Frailty is a pronounced symptom of aging associated with multiple comorbid states and adverse outcomes. The aim of this study was to evaluate the impact of 2 interventions, one based on prevention of falls and the other on prevention of loneliness, on total frailty and dimensions of frailty in urban community-dwelling elderly as well as associations with independent living. This prospective interventional study followed up 410 persons aged 75 to 95. The participants of the control and intervention groups were monitored through a public health intervention programme. The level of frailty was measured by the Tilburg Frailty Indicator (TFI) questionnaire and the factors of independent living were analyzed using validated questionnaires. After 1 year, physical frailty measured in the control group showed a statistically significant increase (r = −0.11), while in the intervention groups physical frailty did not increase (both P > .05). Psychological frailty measured after 1 year in the control group was significantly higher (r = −0.19), as well as in the group where the public health interventions to reduce loneliness were carried out (r = −0.19). Psychological frailty did not increase in the group in which public health interventions to prevent falls were carried out, and social frailty did not increase at all in the study period. The total level of frailty in the control group after 1 year was significantly increased (r = −0.19), while no increase was seen in the overall frailty in the intervention group. Multivariate analysis has shown that both interventions where independently associated with lower end frailty. Additionally, higher baseline frailty and visit to a physician in the last year were positively associated with higher end-study frailty level, while higher number of subjects in the household and higher total psychological quality of life (SF-12) were independently associated with lower end-study frailty. Only in the prevention of falls group there was no increase in restriction in the activities of daily living throughout study follow-up. Public health interventions to prevent falls and to prevent loneliness have a positive effect on the frailty and independent living of the elderly living in their own homes in an urban community.

BK virus (BKV) is a polyomavirus with high seroprevalence in the general population with an unremarkable clinical presentation in healthy people, but a potential for causing serious complications in immunosuppressed transplanted patients. Reactivation or primary infection in kidney allograft recipients may lead to allograft dysfunction and subsequent loss. Currently, there is no widely accepted specific treatment for BKV infection and reduction of immunosuppressive therapy is the mainstay therapy. Given this and the sequential appearance of viruria-viremia-nephropathy, screening and early detection are of utmost importance. There are numerous risk factors associated with BKV infection including genetic factors, among them human leukocyte antigens (HLA) and killer cell immunoglobulin-like receptors (KIR) alleles have been shown to be the strongest so far. Identification of patients at risk for BKV infection would be useful in prevention or early action to reduce morbidity and progression to frank nephropathy. Assessment of risk involving HLA ligands and KIR genotyping of recipients in the pre-transplant or early post-transplant period might be useful in clinical practice. This review summarizes current knowledge of the association between HLA, KIR and BKV infection and potential future directions of research, which might lead to optimal utilization of these genetic markers.

Background: We have previously shown that metzincin protease ADAMTS-4 accompanies renal fibrogenesis, as it appears in the blood of hemodialysis patients. Methods: Native kidney (NKB) and kidney transplant (TXCI) biopsy samples as well as plasma from patients with various stages of CKD were compared to controls. In paired analysis, 15 TXCI samples were compared with their zero-time biopsies (TX0). Tissues were evaluated and scored (interstitial fibrosis and tubular atrophy (IFTA) for NKB and Banff ci for TXCI). Immunohistochemical (IHC) staining for ADAMTS-4 and BMP-1 was performed. Plasma ADAMTS-4 was detected using ELISA. Results: ADAMTS-4 IHC expression was significantly higher in interstitial compartment (INT) of NKB and TXCI group in peritubular capillaries (PTC) and interstitial stroma (INT). Patients with higher stages of interstitial fibrosis (ci > 1 and IFTA > 1) expressed ADAMTS-4 in INT more frequently in both groups (p = 0.005; p = 0.013; respectively). In paired comparison, TXCI samples expressed ADAMTS-4 in INT and PTC more often than TX0. ADAMTS-4 plasma concentration varied significantly across CKD stages, being highest in CKD 2 and 3 compared to other groups (p = 0.0064). Hemodialysis patients had higher concentrations of ADAMTS-4 compared to peritoneal dialysis (p < 0.00001). Conclusion: ADAMTS-4 might have a significant role in CKD as a potential novel diagnostic indicator.

The role of adiponectin in hypertension is still a matter of debate. Obtained conflicting results could be mostly explained with diversity of subjects included in different studies. Our aim was to analyze association of adiponectin with blood pressure (BP) in a group of normotensive and untreated hypertensive subjects. Participants (N = 257) were selected from a random sample of 2487 subjects enrolled in an observational cross-sectional study. Subjects with diabetes and chronic kidney diseases were excluded. BP was measured using Omron M6 device following ESH/ESC guidelines. Adiponectin concentration was determined by ELISA. There were no differences in adiponectin values (mg/L) between hypertensives and normotensives (median 9.75; iqr: 7.44-17.88 vs 11.35; iqr: 7.43-12.63; P = 0.17). On univariate linear regression adiponectin was not associated with systolic or diastolic BP (P > 0.05). Furthermore, multivariate analysis did not show significant contribution of log-transformed adiponectin either to systolic (beta = -0.040; P = 0.43) or diastolic BP (beta = 0.066; P = 0.33). In our group of normotensives and untreated hypertensives with normal kidney function adiponectin was not associated with BP even after adjustment for other risk factors. Our results and conclusions should not be extrapolated to subjects with other characteristics.