Pathogenic Effects of a High Peritoneal Transport Rate

Abstract

Recent studies have shown that patients with high peritoneal transport characteristics have substantially increased morbidity and mortality. This finding is counter-intuitive, since HTs will a priori achieve higher clearances. There are many possible causes: increased protein losses with consequent hypoalbuminemia; poor ultrafiltration capacity causing fluid retention, ventricular hypertrophy and hypertension; increased glucose absorption leading to anorexia, hyperinsulinism, and local AGE formation; and the development of an atherogenic lipid profile. While common pathogenic causes of high peritoneal transport and atherosclerosis have been hypothesized, it is more likely that CAPD as currently practiced is unsuitable for HTs, who should be switched to HD or NIPD. Renal and peritoneal clearances have different clinical effects and should be assessed separately. Current measures of dialysis adequacy, such as total Kt/V, do not therefore describe the patient's clinical situation accurately and are insufficient.

The Association between Interleukin 10 Gene Polymorphism -592 (A/C) and Peritoneal Transport in Patients Undergoing Peritoneal Dialysis

“…19 Therefore, the concept of chronic inflammation in influencing peritoneal transport rate had been proposed. 7 Previous study had demonstrated that the higher peritoneal transport rate status, regardless of before dialysis or with time after starting PD, was positively correlated with serum CRP level but had a reciprocal relationship with serum albumin levels, which both were as surrogate markers of inflammation. 20,21 Furthermore, Pecoits-Filho et al reported the plasma and dialysate IL-6 levels were significantly higher in patients with increasing peritoneal transport rate.…”

“…Despite pathogenic effects of high peritoneal transport status being documented, 7 the determinants on the peritoneal transport characteristics have not been well clarified. The clinical factors (e.g.…”

“…Assessing the individual variation in peritoneal transport is of major clinical importance because the results of PET prompt nephrologists to determine the dialysis prescription and provide the predictor of patient outcome about death and technique failure. Recent studies demonstrated the substantial association of high peritoneal transporter characteristics and increased mortality 2,3 and decreased technique survival 4–6 as a consequence of increased glucose absorption from peritoneum and inadequate dialysis, leading to suboptimal ultrafiltration capacities, fluid overload, increased protein losses and malnutrition, 7 and resulting in the usual cause of conventional PD patients switching to short‐dwell therapies (e.g. automatic PD) or hemodialysis.…”

High Peritoneal Transport Status is Not an Independent Risk Factor for High Mortality in Patients Treated with Automated Peritoneal Dialysis

“…Patients who have a greater rate of membrane solute transport are classified as high (or fast) transporters, and will tend to have enhanced clearance of small solutes, such as urea and creatinine, early in short dwells. However, these patients will have larger peritoneal loss of protein, will be more likely to fluid overload as a result of rapid reabsorption of glucose from the dialysate and subsequent ultrafiltration dysfunction, and will have greater systemic exposure to glucose (15-19). In addition, high transporters have been associated with poor nutritional status, more prevalent comorbid diseases, and chronic inflammation (3, 9-13).…”

Different patterns of inflammatory and angiogenic factors are associated with peritoneal small solute transport and peritoneal protein clearance in peritoneal dialysis patients

“…The most common functional alteration during long-term PD is increased peritoneal small-solute transport rate measured by dialysate-to-plasma (D/P) ratios or mass transfer area coefficients (MTAC) [ 3 , 4 ], which is the major contributor to impaired ultrafiltration and ultimately discontinuation of treatment [ 5 ]. It has been well appreciated that high D/Pcr represented an independent risk factor for mortality and technique failure in PD patients [ 6 – 8 ] as a consequence of increased glucose absorption from peritoneal cavity and inadequate dialysis, leading to suboptimal ultrafiltration capacities, fluid overload and malnutrition [ 9 ]. On the other hand, patients may lose approximately 5 g total protein or 4 g albumin daily from the peritoneal cavity during PD therapy [ 10 ].…”