Background and objectives: Nearly 30% of renal transplant recipients develops BK viremia, a prerequisite for BK nephropathy. Case reports have evaluated treatment options for BK virus, but no controlled studies have assessed prophylactic therapies. Fluoroquinolone antibiotics were studied for prevention of BK viremia after renal transplantation.Design, setting, participants, & measurements: This retrospective analysis evaluated adult renal transplant recipients with at least one BK viral load (blood) between 90 and 400 days after transplantation. Six to 12 months of co-trimoxazole was used for Pneumocystis prophylaxis. In sulfa-allergic/-intolerant patients, 6 to 12 months of atovaquone with 1 month of a fluoroquinolone was used. Fluoroquinolones can inhibit BK DNA topoisomerase. The two groups studied were those that received 30 days of levofloxacin or ciprofloxacin after transplantation and those that did not. The primary endpoint was BK viremia rates at 1 year. Of note, of the 160 patients not receiving fluoroquinolone prophylaxis, 40 received a fluoroquinolone for treatment of a bacterial infection within 3 months after transplantation. Subgroup analysis evaluating these 40 patients against the 120 who had no exposure to fluoroquinolones was completed.Results: A 1-month fluoroquinolone course after transplantation was associated with significantly lower rates of BK viremia at 1 year compared with those with no fluoroquinolone. In the subgroup analysis, exposure to fluoroquinolone for treatment of bacterial infections within 3 months after transplantation was associated with significantly lower 1-year rates of BK viremia.Conclusions: This analysis demonstrates that fluoroquinolones are effective at preventing BK viremia after renal transplantation.

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Background-Allograft vasculopathy is a major limiting factor in the long-term success of cardiac transplantation. T cells play a critical role in initiation of cardiac allograft rejection and allograft vasculopathy. The negative T-cell costimulatory pathway PD-1:PDL1/PDL2 (programmed death-1:programmed death ligand-1/2) plays an important role in regulating alloimmune responses. We investigated the role of recipient versus donor PD-1 ligands in the pathogenesis of allograft rejection with emphasis on the role of tissue expression in regulating this alloimmune response in vivo. Methods and Results-We used established major histocompatibility complex class II-and class I-mismatched models of vascularized cardiac allograft rejection, blocking anti-PDL1 and anti-PDL2 antibodies, and PDL1-and PDL2-deficient mice (as donors or recipients) to study the role of the PD-1:PDL1/PDL2 pathway in chronic rejection. We also used PDL1-deficient and wild-type mice and bone marrow transplantation to generate chimeric animals that express PDL1 exclusively on either hematopoietic or parenchymal cells. PDL1 but not PDL2 blockade significantly accelerated cardiac allograft rejection in the bm12-into-B6 and B6-into-bm12 models. Although wild-type cardiac allografts survived long term, PDL1 Ϫ/Ϫ donor hearts transplanted into wild-type bm12 mice exhibited accelerated rejection and vasculopathy associated with enhanced recipient T-cell alloreactivity. Interestingly, PDL1Ϫ/Ϫ recipients did not exhibit an accelerated tempo of cardiac allograft rejection. Using chimeric animals as donors, we show that PDL1 expression on cardiac tissue alone significantly prolonged graft survival compared with full PDL1 Ϫ/Ϫ donor grafts in transplanted wild-type recipients. Conclusions-This is the first report to demonstrate that expression of the negative costimulatory molecule PDL1 on donor cardiac tissue regulates recipient alloimmune responses, allograft rejection, and vasculopathy. (Circulation. 2008;117: 660-669.)

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Taken together, these data suggest that in vivo-activated monocytes in peripheral blood spontaneously secrete proinflammatory cytokines in renal allograft recipients with transplant glomerulopathy and seem to be under the regulation of functional regulatory T cells in this setting.

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CASE PRESENTATIONA 53-year-old Caucasian lady was evaluated in our center as a potential kidney donor. She volunteered to donate a kidney to her brother with whom she shared a 6/6-antigen match. The exact etiology of her brother's end-stage renal disease (ESRD) could not be determined. On evaluation she was noted to be in good health and a review of systems was unremarkable. Family history was significant for functional pituitary tumor leading to acromegaly and diabetes in her father and renal cell carcinoma in her uncle. Physical examination revealed that she was overweight with a body mass index of 31.2 kg/m 2 . Her blood pressure was 120/68 mm Hg, her heart rate was 79 beats per minute and she was afebrile. The remainder of the systemic examination was unremarkable.A transplant donor workup was completed (Table 1). The pertinent abnormality was persistent microscopic hematuria with two out of three urine analyses positive for trace to 1 þ blood in dipstick and 1-4 red cells on microscopy. These urinalyses were performed on three separate occasions at least 1 month apart. Urine cultures were negative throughout. Gynecological examination, which included a papanicolaou (PAP) smear, was unremarkable.The differential diagnosis for the microhematuria was discussed with the patient. The patient was determined to be considered as a candidate for kidney donation and requested that we proceed to a percutaneous renal biopsy in order to definitively identify the cause of hematuria.