Hyponatremia is a surrogate marker of poor outcome in peritoneal dialysis-related peritonitis.

BACKGROUND: Hyponatremia is known to be a marker of poor prognosis in many clinical conditions. The association between hyponatremia and clinical outcomes in peritoneal dialysis-related peritonitis (PDRP) has not been studied. We evaluated the association between hyponatremia and clinical parameters of patients with PDRP. METHODS: We conducted a retrospective analysis of medical records of patients with PDRP admitted to a medical center in the period 2004-2011. Patients with serum Na+ <130 mEq/L and ≥ 130 mEq/L at admission were divided into hyponatremic and normonatremic groups, respectively. The demographic and laboratory characteristics, pathogens of peritonitis, length of hospital stay and mortality rate were analyzed. RESULTS: Hyponatremia occurred in 27% (27/99) patients with PDRP. Gram-negative bacilli were the major pathogen responsible for 78% (21/27) PDRP in hyponatremic group while gram-positive cocci were found in 75% (41/55) PDRP in normonatremic groups. There was no significant difference in age, duration of dialysis, PD catheter removal rate and technique failure between two groups. Hyponatremic group had significantly higher serum CRP (p <0.001), lower serum albumin (p < 0.001) and phosphate (p < 0.05). Of note, serum Na+ level was positively correlated with serum albumin (p < 0.001), phosphate (p < 0.04) levels, and subjective global assessment (SGA) score (p < 0.001). Moreover, the length of hospital stay was longer and in-hospital mortality rate was higher in hyponatremic group (p < 0.001). Using a multivariable logistic regression, we showed that hyponatremia at admission is an independent predictor of in-hospital mortality (OR 76.89 95% CI 3.39-1741.67, p < 0.05) and long hospital stay (OR 5.37, 95% CI 1.58- 18.19, p < 0.05). CONCLUSIONS: In uremic patients with PDRP, hyponatremia at admission associated with a high frequency of gram negative bacilli infection, low serum albumin and phosphate levels, low SGA score, and poor prognosis with long hospital stay and high mortality rate.

Serum fetuin-A levels increased following parathyroidectomy in uremic hyperparathyroidism.

BACKGROUND: Both fetuin-A and hyperparathyroidism play crucial roles in vascular calcification (VC) and bone metabolism. However, the correlation between secondary hyperparathyroidism (SHPT), parathyroidectomy (PTX) and fetuin-A levels in dialysis patients has not yet been studied. METHODS: For this study, we included 27 consecutive dialysis patients with severe SHPT who underwent total PTX with autotransplantation over a period of 2 years (from Oct 2006 to Sep 2008). Serum ionized calcium (iCa), phosphorus (Pi), bone-specific alkaline phosphatase (bAP), intact parathyroid hormone (iPTH), and fetuin-A were checked basally and 2, 7, 14, 30, and 60 days after PTX. RESULTS: Two days after PTX, the iPTH, serum iCa, and Pi concentrations significantly decreased. Serum bAP levels gradually increased after PTX, peaked after 14 days (p < 0.05), and then gradually decreased. Serum fetuin-A levels significantly increased during the first 7 days after PTX, peaked 14 days after PTX (0.21 ± 0.05 vs. 0.35 ± 0.07 mg/ml, p < 0.05), and then remained at a stable level 60 days after PTX. There were significant correlations between percentage increase in serum fetuin-A levels and percentage decrease in serum iPTH levels 2 days and 7 days after PTX (r = 0.526, p < 0.01; r = 0.403, p < 0.05, respectively) and correlations between percentage increase in serum fetuin-A levels and percentage decrease in serum iCa levels 30 and 60 days after PTX (r = 0.449, p < 0.05; r = 0.474, p < 0.05, respectively). CONCLUSIONS: Serum fetuin-A significantly increased after PTX in uremic patients with SHPT. The percentage increase in serum fetuin-A after PTX was closely correlated with the percentage decrease in serum iPTH levels immediately after PTX, and with the percentage decrease in serum iCa levels in the later stage after PTX. Further investigations are necessary to further understand the regulation of fetuin-A in dialysis patients with sSHPT.