Background: Although relationship between dialysate sodium concentration and hemodynamic stability has been well studied over the years, outcomes of absolute blood volume (ABV) maintenance and vascular refilling volume (V ref ) modifications were not included, as its analysis has not been easily accessible to direct investigation. However, recent studies report a simple and feasible methodology to assess ABV and V ref during hemodialysis (HD) treatments. It is the aim of this study to analyze whether sodium concentration in dialysate modifies ABV drop and V ref . Methods: The study was performed in 19 patients under HD. During three different sessions, sodium concentration in dialysate was randomized to three different profiles: low sodium concentration (LNa, 138 mEq/L), neutral sodium concentration (NNa, 140 mEq/L), and high sodium concentration (HNa, 143 mEq/L). ABV and V ref were calculated using Kron et al methodology. Results: Predialysis values of the measured parameters showed similar results for the three profiles. Sodium concentration showed an effect on ABV drop, V ref, and vascular refilling fraction (F ref ). Pair-wise comparison revealed mean ABV decreased 0.21 L less when using HNa profile versus LNa profile (p = 0.027), a mean V ref increase of 0.39 L (p = 0.038), and a mean F ref increase of 9.94% (p = 0.048). Conclusions: This study shows that the use of HNa profiles increases V ref and F ref and reduces ABV drop during dialysis treatments when compared to LNa profiles.

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), characterized by the presence of autoantibodies to neutrophil cytoplasmic antigens, proteinase 3 (PR3), and myeloperoxidase (MPO), typically involves small blood vessels of the respiratory tract and kidneys. It includes distinct clinical syndromes: microscopic polyangiitis (MPA), granulomatosis with polyangiitis (GPA), and eosinophilic GPA. GPA is commonly associated with PR3-ANCA, while MPA is associated with MPO-ANCA. AAVs have a complex pathogenesis, influenced by genetics and environmental factors. There is evidence for a loss of tolerance to neutrophil proteins, which leads to ANCA-mediated neutrophil activation and injury, with effector T cells and activation of the alternative pathway of the complement also involved. Advances in immunosuppressive treatment have drastically reduced mortality of AAV in the past decades, opting for a more individualized approach. Careful assessment of ANCA specificity, disease activity, organ damage, and quality of life allows for a tailored immunosuppressive therapy. Contemporary AAV treatment is characterized by regimens that minimize the cumulative exposure to glucocorticoids and cyclophosphamide, and novel approaches including complement blockage and immunosuppressant combinations might be the standard of care in the future. In this review, we examine the pathogenesis, clinical approach, and evidence-based treatment options for the management of AAV patients.