Search

The timing of the first episode of peritonitis in peritoneal dialysis (PD) might have some special characteristics and may depend on many factors such as a patient's attitudes, age, comorbidity, or training capacity. It may also have a significant impact on further peritonitis episodes and technique failure. We retrospectively analyzed data for 168 PD patients who were undergoing continuous ambulatory PD by a twin-bag system, automated PD, or in-center intermittent PD over 12 years. There were 121 cases of peritonitis recorded in 60 patients, with an overall peritonitis rate of 1 episode per 45.75 patient-months. The mean time to the first episode of peritonitis after commencement of PD was 26.4 +/- 22 months (range: 1-110 months). In 20 patients, a first peritonitis episode presented rather early--during the first 12 months on PD (group A)--and in 27 patients, a first episode presented rather late-after at least 24 months on PD (group B). Group A had lower technique survival (30.4 +/- 26.5 months), were more prone to further episodes of peritonitis during follow-up, and had a total peritonitis rate of 1 episode per 14.85 patient-months. In group B, technique survival was longer (69.3 +/- 33.8 months), and the total peritonitis rate was 1 episode per 45.68 patient-months. We observed no differences between the two groups in comorbidity, age, or PD modality. These results indicate that patients with early-onset peritonitis are prone to making mistakes during connection, resulting usually in infection with gram-positive pathogens. These patients may present repeated peritonitis episodes and experience decreased technique survival.

Metabolic acidosis correction is one of the goals of renal replacement therapy. Correction of acidosis in peritoneal dialysis (PD) may be affected by PD modalities such as automated PD (APD) or by new solutions containing a combination of bicarbonate and lactate as a buffer [bicarbonate continuous ambulatory PD (CAPD)]. The aim of the present study was to examine the acid-base status of our PD population and to compare the effects of APD, lactate CAPD, and bicarbonate CAPD on serum bicarbonate levels. We studied 35 stable patients undergoing APD (n = 15), lactate-buffered (35 mEq/L) CAPD (n = 14), and bicarbonate/lactate-buffered CAPD (n = 6) for 48.5 +/- 38.1 months. Most of our patients had serum bicarbonate levels in the normal range. In 3 patients (8%), HCO3 was below 22 mEq/L, and in 8 patients (22%; APD = 2, lactate CAPD = 2, bicarbonate CAPD = 4), HCO3 was above 28 mEq/L. We found no statistically significant correlations between HCO3 serum levels and PD prescription, peritoneal membrane characteristics, or intake of calcium carbonate and sevelamer hydrochloride. Patients on bicarbonate CAPD had higher HCO3 serum levels, but this difference disappeared when corrections for duration of dialysis, residual urine volume, and PD adequacy indices were applied. In the studied PD population, adequate correction of metabolic acidosis was achieved, as reflected in serum bicarbonate levels. We observed no difference in serum bicarbonate levels between APD and lactate CAPD patients. The new bicarbonate-buffered PD solutions are more biocompatible and can result in higher serum bicarbonate levels. However, a significant number of PD patients on bicarbonate-buffered solutions may become alkalotic. The clinical significance of these results needs further examination in prospective studies.