title: The fate of glomerular mesangial IgA deposition in the donated kidney after allograft transplantation.
abstract: OBJECTIVE
  To investigate the fate of the mesangial IgA deposits in the donor kidney after allograft transplantation.
  
  
  METHODS
  Routine pre-transplant cadaveric donor kidney biopsy and repeated renal biopsies were performed at months 1, 3, and 6 after renal transplantation. The patients, 342 in number, were divided into IgA positive deposition kidney group (group A, n = 83) and non-IgA deposition kidney group (group B, n = 259). There were no significant differences between the two groups' sex, age, time of hemodialysis, warm ischemia time, cold ischemia time, complement-dependent cytotoxicity, level of panel-reactive assay, and the distribution of original disease.
  
  
  RESULTS
  Recipients in group A received donor kidney with glomerular mesangial proliferation and marked diffuse granular IgA deposition. All of them showed edema, nephrotic range protienuria, microhematuria, hypoalbuminemia, hypertension, and delayed graft function. Borderline change was higher in group A than in group B, 37.3 and 16.2% (p < 0.001), respectively. Acute allograft rejection was higher in group A than in group B, 31.3 and 19.3% (p < 0.001), respectively. The glomerular mesangial IgA deposits gradually disappeared from the mesangial regions in grafts of acute rejection. Graft survival in both groups was not significant, being 93.8 and 95.6% in 1 yr, and 86.7 and 88.3% in 3 yr.
  
  
  CONCLUSIONS
  Clinical features of the recipients which received from donor kidney with glomerular mesangial proliferation and marked diffuse granular IgA deposition: edema, proteinuria, microhematuria, hypoalbuminemia, hypertension, and delayed graft function. The presence of IgA deposits on donated kidney, by a possible increase of the immunogenicity of these kidneys, might be a cause of increased rejection. There were no significant differences between the two groups on long-term allograft survival.
authors.affiliation: Research Institute of Nephrology, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China. jishuming@medmail.com.cn
authors.forename: Shuming
authors.initials: S
authors.lastname: Ji
authors.forename: Min
authors.initials: M
authors.lastname: Liu
authors.forename: Jinsong
authors.initials: J
authors.lastname: Chen
authors.forename: Liping
authors.initials: L
authors.lastname: Yin
authors.forename: Guozhu
authors.initials: G
authors.lastname: Sha
authors.forename: Huiping
authors.initials: H
authors.lastname: Chen
authors.forename: Zhihong
authors.initials: Z
authors.lastname: Liu
authors.forename: Leishi
authors.initials: L
authors.lastname: Li
mesh_terms: D000328:Adult; D000367:Age Factors; D002102:Cadaver; D003165:Complement System Proteins / Q000276:immunology; D003602:Cytotoxicity, Immunologic / Q000276:immunology; D004487:Edema / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D005920:Glomerular Mesangium / Q000276:immunology* / Q000473:pathology; D006084:Graft Rejection / Q000276:immunology / Q000473:pathology; D006085:Graft Survival; D006417:Hematuria / Q000473:pathology; D006801:Humans; D006973:Hypertension / Q000473:pathology; D034141:Hypoalbuminemia / Q000473:pathology; D007070:Immunoglobulin A / Q000032:analysis*; D016030:Kidney Transplantation / Q000276:immunology* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009401:Nephrosis / Q000473:pathology; D009926:Organ Preservation; D011507:Proteinuria / Q000473:pathology; D006435:Renal Dialysis; D012737:Sex Factors; D014184:Transplantation, Homologous
chemical_list: D007070:Immunoglobulin A; D003165:Complement System Proteins