No clinical risk factors for recurrence of immunoglobulin A (IgA) nephropathy in kidney transplants have been defined. This is a single-centre retrospect analysis of recurrence in 104 first kidney transplant patients with biopsy-verified IgA nephropathy. Fifty patients had living donors. All but an identical twin were treated with cyclosporin A. The median follow-up time was 5 yr. Graft biopsies had been obtained from 35 grafts later than 6 months after transplantation, due to deteriorating graft function or gross proteinuria. Thirteen biopsies showed mesangial glomerulopathy proliferative in eleven cases with IgA deposits. Recurrence caused failure of six grafts. Eleven grafts with recurrence were from living donors (p = 0.005). No specific human leukocyte antigen (HLA) was identified as a risk factor. Known duration of original disease until end-stage renal failure was significantly shorter in patients with recurrence (median 5 yr, range 0-25 yr) compared with those without (median of 10 yr, range of 0-37 yr) (p = 0.015). Cumulative graft survival was not reduced in living versus cadaveric donor recipients.

The CAN grade is predictive of further graft survival independently of the serum creatinine level. Interstitial fibrosis and tubular atrophy are more prominent features of chronic graft damage than vascular rejection. Unspecific arterial wall thickening is partly dependent on baseline conditions and lacks prognostic impact in this late stage.

Aim: Morphologic risk factors for developing end-stage renal failure (ESRD) due to IgA nephropathy may be difficult to identify in populations where the course is benign in the vast majority. Ours is a high-risk population. Methods: Protocols of 67 biopsies from native kidneys of kidney transplant patients with IgA nephropathy were reevaluated with respect to the prevalence of certain structural findings. Time points for onset of symptoms, biopsy procedure, and ESRD were recorded. Results: Features seen with more than expected frequency were: extracapillary proliferation in 49%, cellular infiltrates in the interstitium in 89%, marked tubular atrophy in 54%, and IgA deposits in the peripheral capillary loops in 71%. With extracapillary proliferation the remaining time to ESRD was 3.5 ± 3.2 versus 7.0 ± 4.2 years without (p < 0.0004). With marked tubular atrophy the remaining time was 3.5 ± 2.7 and 8.2 ± 4.2 years without (p = 0.0002). Cellular infiltrates in the interstitium also signified shorter progression (p = 0.009). Except for the presence of IgA in the periphery, no finding by immune fluorescence was more frequent than expected or correlated with progression. Conclusion: Extracapillary proliferation, interstitial cellular infiltrates, marked tubular atrophy, and IgA deposits in the peripheral capillary loops indicate risk of progressive renal failure in IgA nephropathy, but other findings by immune fluorescence do not.

Rejection rates were not reduced in patients with IgA nephropathy and survival of grafts and patients not better than for matched controls.