We examined the prevalence of vitamin D deficiency in hemodialysis patients and tested the hypothesis that decreased levels of 25-hydroxyvitamin D (25D) are associated with an increased risk for early all-cause mortality. One hundred and two patients, 57 (56%) men and 45 (44%) women, mean age 60.5 +/- 13.1 years, were included in our study. Serum calcium and phosphorus levels were measured by routine laboratory methods. Parathyroid hormone (PTH) was measured by immunoassay and 25D by enzyme immunoassay. Patients were divided into two groups depending on the serum concentration of 25D: below or above 50 nmol/L. Survival rates were analyzed using the Kaplan-Meier survival curves. The Cox regression model was used to define potential variables effecting all-cause mortality. The mean level of 25D in all patients was 58 +/- 35.6 nmol/L, 52% of patients had 25D levels >50 nmol/L and 48% had levels of 10.5-50 nmol/L. Compared with men, women were more likely to be 25D deficient (67% vs. 37%; P = 0.005). Patients were observed from the date of laboratory measurement until their death or to a maximum of 730 days. Kaplan-Meier survival analysis showed that mortality in patients was significantly higher in the group with 25D levels < or =50 nmol/L (P < 0.033). With Cox multivariable regression modeling, the PTH level (P < 0.029) turned out to be the only predictor of mortality in our patients. Using the definitions recommended in the National Kidney Foundation Kidney Disease Outcomes Quality Initiative guidelines, we found that our hemodialysis patients on average have vitamin D insufficiency. Our results indicate that patients with 25D levels < or =50 nmol/L are associated with higher all-cause early mortality.

Chronic kidney disease-mineral and bone disease (CKD-MBD) is associated with uraemic bone disease, vascular calcification, reduced quality of life and reduced survival. This study evaluated the efficacy of parathyroidectomy (PTX) with autotransplantation in improving short-term and long-term outcomes. Dialysis patients who underwent PTX showed significantly more favourable biochemical parameters after PTX. These changes were accompanied by a lower coronary artery calcification score, reduced thickness of the intimae media and comparable bone mineral density measures compared with control dialysis patients who did not undergo PTX. Despite the risk of a substantially lower intact parathyroid hormone level postoperatively that might lead to adynamic bone disease, none of the patients reported clinical signs of this disease, such as bone pain or fractures. In conclusion, PTX with autotransplantation led to improvement of CKD-MBD so may be considered in patients with secondary hyperparathyroidism that is resistant to treatment with vitamin D analogues and calcimimetics.

We found no significant differences in total homocysteine concentrations between group A (thrombosis non-prone) and group B (thrombosis prone) patients. Our results suggest that thrombosis of native arteriovenous fistulas may not be caused by hyperhomocystinemia in these patients.

Vascular calcifications are very frequent extraosseous calcifications in patients with chronic renal disease. They occur in the intima and in the media. They are associated with decreased arterial elasticity and increased mortality. The risk factors are: advanced age, duration of dialysis treatment, diabetes, increased phosphate concentration, the dose of Ca-containing phosphate binders and inflammation. It is now well established that vascular smooth muscle cells actively take up phosphate to form bioapatite. This process is associated with a phenotypic transformation of vascular smooth muscle cells during which they express osteoblast markers. Lipids and inflammatory cytokines also increase bioapatite formation. Calcification inhibitors are matrix Gla protein and fetuin-A. Decreased serum fetuin-A concentration is associated with a higher mortality rate in dialysis patients. An important preventive measure for vascular calcification is the substitution of Ca-containing by non-Ca-containing phosphate binders.