Metabolic acidosis in peritoneal dialysis patients: the role of residual renal function.

BACKGROUND

Metabolic acidosis (MA) is common in chronic renal insufficiency (CRI) patients, and its pattern changes as renal function deteriorates. Although the prevalence of acidosis in peritoneal dialysis has been reported to be rather high, the causes of it have not been well studied. The present study was performed to examine the prevalence of metabolic acidosis in our continuous ambulatory peritoneal dialysis (CAPD) patients and its possible causes.

METHODS

In this cross-sectional study, we analyzed data from patients who received maintenance CAPD in our hospital and had been on dialysis for at least one month. Patients' demographic features, medications, and intercurrent medical conditions were recorded. Data including blood biochemistry, dialysis adequacy, and nutrition were collected. A serum bicarbonate concentration of less than 23 mmol/l was defined as having acidosis. The normal value of the serum anion gap (AG) was defined as 12+/- 4 mmol/l.

RESULTS

A total of 154 patients (76 males and 78 females) with age of 60.04+/- 13.92 years and the time on dialysis of 16.83+/- 21.59 months were included in this study. Sixty-six patients (43%) had a serum bicarbonate of less than 23 mmol/l, among whom 12 patients (8%) were identified as having MA with increased AG, 54 (35%) were identified as having MA with normal AG. Patients who had better residual renal function (RRF) had a significantly lower serum bicarbonate level despite their higher total KT/V(urea) as compared to those with lower RRF. In addition, patients with MA and normal AG had the highest RRF and highest total KT/V(urea). All patients with MA and increased AG had significantly lower values of dietary protein intake (DPI) as compared to their values of normalized protein nitrogen appearance (nPNA), and had higher serum urea and phosphate levels as compared with those patients without MA.

CONCLUSION

Our study suggested that CAPD patients with better RRF were more susceptible to metabolic acidosis, which was characterized by normal anion gap and hyperchloremia. Thus, we speculate that renal loss of bicarbonate may to a large extent be responsible for the occurrence of MA in these patients.