immunoglobulin a nephropathy ( igan ) is the most common primary glomerulonephritis , characterized by dominant or co - dominant diffuse mesangial deposition of iga . progression to end - stage renal disease ( esrd ) occurs in 3050% of patients after 25 years of follow - up . the incidence of posttransplant recurrence of igan varied between 20% and 60% at 5 years follow - up in various studies . we describe here a young male who developed crescentic igan in two consecutive renal transplantation . he had not received induction immunosuppression and his maintenance immunosuppression included prednisolone , mycophenolate mofetil , and cyclosporine . after a year of normal graft function allograft biopsy revealed crescentic glomerulonephritis with crescents [ figure 1 ] in four out of eight glomeruli and 3 + mesangial deposits of iga . there was a rapid loss of graft function , and he became dialysis dependent within few months and he was on maintenance hemodialysis for next 2 years . renal biopsy of first allograft showing cellular crescents ( h and e , 40 ) in 2012 , he received a second renal transplant from a deceased donor in our institution . although anti - thymocyte globulin ( atg ) was the preferred induction agent , we could not give due to logistic reason , and he received two doses of basiliximab . graft function remained stable over the next 3 years with a serum creatinine of 1.3 mg / dl . three years after the second transplant , he presented with macroscopic hematuria , nephrotic proteinuria ( urine protein creatinine ratio : 5.1 ) and severe graft dysfunction ( serum creatinine 5.2 mg / dl ) . serological tests for antinuclear antibody and anti - neutrophil cytoplasmic antibodies were negative . graft biopsy revealed crescents in nine out of 16 glomeruli [ figure 2 ] . immunofluorescence showed 3 + positivity for iga [ figure 3 ] in the mesangium consistent with the diagnosis of crescentic igan . he was given pulse methyl prednisolone ( 1 g  3 doses ) and his serum creatinine declined to 2.4 mg / dl . renal biopsy of second allograft showing cellular crescents ( pas , 40 ) immunofluorescence showing intense staining of immunoglobulin a deposits this case exemplifies the rare phenomenon of igan recurrence as crescentic glomerulonephritis in two successive renal allografts , one from a living related donor and the other a cadaveric donor . even though , native kidney biopsy had not been done in our patient , history of macrohematuria during childhood the incidence of posttransplant recurrence of igan varied between 20% and 60% at 5 years follow - up in various studies . the variation in incidence may be related to differences in indications for allograft biopsy in different centers . the predictors for recurrence of igan after transplantation are crescentic glomerulonephritis in native kidney , rapid progression of original disease , younger age at transplantation , zero human leukocyte antigen ( hla ) mismatch and use of <3 immunosuppressive medications . recurrence of igan has declined progressively from 1980 to 2010 , probably due to the use of more potent immunosuppressives . in an analysis of 116 cadaveric donor renal transplant recipients , 10 years cumulative recurrence rate of igan was 9% in those who had received atg induction , whereas it was 41% in the patients who had not received atg . in a study of 487 patients with igan in the indian subcontinent , the renal survival rate was 84 , 55 and 33% at 1 , 5 and 10 years , respectively . moroni et al . have reported a recurrence rate of 22% and graft loss of 8.4% in a 10 years follow - up study of 190 renal transplant recipients . if previous graft loss had been due to recurrent igan , the risk of subsequent graft loss rose to 25% . the presence of hla b8 and dr3 in the recipient is associated with 66% increased the risk of graft loss due to recurrent igan . posttransplant crescentic igan portends a poor graft survival . in a study by kowalewska et al . , de novo or recurrent igan was detected in 10 out of 48 patients with crescents in posttransplant graft biopsy . of them , nine patients progressed to end - stage renal failure at 3 years . posttransplant recurrent crescentic igan has been treated with different regimens including pulse steroids , plasmapheresis followed by high - dose oral steroids and cyclophosphamide . one each from a living related donor and a cadaveric donor . the second graft could be salvaged with intensive immunosuppressants . to the best of our knowledge , there has not been a similar scenario reported in literature .
we report a 21-year - old male who developed end - stage renal disease , probably due to immunoglobulin a nephropathy ( igan ) , received a renal transplant from his mother , which was lost due to crescentic igan after 18 months . 
 two years later , he received a second transplant from a deceased donor . 
 he developed rapidly progressive graft dysfunction 3 years later . 
 allograft biopsy revealed crescentic igan , which was successfully treated with intravenous steroids and cyclophosphamide . 
 recurrence of igan in two successive allografts in one patient has not been reported previously .