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Until recently, basophils and mast cells were considered mainly effector cells with an innate immune response linked to allergy and parasite infection. Only in the past few years they were recognized as important regulators of adaptive immunity. The development of new methods and reagents has enabled detection and functional analysis of these rare cells in patients and murine disease models. Basophils are normally present in the peripheral blood, spleen, and bone marrow, but migrate into lymph nodes and tissues during inflammation. They are rapidly activated by cytokines (e.g., interleukin (IL)-3) and intact antigens that cross-link surface-bound immunoglobulins. Activated basophils change the phenotype of T cells toward Th2 and markedly support humoral memory responses. Mast cells also migrate into lymph nodes and interact with dendritic cells, T cells, and B cells. In this review, we describe how mast cells and basophils affect immune responses and discuss implications for renal diseases and transplant rejection. [ABSTRACT FROM AUTHOR]

Evaluates the contribution of dialyzer membranes on the induction of apoptosis in human neutrophils. Adverse reactions associated with hemodialysis; Factors influencing apoptosis of peripheral nucleated cells in uremia; Effects of the complement factors C3 and C5 serum on the rate of apoptosis.

Examines the role of alphabeta and gammadelta cells in glomerulonephritis (GN) pathogenesis. Influence of cellular immune mechanisms in GN; Importance of sensitized nephritogenic T cells in inflammatory renal lesions amplification; Effector steps of cellular immunity in GN.

Presents a letter to the editor about data published on the prevention of radiocontrast-induced nephropathy by N-acetylcysteine.

Patients with advanced chronic kidney disease should be vaccinated against hepatitis B. In observational studies vitamin D insufficiency is associated with a reduced seroconversion rate. The effect of cholecalciferol supplementation on hepatitis B vaccination response in haemodialysis patients with vitamin D insufficiency is unknown. In this randomized open label pilot study 40 unvaccinated haemodialysis patients with 25(OH)D insufficiency (<30 ng/mL) were enrolled. In the supplementation group, we administered cholecalciferol orally in a dose of 28,000 IU weekly for a maximum of 12 weeks. Hepatitis B vaccination (HBvaxPRO 40 µg i.m. months 0, 1, 6) was performed after achieving a 25(OH)D level >30 ng/mL or after completing three months of supplementation despite failure to achieve the target level. In the control group, patients were vaccinated immediately after randomization. Anti-hepatitis B-antibody titer (anti-HBs) was measured eight weeks after completing the vaccination course. Thirty-seven (26 male, 11 female) patients aged 65 (13.5) years underwent randomization with 17 patients allocated to the control group and 20 patients included in the supplementation group. After 12 weeks of cholecalciferol supplementation, mean (SD) 25(OH)D concentration increased from 15.0 (8.0) to 31.0 (7.1) ng/mL, but remained unchanged in the control group (14.0 (7.1) to 11.6 (7.5) mg/mL). Neither the number of patients with seroconversion (anti-HBs titer ≥ 10 IU/L; n = 6 (35.3%) vs n = 3 (27.3%), p = 0.704), nor the number of patients with seroprotection (anti-HBs titer >100 IU/L; n = 4 (23.5%) vs n = 2 (18.2%) differed between treatment groups. Cholecalciferol supplementation was safe without treatment-related adverse events. In this small pilot study, high-dose oral cholecalciferol supplementation did not improve the hepatitis B vaccination response in haemodialysis patients with vitamin D insufficiency. This clinical trial was registered within EudraCT (EudraCT number 2011-004621-26). [ABSTRACT FROM AUTHOR]

All patients with advanced chronic kidney disease or on renal replacement therapy should receive active hepatitis B vaccination. The aim of this retrospective cohort study was to investigate the association between the immune response to hepatitis B vaccination and all-cause, cardiovascular or infection-related mortality in incident dialysis patients starting dialysis between 2001 and 2008 (n = 426) in two Austrian dialysis centers. Vaccination response was defined as follows: absent anti-HBs antibody titer or a titer <10 IU/L was classified as non-response, seroconversion (SC) was defined as a titer ⩾10 IU/L, and seroprotection (SP) as a titer ⩾100 IU/L. Kaplan-Meier survival curves and multivariable adjusted Cox Proportional Hazards Models were used to determine the association between vaccination response and all-cause, cardiovascular and infection-related mortality. Of all patients 207 (48.6%) were non-responders, SC was observed in 219 (51.4%), SP in 118 (27.7%) patients. During a median follow-up of 51.2 months 228 (53.5%) patients died. Patients with SP and SC showed a significantly lower all-cause (p < 0.001 for both) and cardiovascular mortality (p = 0.006 for SP, p = 0.01 for SC). SP and SC were independently associated with a significant risk reduction for all-cause mortality (SP: HR 0.69, 95% CI 0.49–0.97, p = 0.03; SC: HR 0.72, 95% CI 0.55–0.95, p = 0.02). In conclusion, achieving seroconversion and seroprotection after active hepatitis B vaccination is associated with significantly reduced all-cause mortality in incident dialysis patients. This simple and readily available tool allows estimation of patient survival independently of other well-known key parameters such as age, gender, the presence of diabetes and markers of malnutrition and inflammation. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor about the treatment of glomerulonephritis by antigen-specific therapy and double-stranded DNA molecules.

Statins mediate many of their protective effects by lowering lipids as well as by modulating inflammation. Here, we studied their potential immunomodulatory role in renal inflammation using an autoimmune mouse model of anti-glomerular basement membrane glomerulonephritis. Oral treatment with Atorvastatin dramatically reduced albuminuria and histological changes in the kidneys as compared to vehicle-treated control animals. There was a significant decrease in the Th1 and Th17 response in the regional lymph nodes draining the kidneys. This systemic effect was accompanied by decreased infiltration of the kidneys with inflammatory CD4+ T and Th17 cells, macrophages, and neutrophils in statin-treated mice. Regulatory T cells were not altered in their number, FoxP3 expression, or suppressive capacity, but their interleukin-10 production was significantly increased by statin treatment. Hence, Atorvastatin systemically and locally decreased the Th1 and Th17 response, thereby protecting the mice against anti-glomerular basement membrane glomerulonephritis. Whether statins can be used to treat human autoimmune renal diseases will require more direct studies. [ABSTRACT FROM AUTHOR]