 Patients on renal replacement therapy exhibit an increased cardiovascular mortality 10-30 fold higher than in the general population associated with accelerated vascular calcification. The KIDNEY DISEASE IMPROVING GLOBAL OUTCOMES KDIGO-work group introduced the term CKD-Mineral and Bone Disorder CKD-MBD which describes a clinical syndrome encompassing mineral, bone, and calcific cardio-vascular abnormalities that develop as a complication of CKD. This syndrome emerges as a result of a declining kidney function and is characterized by changes of circulating levels of parathyroid hormone PTH, 25-hydroxyvitamin D 25OHD,1,25-dihydroxyvitamin D 1,25OH2D, other vitamin D metabolites and fibroblast growth factor-23 FGF-23. The ability of the failing kidneys to excrete phosphate is diminished and hyperphosphatemia occurs. High phosphate levels together with calcium as well as low concentrations of fetuin A, the main calcification inhibitor under physiological conditions, lead to increased vascular and extravascular calcification and renal bone disease. Another important calcification inhibitor is the vitamin K2-dependent matrix Gla-protein MGP. Dialysis patients exhibit a low vitamin K intake and suffer substantially from vitamin K deficiency. Insufficient vitamin K intake leads to the production of non-carboxylated, inactive MGP and deficiency of carboxylated MGP may contribute substantially to the development and progression of arterial calcification. Bacterial infection and sepsis, although decreasing over the last decades, also account for up to 20 of deaths in ESRD-patients and are the second most common cause of mortality and hospitalization. Mortality due to sepsis is 100 - 300 times higher in dialysis patients as compared to the general population. The mechanisms of the increased susceptibility to infection are unclear but recent studies suggest that in patients with ESRD, innate immune response is defective. One reason for defective innate immunity might lie in an increased risk for endotoxemia. Hemodialysis HD-induced regional splanchnic ischemia leads to increased gut permeability and consecutive endotoxin translocation. This possibly results in alterations in gut microbiome composition. 