomerulopathy was the leading (40.8%) cause of post-transplant proteinuria. Immunological causes, including transplant glomerulopathy, acute rejection, and chronic rejection accounted for the majority of all pathological causes of proteinuria. Nevertheless, almost all patients that developed proteinuria had immunological lesions in the graft, especially for interstitial inflammation. Intraglomerular C3 deposition was unexpectedly correlated with the severity of proteinuria. Moreover, the severity of interstitial inflammation was an independent risk factor for graft loss, while high level of hemoglobin was a protective factor for graft survival. This study revealed a predominance of immunological parameters in renal allografts with post-transplant proteinuria. These parameters not only correlate with the severity of proteinuria, but also with the outcome of the graft.
authors.affiliation: Research Institute of Nephrology, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China. sunqiquan@hotmail.com
authors.forename: Qiquan
authors.initials: Q
authors.lastname: Sun
authors.forename: Song
authors.initials: S
authors.lastname: Jiang
authors.forename: Xue
authors.initials: X
authors.lastname: Li
authors.forename: Xianghua
authors.initials: X
authors.lastname: Huang
authors.forename: Kenan
authors.initials: K
authors.lastname: Xie
authors.forename: Dongrui
authors.initials: D
authors.lastname: Cheng
authors.forename: Jinsong
authors.initials: J
authors.lastname: Chen
authors.forename: Shuming
authors.initials: S
authors.lastname: Ji
authors.forename: Jiqiu
authors.initials: J
authors.lastname: Wen
authors.forename: Mingchao
authors.initials: M
authors.lastname: Zhang
authors.forename: Caihong
authors.initials: C
authors.lastname: Zeng
authors.forename: Zhihong
authors.initials: Z
authors.lastname: Liu
mesh_terms: D000293:Adolescent; D000328:Adult; D002681:China; D003176:Complement C3 / Q000378:metabolism*; D005260:Female; D006084:Graft Rejection / Q000276:immunology / Q000473:pathology; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D016030:Kidney Transplantation / Q000009:adverse effects* / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D016016:Proportional Hazards Models; D011507:Proteinuria / Q000209:etiology / Q000276:immunology / Q000473:pathology; D012307:Risk Factors; D014184:Transplantation, Homologous / Q000009:adverse effects* / Q000276:immunology / Q000473:pathology
chemical_list: D003176:Complement C3; D007074:Immunoglobulin G