Vitamins in dialysis: who, when and how much?

Despite the significant technical evolution of the blood purification methods, cardiovascular morbidity and mortality in dialysis patients is still several times higher than that observed in the general population. Vitamins are playing a crucial role in multiple key metabolic pathways. Due to multiple factors, dialysis patients present very often hypo- or hypervitaminosis for a broad range of vitamins. Dialysis in the context of renal replacement therapy is associated with a non-physiological potassium-sparing dietetic regime. Additionally, there is a non-selective intradialytic loss of micro- and macronutrients, deranged intracellular kinetics and gastrointestinal malabsorption due to uratemia. Frequent treatment with antibiotics due to infections associated with the acquired uremia-related immunosuppression may derange the vitamin-producing intestinal microflora. Certain agents prescribed in the context of renal failure or other conditions may reduce the absorption of vitamins from the gastrointestinal tract. These factors may deplete a dialysis patient from vitamins, especially the ones with antioxidant activity that may be associated with cardioprotective properties. In other cases, vitamins metabolized and excreted by the kidneys may be accumulated and exert toxic effects. The scope of this paper is to describe the main issues on vitamin therapy in dialysis patients in view of the ever contradictory opinions and practices.

Increased soluble Flt-1 correlates with delayed graft function and early loss of peritubular capillaries in the kidney graft.

BACKGROUND: Ischemia-reperfusion induces tubular and endothelial damage in the renal graft and leads to delayed graft function (DGF) and to an early loss of peritubular capillaries (PTC). Few, if any, clinical studies have assessed the impact of proangiogenic and antiangiogenic factors on endothelial repair during renal transplantation (RT)-related ischemia-reperfusion. METHODS: We prospectively assessed the kinetics of the antiangiogenic factor soluble Fms-like tyrosine kinase-1 (sFlt-1) in 136 consecutive RT patients and analyzed sFlt-1 impact on DGF and PTC loss. RESULTS: sFlt-1 plasma levels increased by twofold to threefold throughout the first week after RT. This increase was more marked in recipients of grafts from deceased donors compared with living donors. Patients with DGF had higher sFlt-1 levels at all time points during the first 7 days after RT and a higher peak sFlt-1 compared with those without DGF. In multivariate analysis, a peak plasma sFlt-1 of 250 pg/mL or higher was associated with 2.5-fold increase in the risk of DGF (P=0.04). Similarly, patients with a peak plasma sFlt-1 of 250 pg/mL or higher had a more pronounced early decrease in PTC compared with those with a peak sFlt-1 less than 250 pg/mL. CONCLUSIONS: sFlt-1 is a new nonimmunologic independent risk factor for DGF and PTC loss. Its inhibition may help improve the outcome of RT.

Pulmonary hypertension in dialysis patients.

Pulmonary hypertension in end-stage renal disease patients is associated with significantly increased morbidity and mortality. The prevalence of pulmonary hypertension in dialysis patients is relatively high and varies in different studies from 17% to 49.53% depending on the mode of dialysis and other selection factors, such as the presence of other cardiovascular comorbidities. The etiopathogenic mechanisms that have been studied in relatively small studies mainly include arteriovenous fistula-induced increased cardiac output, which cannot be accomodated by, the spacious under normal conditions pulmonary circulation. Additionally, pulmonary vessels show signs of endothelial dysfunction, dysregulation of vascular tone due to an imbalance in vasoactive substances, and local as well as systemic inflammation. It is also believed that microbubbles escaping from the dialysis circuit can trigger vasoconstriction and vascular sclerosis. The non-specific therapeutic options that proved to be beneficial in pulmonary artery pressure reduction are endothelin inhibitors, phosphodiesterase inhibitor sildenafil, and vasodilatory prostaglandins in various forms. The specific modes of treatment are renal transplantation, size reduction or closure of high-flow arteriovenous fistulas, and transfer from hemodialysis to peritoneal dialysis-a modality that is associated with a lesser prevalence of pulmonary hypertension.