Peritoneal dialysis (PD) related infections continue to be a serious complication for PD patients. Peritonitis can be associated with pain, hospitalization and catheter loss as well as a risk of death. Peritonitis risk is not evenly spread across the PD population or programs. Very low rates of peritonitis in a program are possible if close attention is paid to the causes of peritonitis and protocols implemented to reduce the risk of infection. Protocols to decrease infection risk in PD patients include proper catheter placement, exit-site care that includes Staphylococcus aureus prophylaxis, careful training of patients with periodic retraining, treatment of contamination, and prevention of procedure-related and fungal peritonitis. Extensive data have been published on the use of antibiotic prophylaxis to prevent exit site infections. There are fewer data on training methods of patients to prevent infection risk. Quality improvement programs with continuous monitoring of infections, both of the catheter exit site and peritonitis, are important to decrease the PD related infections in PD programs. Continuous review of every episode of infection to determine the root cause of the event should be routine in PD programs. Further research is needed examining approaches to decrease infection risk.

Studies with 1.75 mmol/L calcium dialysate have shown that patients gain calcium from dialysate. Thus, hypercalcemia, especially when calcium compounds are used for phosphate control, is a commonly seen complication. Dialysate with 1.25 mmol/L calcium has been available since 1989. Little is known about calcium mass transfer (CMT) with dialysate of this calcium concentration. CMT was measured in 20 stable adult peritoneal dialysis patients. Each CMT study consisted of a 2-L continuous ambulatory peritoneal dialysis (CAPD) exchange with a dwell time of 4 hours. CMT studies were performed using 1.25 and 1.75 mmol/L calcium dialysate with 1.5, 2.5, and 4.25 g/dL dextrose concentrations. CMT with 1.25 mmol/L calcium dialysate was compared to that with 1.75 mmol/L for each dextrose concentration. With a dextrose concentration of 1.5 g/dL, the mean CMT for 1.25 mmol/L calcium dialysate was —0.1 ± 0.3 mmol versus 0.6 ± 0.3 mmol for 1.75 mmol/L calcium dialysate (P < 0.0001). A dextrose concentration of 2.5 gl dL resulted in a mean CMT of —0.4 ± 0.2 mmol for 1.25 mmol/L calcium versus 0.45 ± 0.25 mmol for 1.75 mmol/L calcium (P < 0.0001). Using a dextrose concentration of 4.25 g/dL, the mean CMT was —0.7 ± 0.25 mmol for 1.25 mmol/L calcium versus —0.05 ± 0.35 mmol for 1.75 mmol/L calcium (P < 0.0001). Mean serum ionized calcium (SiCa) was between 1.15 and 1.20 mmol/L for all study groups. CMT inversely correlated with SiCa for each type of dialysate used. CMT was dependent on the concentrations of calcium and dextrose in the dialysate and the SiCa level at the time of the exchange. The use of 1.25 mmol/L calcium dialysate, which does not result in calcium gain to the patient, may prove to be useful in preventing hypercalcemia when peritoneal dialysis patients are using calcium salts as phosphate binders.

Polycythemia in CAPD patients has been rarely described. Over an eight year period, 4 out of 123 CAPD patients (3%) were identified as having Hct values exceeding 50% for 1 month or longer. All of the 4 patients were insulin dependent diabetics (4/47 diabetic patients, 8.5%). Charts were reviewed on 3 of these 4 patients. Polycythemia developed after a mean of 21 +/- 7 months on peritoneal dialysis. Prior to the development of polycythemia, ferritin levels were low and ferrous sulfate therapy was begun at a time the Hct values were 36 to 40%. Erythropoietin levels were obtained in 2 patients, and were 22 U/L (Hct 51%) and less than 5 U/L (Hct 55%). Renal ultrasound failed to show renal masses or cysts. One patient had a plasma volume of 2.1 L (normal 2.4-3.2 L); another patient was clinically volume depleted. Complications during the period of polycythemia included gangrenous feet requiring amputation in 2 patients, CVA in 2 patients, and splenic infarct in 1 patient. One patient died of cerebral thrombosis. We conclude that polycythemia is uncommon in CAPD patients and occurs most often in diabetic patients. Volume depletion and iron therapy may play a role in its etiology. In this high risk group of patients polycythemia may contribute to vascular complications and should be avoided.