BK virus (BKV) infection represents a serious complication in renal transplant patients resulting in BKV-associated nephropathy and subsequent allograft loss. Natural killer cells are crucial in the antiviral immune response; however, an understanding of the role of natural killer cells in protection against BKV is limited. To elucidate whether killer-cell immunoglobulin-like receptors and their interaction between donor-/recipient-related ligands have a role in BKV infection, we performed genotyping analysis in 48 kidney transplant recipients with a history of severe BKV infection/BKV-associated nephropathy and 110 recipients with stable renal function and no BKV reactivation. Of interest, we found that telomeric gene content motif was significantly associated with severe course of BKV infection/BKV-associated nephropathy and detected significantly higher percentage of patients with BKV-associated nephropathy carrying low numbers of activating receptors compared with the control group. Detailed analysis of each single receptor revealed significantly lower frequencies of the activating receptor KIR3DS1 in patients with BKV infection/nephropathy as compared with the controls. Thus, our study supports protective effects of activating receptors in BKV infection and suggest natural killer-cell–related genetic predisposition to the development of BKV-associated nephropathy.

Source: Nature.

Hypertension is the primary risk factor for cardiovascular and renal-disease endpoints. Medications help many patients but not all. Recently, two device-related treatments have been introduced, catheter-based renal denervation and electrical carotid sinus stimulation. Remuneration for these treatments is guaranteed in many countries even though basic information is missing. We draw attention to deficiencies in the database. For catheter-based renal denervation, few large-animal data are available to investigate the effect of the intervention on the histology of the arterial wall. No functional data are available regarding re-innervation. For carotid sinus stimulation, the situation is similar. Acute activation of either treatment seems to reduce sympathetic tone dramatically. However, whether or not the effects are sustained over time is unknown. No ‘end-point’ data are available for either treatment. Devices should be subjected to evidence-based standards before widespread introduction.

Antineutrophil cytoplasm antibody (ANCA)–associated vasculitis (AAV) is a group of vasculitides characterized by small-to-medium-sized blood vessel vasculitis and the presence of ANCA. Although our understanding of the causes of AAV remains limited, new information supporting an autoimmune basis is emerging. This review highlights recent progresses in etiology, pathogenesis, classification, and treatment. A genome-wide association study has confirmed a role for genetic susceptibility in AAV, and links between environmental factors and AAV induction through abnormal neutrophil extracellular traps has been demonstrated. Ongoing international consensus initiatives have revised approaches to the classification of vasculitis that has been enhanced by the analysis of large-scale prospective clinical data sets. New autoantibodies to human lysosome–associated membrane protein-2 antibody, moesin, and plasminogen have been detected in AAV sera and a prognostic classification of renal biopsies developed. Clinical trial networks have extended the evidence base for the treatment of AAV, and rituximab has emerged as an alternative to cyclophosphamide for remission induction. Long-term outcomes following current treatment strategies have been determined and increased risks for cardiovascular and malignant disease reported.

Source: Nature.

Pneumocystis jirovecii is a unicellular organism that in individuals with impaired immunity may cause pneumonia that can progress from minor illness to severe inflammatory pneumonia (PCP) with respiratory failure and death. Despite antimicrobial prophylaxis, which has reduced the incidence of PCP, clusters of late infections have been reported among kidney transplant recipients worldwide. A nosocomial PCP cluster was first recognized in 2010 at a Sydney hospital, but PCP clusters have since occurred in almost half of the renal transplant units on the eastern Australian seaboard, refocussing attention on optimal prophylaxis regimens and the likelihood of patient-to-patient transmission. A consensus meeting was conducted to derive the lessons from this experience for responding to PCP outbreaks. These included: (1) acting quickly—clusters of PCP in kidney transplant recipients with patient-to-patient transmission required transplant programs to act quickly to institute prophylactic and treatment measures; (2) instituting universal prophylaxis for all patients seen in the affected unit; (3) reducing patient-to-patient transmission via airborne droplets in the outpatient waiting areas; (4) examining the P. jirovecii genotypes. The meeting also considered recommendations for the duration of prophylaxis following de novotransplant and, for the individuals in whom long term prophylaxis is required, separating units with and without clusters of PCP.

Source: Nature.