Cytomegalovirus (CMV) is the most common viral infection after transplantation. Valganciclovir (VGC) is established for prophylaxis and treatment of CMV infections, but leukopenia which appears in 10% to 13% (severe in 4.9%) is the principal side effect. We have recently noted an increased incidence of leukopenia and severe neutropenia among our renal transplant patients and thought to identify the associated factors. We conducted a retrospective analysis of all kidney transplantations performed between January 2005 and December 2006. All patients received mycophenolate mofetil (MMF), tacrolimus, and steroids. VGC was used for targeted prophylaxis and preemptive therapy of CMV infection, with doses adjusted to renal function. Of the 64 patients undergoing renal transplantation 13 (20.3%) developed leukopenia within 3 Ϯ 2 months after transplantation with severe neutropenia in 5 (7.8%). All patients were on MMF and VGC (VGC 605 Ϯ 296 mg/d). Leukopenia was significantly associated with simultaneous liver-kidney transplantation and with second kidney transplantations (P Ͻ .01). The incidence of leukopenia was higher among patients under VGC since day 1 of transplantation (P ϭ .008) with maximal incidence observed among patients prescribed 900 mg/d as opposed to those on lower doses (P Ͻ .01). There was no increase in CMV infection among patients with a low dose of VGC. No patient developed clinical CMV disease. In conclusion, VGC prophylaxis was associated with an increased frequency of leukopenia on MMF-tacrolimus treated patients or regimens. Low-dose VGC for CMV prophylaxis appeared to be as effective as high-dose treatment, and associated less frequently with leukopenia and neutropenia. C YTOMEGALOVIRUS (CMV) is a major cause of morbidity and mortality among solid organ transplant recipients.1 Among recipients of kidney transplants, CMV infection and disease are associated with decreased allograft and patient survivals.2 Risk factors for CMV infection and disease include donor (D) and recipient (R) serostatus, with donor-seropositive, recipient-seronegative (Dϩ/RϪ) as well as administration of antilymphocyte antibodies. Valganciclovir (VGC) is an L-valyl ester of ganciclovir with an oral bioavailability 10 times higher than oral ganciclovir, with the convenience of a once-daily oral dosing regimen. 4 It was recently reported that among Dϩ/RϪ patients, 900 mg/d of VGC was as clinically effective as 3 g/d of oral ganciclovir to prevent CMV.5 Several studies have reported that low-dose (450 mg/d) VGC is as effective as oral ganciclovir for CMV prophylaxis.6 -9 Present guidelines recommend 900 mg/d for CMV prophylaxis. 10Leukopenia has been the main side effect of VGC. A recent study showed that full VGC doses are associated with an important risk for neutropenia (12.5%), in conjunction with a cyclosporine (CsA)/tacrolimus-mycophenolate mofetil (MMF)-based regimen.11 In our transplant unit, in the last years we have noticed a higher incidence of leukopenia among our patients, particularly upon the introduct...

Conversion from SRL to EVL in renal transplant recipients receiving a CNI-free immunosuppressive regimen can be performed safely with a low trough level range of EVL. We report for the first time a conversion factor between SRL and EVL.

The authors present a case of urinary infection by a non-tuberculous mycobacteria (NTM) species, Mycobacterium gordonae, in a renal transplant recipient. A 29-year-old female patient had persistent sterile pyuria after her second kidney transplant. An NTM, M. gordonae, was isolated, and the patient was started on antituberculous treatment, with resolution of leukocyturia. Ureteral stenosis with hydronephrosis and deterioration of allograft function was diagnosed later on and, despite the introduction of intraureteral catheter and resolution of hydronephrosis, there was no recovery of baseline renal function. She ultimately resumed dialysis after a severe pyelonephritis. The authors discuss the problems of establishing diagnosis of infection (versus colonization) by NTM and highlight the difficulty of treating these infections, especially because of the possible interaction with immunosuppressant agents, facilitating anti-allograft immune response.

Herein we have described the case of a male renal transplant recipient who developed drug fever apparently related to sirolimus. He had been stable under an immunosuppressive regimen of tacrolimus and mycophenolate mofetil, but developed acute cellular rejection at 5 years after transplantation due to noncompliance. Renal biopsy showed marked interstitial fibrosis, and immunosuppression was switched from mycophenolate to sirolimus, maintaining low tacrolimus levels. One month later he was admitted to our hospital for investigation of intermittently high fever, fatigue, myalgias, and diarrhea. Physical examination was unremarkable and drug levels were not increased. Lactic dehydrogenase and C-reactive protein were increased. The blood cell count and chest radiographic findings were normal. After extensive cultures, he was started on broad-spectrum antibiotics. Inflammatory markers and fever worsened, but diarrhea resolved. All serologic and imaging tests excluded infection, immunemediated diseases, and malignancy. After 12 days antibiotics were stopped as no clinical improvement was achieved. Drug fever was suspected; sirolimus was replaced by mycophenolate mofetil. Fever and other symptoms disappeared after 24 hours; inflammatory markers normalized in a few days. After 1 month the patient was in good health with stable renal function. Although infrequent, the recognition of drug fever as a potential side effect of sirolimus may avoid unnecessary invasive diagnostic procedures. Nevertheless, exclusion of other common causes of fever is essential.

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