Showing papers by "Anil Chandraker published in 2010"
TL;DR: A 1-month fluoroquinolone course after transplantation was associated with significantly lower rates of BK viremia at 1 year compared with those with no fluoroquolone.
Abstract: 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.
101 citations
TL;DR: This review presents animal models that have enabled investigation into chronic allograft injury and discusses pivotal models currently being used and the mechanisms uncovered will ultimately lead to development of new therapeutic options to prevent long-term graft dysfunction.
Abstract: Advances in immunosuppression have reduced the incidence of acute graft loss after transplantation, but long-term allograft survival is still hindered by the development of chronic allograft injury, a multifactorial process that involves both immunologic and nonimmunologic components. Because these components become defined in the clinical setting, development of animal models enables exploration into underlying mechanisms leading to long-term graft dysfunction. This review presents animal models that have enabled investigation into chronic allograft injury and discusses pivotal models currently being used. The mechanisms uncovered by these models will ultimately lead to development of new therapeutic options to prevent long-term graft dysfunction.
42 citations
TL;DR: To the Editor: In an article published in the Journal this past year, Ibrahim et al. provide important, much needed data about long-term outcomes of living kidney donors and generated death rates for participants in the National Health and Nutrition Evaluation.
Abstract: To the Editor: In an article published in the Journal this past year, Ibrahim et al. (Jan. 29, 2009, issue)1 provide important, much needed data about long-term outcomes of living kidney donors. For a comparison group, the investigators used rates of death in the general population, which included adults with coexisting medical conditions (e.g., heart and kidney disease) that would make them ineligible for kidney donation. However, it would be preferable to use as a comparison group persons with a greater similarity to living kidney donors. Therefore, we generated death rates for participants in the National Health and Nutrition Evaluation . . .
26 citations
TL;DR: Peripheral administration of r‐ATG is safe and can be infused without concomitant heparin and hydrocortisone and was shown to be as safe as peripherally administered basiliximab.
Abstract: Antithymocyte globulin rabbit (r-ATG) has been used for the treatment and prevention of acute rejection in renal transplant recipients (RTR). Current manufacturer recommendations for r-ATG dictate the need for administration through a high-flow vein (central line). Previous studies have shown peripheral administration of r-ATG to be safe; however, these studies suggest the co-administration of heparin and hydrocortisone and did not compare the infusion-site reaction rates to a control group. A retrospective analysis was conducted of adult RTR receiving r-ATG or basiliximab between January 2004 and October 2006. Each agent was administered through a dedicated peripheral line. The primary endpoint was the incidence of infusion-site reactions. Other endpoints included the need to replace the intravenous catheter and the incidence of systemic thrombosis within 1 month of transplantation. During the study period, 152 peripheral infusions of r-ATG and 92 peripheral infusions of basiliximab were administered. No difference in infusion-site reactions was noted between the groups. There was also no difference either in the need for peripheral line replacement or the rates of systemic thrombosis. Peripheral administration of r-ATG is safe and can be infused without concomitant heparin and hydrocortisone. This method of r-ATG infusion was shown to be as safe as peripherally administered basiliximab.
14 citations
01 Jan 2010