Efficacy and safety of body weight-adapted oral cholecalciferol substitution in dialysis patients with vitamin D deficiency.

BACKGROUND: Vitamin D deficiency is highly prevalent in dialysis patients. Whether substitution of native vitamin D in these patients is beneficial is a matter of ongoing discussion, as is the optimal dosing schedule. The purpose of this study was to investigate the efficacy and safety of a body-weight adapted oral dosing regimen of cholecalciferol in dialysis patients. METHODS: In a prospective single-center study 56 prevalent dialysis patients with a baseline 25OHD3 level <20 ng/mL received 100 IU of cholecalciferol per kg body weight once weekly orally for 26 weeks. 25OHD3 was measured at baseline and at study end, iPTH every three months, serum calcium and phosphorous monthly. Concurrent medication including phosphate binders, calcitriol and cinacalcet and dialysate calcium concentration remained unchanged throughout the study. RESULTS: Baseline 25OHD3 was 9.9 ± 4.1 ng/mL and increased to 26.1 ± 8.8 ng/mL (P = 0.01). Fourteen patients (27 %) achieved a level > 30 ng/mL and all others above 20 ng/mL. Cinacalcet therapy was positively associated with the increase in 25OHD3 (P = 0.024). The plasma iPTH level significantly decreased from median 362 pg/mL to 297 pg/mL (P = 0.01). This decline was more pronounced in patients with higher baseline iPTH levels (P < 0.01) and differed significantly dependent on concurrent calcitriol therapy. A significant iPTH decrease was observed in patients receiving calcitriol (P = 0.031). Serum calcium and phosphorous did not change significantly throughout the study period. Cholecalciferol substitution was well tolerated without adverse effects. CONCLUSION: The dosing regimen of oral cholecalciferol supplementation with 100 IU per kg body weight per week for 26 weeks in dialysis patients with vitamin D deficiency causes a significant increase in 25OHD3 close to the supposed target level of 30 ng/mL and a significant reduction in iPTH, without affecting serum calcium or phosphorous levels.

Exit-site care in Austrian peritoneal dialysis centers -- a nationwide survey.

BACKGROUND: Catheter-associated infections markedly contribute to treatment failure in peritoneal dialysis (PD) patients. There is much controversy surrounding prophylactic strategies to prevent these infections. METHODS: In this nationwide multicenter study we analyzed strategies to prevent catheter-associated infections as performed in Austrian PD centers in 2006. A questionnaire was sent to all 23 PD centers in Austria. RESULTS: Ten different catheter models were used in the 332 patients being treated in the 23 Austrian PD centers. Systemic antibiotics prior to catheter placement were given by 17 of the 23 PD centers (glycopeptides, n = 7; cephalosporins, n = 10). Nasal swabs were taken preoperatively by 17 PD centers; nasal Staphylococcus aureus carriers were treated prophylactically with mupirocin cream in 15 of these centers. Dressing change was routinely performed in 318 of 332 chronic PD patients (nonocclusive film dressing, n = 58; gauze dressing, n = 260). Disinfectants for chronic exit-site care included povidone iodine (n = 155), sodium hypochlorite (n = 31), povidone iodine + sodium hypochlorite together (n = 102), and octenidine dihydrochloride/phenoxyethanol (n = 17). Water + non-disinfectant soap or 0.9% sodium chloride was administered as a cleansing agent to the exit site by 27 patients. Routine S. aureus screening (nasal and/or exit-site swabs) in chronic PD patients was performed in 12 PD centers; carriers were treated with mupirocin cream in 11 of these centers. Dialysis staff members were screened for S. aureus in 8 PD centers and spouses were screened for S. aureus in 5 PD centers. The overall exit-site infection rate was 1 episode/43.9 patient-months, tunnel infection rate was 1 episode/88.9 patient-months, and peritonitis rate was 1 episode/51.0 patient-months. Patients of centers that have installed a prophylaxis protocol for treating S. aureus carriers had lower mean infection rates compared with those not using such a protocol. CONCLUSION: Various individual prophylactic strategies are used to prevent catheter-associated infections in Austrian PD centers. Infection rates are within the range reported in the literature. There is still scope for improvement in some centers (e.g., by establishing a prophylaxis protocol).

Prevalence and progression of peripheral arterial calcifications in patients with ESRD.

BACKGROUND: Peripheral arterial calcifications are seen frequently in patients with end-stage renal disease (ESRD). However, prevalence and progression, as well as contributing factors, never were investigated in an unselected incident cohort of dialysis patients. METHODS: We investigated 155 patients with ESRD at the beginning of dialysis therapy and followed them up prospectively during the first year of either hemodialysis (n = 106) or peritoneal dialysis treatment (n = 49). The prevalence and progression of arterial calcifications during the first year were graded by a single radiologist on standardized plain radiographs of the pelvis and calves. Findings were analyzed in relation to sex, age, diabetes mellitus, dialysis modality, total and high-density lipoprotein cholesterol levels, lipoprotein(a) (Lp[a]) level, apolipoprotein(a) kringle-IV repeat polymorphism, calcium level, phosphorus level, intact parathyroid hormone level, and homocysteine level. RESULTS: Patients with peripheral arterial calcifications at the start of renal replacement therapy (RRT) (n = 104) were significantly older (P < 0.001), had diabetes more often (P < 0.001), and had greater Lp(a) concentrations (P = 0.03) and a trend to greater total cholesterol concentrations. Patients with progression of calcifications during the first year of RRT had significantly greater homocysteine levels (P = 0.036). Logistic regression analysis showed that patients without calcifications either at the beginning or after 1 year of RRT were younger (P = 0.01) and had significantly lower homocysteine (P = 0.004) and Lp(a) levels (P = 0.03) and less frequently had diabetes mellitus (P = 0.04). CONCLUSION: Our observations suggest that the prevalence of peripheral arterial calcifications in patients with ESRD is related to age, diabetes mellitus, and Lp(a) and homocysteine levels. Progression of arterial calcifications might be related to high plasma homocysteine concentrations.