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BK virus nephritis is an increasing problem and is posing a threat to improving renal transplant graft survival. The pathogenesis of this condition remains to be investigated. Higher prevalence of BK virus infection in recent years has been correlated with declining acute rejection rates and the use of potent immunosuppressive agents. Patients with this infection usually have asymptomatic viremia and/or nephritis with or without worsening of renal function. The diagnosis of this disease is based on detecting the virus or its effects in urine, blood, and renal tissue. In the past, approximately 30 to 60% of patients with BK virus nephritis developed graft failure. In recent years, the combination of early detection, prompt diagnosis, and therapies including preventive measures have resulted in better outcomes.Clin J Am Soc Nephrol 3: S68 -S75, 2008. doi: 10.2215/CJN.02770707 T he term "BK" originated from a patient's initials, in whom it was first detected in 1971 (1). The next observed case was published by investigators from the University of Pittsburgh in 1995 (2). Since then, there have been numerous reports on BK virus (BKV) infection and BKV nephritis (BKVN) in renal transplant recipients (3-8). The factors that lead to its higher incidence in recent years and its pathogenesis remain poorly understood. Increased awareness, the ability of clinicians to recognize this infection, and the availability of better diagnostic tools may be contributing to higher prevalence of this disease in recent years (9). The use of potent immunosuppressive combination therapy with mycophenolate mofetil (MMF) and tacrolimus has been thought to play a role in the occurrence of this infection (10 -12); however, this infection is also seen with cyclosporine and sirolimus therapy (13). Prevalence of BK viremia within 1 yr after transplantation is approximately 20% (6,14) and is higher than the prevalence of acute rejection of 13% reported for the year 2003 (15). This review discusses the pathogenesis, clinical features, therapy, and the short-and long-term renal graft survival with reference to BKV infection. Pathogenesis of BKV InfectionPotential factors that contribute to the pathogenesis of BKVN may be a combination of (1) ineffective immune surveillance by the host T lymphocytes, (2) the absence of previous humoral immunity to BKV, (3) molecular sequence variability of the virus, and (4) alloimmune activation. These details have been reviewed elsewhere (9) and are also discussed next.Cellular immunity in the development and clearance of BKV infection has remained an important area of research in the past several years. Comoli et al. (16) showed a reduction in BKVspecific IFN-␥-secreting lymphocytes in patients with BKVN compared with healthy control subjects. The authors noted an increase in patient IFN-␥-secreting lymphocyte levels with reduction in immunosuppressive therapy similar to that of their healthy counterparts (16). Prosser et al. (17) used an IFN-␥ enzyme-linked immunosorbent spot (ELISPOT) assay to measure cellula...

The efficient exit of HIV-1 particles from cells requires the action of the viral encoded protein Vpu. Vpu-binding protein (Ubp) is a cellular protein that interacts with both Vpu and the major structural component of the viral capsid (Gag) and appears to affect the efficiency of particle exit. Elucidation of the function of Ubp and characterization of the spatial distribution of Ubp may provide information pertinent to understanding the role of Ubp in virus replication. To investigate the subcellular location of Ubp, and to see whether Vpu affects the intracellular distribution of Gag, we carried out immunofluorescence localization in conjunction with confocal microscopy. Based on this analysis Ubp is present in both the nucleus and the cytoplasm. In the cytoplasm, Ubp appeared to be associated with microtubules as evidenced by cofluorescence with tubulin in the absence and in the presence of colchicine. However, cytoskeletal isolation and detergent extraction of cells resulted in association of Ubp with the soluble fractions, indicating that Ubp is not in tight association with microtubules. Moreover, flotation gradient analysis demonstrated that Ubp is cytoplasmic and not stably associated with the plasma membrane. Interestingly, expression of Vpu in cells resulted in redistribution of both Ubp and Gag to a location near the periphery of the cell. The effect of Vpu on both Ubp and Gag protein has implications for Vpu-mediated particle exit from cells.

Both NGAL and IL-18 are early predictive biomarkers of AKI, and both increase in tandem after surgical PVR. Importantly, both rise before an increase in creatinine or a decrease in eGFR is present. Monitoring both biomarkers may allow for earlier detection and subsequent interventions to prevent AKI at time of surgery for CHD.

Long-term survival after tetralogy of Fallot (TOF) repair is excellent. However, little is published regarding late noncardiac complications. This study aimed to determine the prevalence and risk factors for renal dysfunction among adults after TOF repair. For this study, 56 adult patients with complete repair of TOF were identified, and their charts were retrospectively reviewed. An estimated glomerular filtration rate (eGFR) for each patient was calculated using the Modification of Diet in Renal Disease formula (MDRD). Using each patient's eGFR, he or she was classified into stages based on the National Kidney Foundation chronic kidney disease (CKD) staging. Clinical parameters were compared among patients with and those without renal dysfunction to identify risk factors for renal impairment. The median estimated eGFR rate for the cohort was 78 ml/min/1.73 m(2). Based on the National Kidney Foundation CKD staging system, 54 % of the patients had at least stage 2 chronic renal disease. The risk factors identified were hypertension (p < 0.01), type 2 diabetes mellitus (p < 0.05), longer follow-up evaluation (p < 0.005), older age at complete repair (p < 0.05), and use of daily diuretics (p < 0.05). After repair of TOF, renal dysfunction is common at late follow-up evaluation. The study findings show the importance of routine assessment of renal function and the need to limit or avoid future episodes of acute kidney injury in this at-risk population.