Peritoneal protein losses in diabetic patients starting peritoneal dialysis: is there a relationship with diabetic vascular lesions?
Coronel, F.; Cigarrán, S.; Herrero, J.A.; Delgado, J.ús.; Ramos, F.; Gomis, A.
Advances in Peritoneal Dialysis. Conference on Peritoneal Dialysis 25: 115-118
2009
ISSN/ISBN: 1197-8554 PMID: 19886331 Document Number: 637698
During peritoneal dialysis (PD), a significant amount of protein is lost through the peritoneal membrane, and these losses could influence the patient's nutrition status. It has been reported that peritoneal protein loss (PPL) is greater in diabetic (D) patients than in nondiabetic (ND) patients, but the topic is still controversial, and the factors involved are not totally defined. We studied 23 patients on continuous ambulatory PD (12 with diabetes) who had experienced no episodes of infection during the preceding months. We measured peritoneal transport, PPL, proteinuria, and parameters of inflammation and nutrition. Our study was carried out during the first months of PD (2 - 4 months), which coincided with the first evaluation of peritoneal transport. The PPL was higher in D patients than in ND patients (8.4 +/- 2.2 g vs. 5.7 +/- 1.7 g daily, p < 0.001), as was proteinuria (3.7 +/- 2.7 g vs. 0.9 +/- 0.7 g daily, p = 0.003). In 83% of D patients and 54% of ND patients, peritoneal transport (p = 0.002) was high or high-average. Dialysate-to-plasma creatinine in D patients was 0.77 +/- 0.12 as compared with 0.66 +/- 0.09 in ND patients (p = 0.031). Parameters of nutrition and inflammation were normal in both groups of patients and showed no significant differences, except for serum total protein, which was significantly lower in D patients. Ultrafiltration, Kt/V, and weekly creatinine clearance were similar in both groups. The D patients with a higher PPL had the highest proteinuria values. We conclude that the higher PPL seen in D patients starting PD seems to be related to high membrane transport in these patients. The condition of high transport in D patients could be a result of diabetic microvascular lesions that cause a similar pattern of permeability in the peritoneal and glomerular membranes.