HOST DEFENSES IN CONTINUOUS AMBULATORY PERITONEAL-DIALYSIS AND THE GENESIS OF PERITONITIS

Authors
Citation
Js. Cameron, HOST DEFENSES IN CONTINUOUS AMBULATORY PERITONEAL-DIALYSIS AND THE GENESIS OF PERITONITIS, Pediatric nephrology, 9(5), 1995, pp. 647-662
Citations number
NO
Categorie Soggetti
Pediatrics,"Urology & Nephrology
Journal title
Pediatric nephrology
ISSN journal
0931041X → ACNP
Volume
9
Issue
5
Year of publication
1995
Pages
647 - 662
Database
ISI
SICI code
0931-041X(1995)9:5<647:HDICAP>2.0.ZU;2-S
Abstract
Continuous ambulatory peritoneal dialysis (CAPD) has come to be extens ively used for the treatment of end-stage renal failure in children, a nd especially infants, such that now more than half of children on dia lysis worldwide receive treatment by this means. Peritonitis, however, is commoner in children than in adults receiving treatment, and is a major source of morbidity and treatment failure in children started on CAPD. Only recently has the immunology of the normal peritoneum been studied extensively, with the need to assess the impact of the install ation of large volumes of fluid into the peritoneal sac during dialysi s. The main phagocytic defences of the peritoneum depend upon a unique set of macrophages which are present free in the peritoneal fluid but also in the submesothelium and in perivascular collections together w ith B lymphocytes in the submesothelial area. Both the number of macro phages per unit volume and the concentration of opsonic proteins, such as IgG, complement and fibronectin, are reduced to between only 1% an d 5% when dialysis fluid is continuously present in the peritoneal sac . In addition, the fluids used for CAPD are toxic to both macrophages and to mesothelial cells. Thus minor degrees of contamination frequent ly lead to peritonitis and in addition the majority of patients have c atheters inserted in their peritoneum which become colonised with orga nisms capable of producing exopolysaccharide (slime), which promotes a dhesion of the organism to the plastic and protects them against phago cytic attack and the penetration of antibiotics. Thus the peritoneum i s in a state of continual inflammation, as well as being a markedly mo re vulnerable site than the normal peritoneum to the entry of organism s. Whether clinical peritonitis appears in this state of chronic conta mination probably depends on perturbation in the balance between host defences and the organism. Whilst Staphylococcus epidermidis is the co mmonest cause of peritonitis, Staphylococcus aureus and Gram-negative organisms are much more serious and more frequently lead either to tem porary catheter removal or discontinuation of dialysis altogether. Thi s review describes the peritoneal defences in relation to the genesis of peritonitis.