Renal Allograft Dysfunction During Acute Hemorrhagic Cystitis

H Kobayashi; K Tanabe; T Tokumoto; N Ishikawa; K Takahashi; T Yagisawa; H Toma; S Fuchinue; T Kawai and K Ota, Department of Urology and Surgery, Kidney Center, Tokyo Women's Medical College

Purpose: The purpose of this study is to clarify the relationship between graft dysfunction due to acute hemorrhagic cystitis (AHC) and acute rejection, and determine the appropriate management of these patients following renal transplantation.

Materials and Methods: We performed 1206 kidney transplants and 27 patients (2.2%) were diagnosed with AHC. All 27 patients were retrospectively reviewed.

Results: The average onset of AHC was 89.8 ± 78.6 days postoperatively. All patients had gross hematuria and irritative voiding symptom. 24 of the 27 patients studied had an elevated serum creatinine (S-Cr). The S-Cr levels of the patients rose from 1.3 ± 0.3 mg/dl (baseline S-Cr level before the onset of AHC) to 2.1 ± 0.8 mg/dl (maximum S-Cr level after the onset of AHC). 12 of 27 patients (Group 1) underwent methylplednisolone (MP) pulse therapy and 15 of 27 patients (Group 2) did not. Graft biopsies were performed in 7 patients in Group 1 and only one patient had histologically proven acute cellular rejection. Graft biopsies were also performed in 5 patients in Group 2, however, there was no evidence of histologically proven acute rejection. Of the 12 patients who underwent graft biopsy, only one patient (8%) had histologically proven acute cellular rejection. Maximum S-Cr levels were reached within 5 days after the onset of AHC. S-Cr levels started to decrease within 11 days and returned to baseline level within 4 weeks. There were no significant differences in the duration of graft dysfunction between Group 1 and Group 2. Although, Group 2 had a significantly shorter duration (9.9 ± 5.2 days) of clinical symptoms (hematuria and irritative voiding symptoms) than Group 1 (14.8 ± 7.0 days, p<0.01). There was no graft loss due to AHC, whereas three patients lost their graft due to causes unrelated to AHC (recurrent IgA nephropathy; 2 patients and acute rejection; 1 patient).

Conclusions: AHC is a self limiting disease and MP pulse therapy should be contraindicated without histological evidence of acute rejection. Elevated S-Cr levels in the presence of AHC was a common cause of graft dysfunction but was not related to biopsy proven acute rejection.