Abstract

P285 Aims: It has been proposed that proteinuria occurring after renal transplantation may be not only a marker but also a culprit of allograft dysfunction. However, it remains to be clarified whether the proteinuria promotes graft loss. This study was undertaken to elucidate the role of proteinuria in the outcome of renal transplants who required allograft biopsy during the long-term follow-up. Methods: We retrospectively analyzed the data from 56 patients who underwent transplant renal biopsy for proteinuria and/or azotemia occurring beyond 1 year after transplantation. Proteinuria was considered as significant when ≥ 30 mg/dL on dipstick, and the results of transplant renal biopsy were categorized as acute rejection (AR), chronic allograft nephropathy (CAN), cyclosporine nephrotoxicity (CN), recurrent or de novo glomerulonephritis (GN), and acute tubular necrosis (ATN) according to the Banff 97 classification. Logistic regression was used to estimate the relative risk (RR) of graft loss associated with proteinuria and renal pathology. Results: Recipients were 35.4 ± 9.9 (mean ± SD) years old at the time of transplantation, and 78.6% were male. The number of HLA mismatches was 4.6 ± 1.4. Donors were 43.1 ± 12.2 years old. Transplant renal biopsy was performed at 53.7 ± 30.7 months (range, 15 to 130 months) after transplantation, and thereafter the patients were followed up additionally for 87.7 ± 31.8 months (range, 30 to 155 months). Serum creatinine measured at the time of transplant renal biopsy was 3.4 ± 3.1 mg/dL. Graft loss occurred in 26 patients (46.4%) during the whole follow-up period. Proteinuria at 1 year after transplantation was noted in 27.0% of the patients, and it was not significantly associated with graft loss (RR=1.46, 95% CI 0.68-3.13). In addition, the presence of proteinuria at the time of transplant renal biopsy was not significantly associated with graft loss (RR=3.50, 95% CI 0.73-16.9), and none of each category (AR, CAN, CN, GN, and ATN) of the renal pathology was significantly associated with graft loss. Only the category of GN was significantly associated with the presence of proteinuria at the time of transplant renal biopsy (P<0.01). On the other hand, the presence of proteinuria at 1 year after transplant renal biopsy was significantly associated with graft loss (RR=11.0, 95% CI 1.42-85.2). In the last follow-up tests all patients with graft loss had proteinuria, whereas 51.7% (15/29) of the patients without graft loss revealed proteinuria (P<0.001). Conclusions: These results suggest that proteinuria after renal transplantation is an important marker of graft dysfunction but is not predictive of the risk of graft loss in biopsy-indicated cases. Appropriate management guided by the results of transplant renal biopsy may improve the outcome.

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