Abstract

P824 Although, polyoma virus infection was first reported in renal transplant recipients 30 years ago, there are still salient questions that have not been answered as to disease pathogenesis. Aim: The differential diagnosis of rejection has been difficult to dissociate from viral cytopathic effects in biopsy histology. The relationship between viral shedding in the urine and interstitial nephritis has also been unclear. The utility of the polymerase chain reaction (PCR) in amplifying minute amounts of viral DNA has distinct sensitivity advantages over other detection methods. Methods: In a preliminary report we demonstrated that when this virus was detected by PCR in the blood and plasma, there was a strong correlation with poorer graft function leading to failure. In the present more complete study during a period in which 419 kidney transplants were performed between June 30, 1999 to December 10, 2002. There were assays performed on 85 urine specimens, 141 blood specimens, from 21 renal transplant recipients. There were also 378 cadaver kidney (tissue) biopsies prospectively evaluated by PCR. Thirty recipient urine samples and 10 recipient blood samples that were PCR-positive were detected between 5 and 45 months post-transplant. None of the cadaver donor biopsies were positive. In a clinical correlation in seven patients demonstrating at least one urine and blood sample positive at the same time for polyoma by PCR, there was renal transplant biopsy-proven polyoma histochemical staining. Two of these seven lost their grafts and three have continued to elevate serum creatinine concentrations. Of the 378 PCR negative cadaver donors kidney biopsies from 211 donors that were tested between 2-10-01 and 1-1-03 resulted in 189 transplants. One of the recipients of the tested grafts has thus far been diagnosed with polyoma virus at another center, however 188 recipients at our center have been negative (between 6 months and 21 months post-operatively). Conclusion: The use of routine molecular testing and screening of renal transplant donor and recipient populations will ultimately result in a better understanding of the pathogenesis of polyoma virus infection in renal allografts.

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