Peritoneal dialysis (PD) is an effective and beneficial treatment for patients with end-stage renal disease;[sup], however, peritoneal fibrosis remains a serious complication of long-term PD patients, and a major cause of PD failure.[sup],, Peritoneal fibrosis usually occurs in response to a variety of insults (including bioincompatible
glucose dialysate fluids, peritonitis, uremic toxins, and chronic inflammation).[sup] Epithelial–mesenchymal transition (EMT) has been identified as a key mechanism of peritoneal fibrosis in vitro and in PD patients.[sup],, Various studies have suggested that drugs and peptides could be useful for inhibiting EMT; however, these studies are limited as they block only one signaling pathway.
End-stage renal disease (ESRD) and HD itself lead to an inflammatory status induced by multiple factors, including uremic syndrome per se, heart failure, vascular access infections, bioincompatible
dialysis solutions, the accumulation of advanced glycation products, progressive decrease of glomerular filtration rate [3-5], and blood-membrane interaction .
Hemodialysis (HD), as one of the therapeutic procedures performed on patients with renal failure, is believed to contribute to chronic inflammation due to exposure of blood to bioincompatible
system causing activation of circulating phagocytes .
The mechanism by which peritonitis promotes progression to SP may start by the denudation of the mesothelium, which facilitates the peritoneal damage by the bioincompatible
compounds from PD solutions, increases peritoneal permeability to glucose, and favours nonenzymatic glycosylation of submesothelial structural proteins and decrease in fibrinolytic capacity.
It has also been proposed that hemodialysis triggers inflammation as a result of exposure of blood to the bioincompatible
system stimulating monocyte and macrophage cells [148,149].
(16) Cytokine production may be stimulated by contact of the blood with bioincompatible
dialysis membranes, and cytokines have been shown to stimulate the synthesis of HA.
Baj, "Increased levels of soluble TNF-[alpha] receptors and cellular adhesion molecules in patients undergoing bioincompatible
hemodialysis," American Journal of Nephrology, vol.
Table 1 Factors Associated with an Increase in CRP in Patients on Dialysis * Infection * Surgery * Bioincompatible
membranes * Daily dialysis * Congestive heart failure * Atherosclerosis * Volume overload * Malignancy * Periodontal disease * Inflammation * Uremia * High flux dialysis * Impure dialysate * Type of access (e.g., catheters) * Vascular diseases * Increased truncal fat mass * Arthritis * Failed kidney transplant Source: Adapted from Stenvinkel, 2006.
Increased protein catabolism can be related to bioincompatible
membranes secondary to the release of cytokines and inflammatory mediators.
Most patients are affected to some degree by mechanical irritation caused by the dialysis procedure, compounded in some cases by bioincompatible
Several potential inflammatory triggers may be responsible for the response in ESRD patients, including the hemodialysis (McKenna, Macdonald, Bernstein, & Rush, 1994) or peritoneal dialysis (Brauner, Hylander, & Wretlind, 1996) procedures themselves, development of peritonitis in peritoneal dialysis patients (Bistrian, McCowen, & Chan, 1999; Brauner et al., 1996) or other infections, and exposure to bioincompatible
dialysis membranes that causes the immune activation (Lin et al., 1996).
The authors found there were a number of bioincompatible
aspects of reuse.