title: IgA nephropathy in kidney allograft recipients-therapeutic perspective.
abstract: BACKGROUND
  A growing number of patients are losing their kidney allografts due to glomerulonephritis. Although posttransplant IgA nephropathy (IgAN) is regarded as benign, it may lead to late allograft loss in a substantial number of patients. The aim of this study was to evaluate the influence of posttransplant IgAN on long-term transplantation outcomes, risk factors for progression of graft dysfunction, and effectiveness of therapeutic interventions.
  
  
  METHODS
  We evaluated, potential risk factors for accelerated graft loss among 27 kidney allograft recipients with posttransplant IgAN, comparing graft survival in a control group matched for population and transplantation-related parameters. We evaluated the effectiveness of therapeutic interventions regarding immunosuppressive regimen, and hypertension control including angiotensin converting enzyme inhibitor (ACEI) usage with Kaplan-Meier, Cox proportional hazard plots, and log-rank tests in statistical analyses.
  
  
  RESULTS
  Compared with the control group, patients with IgAN experienced a 6.57 higher risk for dialysis dependence (P < .01, 95% CI 1.4 to 30.83). The risk for accelerated graft loss in the course of IgAN was associated with graft dysfunction (RR = 2.16 for additional 1 mg/dL of serum creatinine at glomerulonephritis presentation; P < .03, 95% CI 1.2 to 4.36) and intense proteinuria as evidenced by a RR = 4.67 for the presence of the nephrotic syndrome (P < .05, 95% CI 0.95 to 22.8). Immunosuppression enhancement resulted in a significantly decreased risk of dialysis dependence, namely, RR = 4.76 (95% CI 1.12 to 20, P < .04). With ACEI treatment there was a tendency for a 2.8-fold decreased risk of dialysis dependence, without reaching statistical significance (P = .14).
  
  
  CONCLUSIONS
  Patients with posttransplant IgAN may benefit from intensifying maintenance immunosuppression, which slows progression to end-stage graft dysfunction.
authors.affiliation: Transplantation Institute, Department of Transplant Medicine and Nephrology, Warsaw Medical University, Nowogrodzka 59, 02-006 Warsaw, Poland. jpazik@poczta.fm
authors.forename: J
authors.initials: J
authors.lastname: Pazik
authors.forename: T
authors.initials: T
authors.lastname: Baczkowska
authors.forename: Z
authors.initials: Z
authors.lastname: Lewandowski
authors.forename: D
authors.initials: D
authors.lastname: Lewandowska
authors.forename: J
authors.initials: J
authors.lastname: Ostrowska
authors.forename: A
authors.initials: A
authors.lastname: Perkowska Ptasińska
authors.forename: A
authors.initials: A
authors.lastname: Mróz
authors.forename: D
authors.initials: D
authors.lastname: Miszewska-Szyszkowska
authors.forename: W
authors.initials: W
authors.lastname: Rowinski
authors.forename: M
authors.initials: M
authors.lastname: Durlik
mesh_terms: D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D018450:Disease Progression; D005260:Female; D005922:Glomerulonephritis, IGA / Q000453:epidemiology* / Q000517:prevention & control / Q000628:therapy*; D006650:Histocompatibility Testing; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D016030:Kidney Transplantation / Q000276:immunology* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000453:epidemiology; D011507:Proteinuria / Q000209:etiology; D012307:Risk Factors; D014184:Transplantation, Homologous
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D007166:Immunosuppressive Agents