Sclerosing Encapsulating Peritonitis during CAPD. Evaluation of the Potential Risk Factors

Rottembourg, Jacques; Issad, B.; Langlois, Patrice; deGroc, F.; Legrain, M

doi:10.1007/978-3-662-11784-2_125

Cited by 30 publications

(34 citation statements)

References 14 publications

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“…In addition, frequent episodes of bacterial peritonitis have been associated with loss of ultrafiltration across the peritoneal membrane and with formation of fibrous adhesions in the peritoneal cavity. Peritonitis has also been implicated as an important factor in the development of encapsulating sclerosing peritonitis (5). A great deal of attention has been focused over the years on designing connec.…”

mentioning

confidence: 99%

Dialysis fluids and local host resistance in patients on continuous ambulatory peritoneal dialysis

Bronswijk

Verbrugh

Heezius

et al. 1988

Eur. J. Clin. Microbiol. Infect. Dis.

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The ability of polymorphonuclear leukocytes, monocytes and peritoneal macrophages to mount a respiratory burst in continuous ambulatory peritoneal dialysis (CAPD) fluids was tested in a phorbol-myristate acetate stimulated chemiluminescence assay. Fresh CAPD fluids depressed the chemiluminescence response of all three types of phagocytes tested to less than 18% of their chemiluminescence response in control buffer. When tested in spent CAPD fluids the suppression of chemiluminescence was 30-32%. Oxygen consumption of polymorphonuclear leukocytes was depressed in fresh CAPD fluids to below 40%. Both phagocytosis of Escherichia coli by and bactericidal capacity of polymorphonuclear leukocytes and monocytes were suppressed in fresh CAPD fluids but not in spent effluents. The influence of acidic pH and hyperosmolality on phagocytic functions were studied separately by modifying the acidity or the glucose content of the control buffer. pH values below 6.0 significantly inhibited chemiluminescence but not phagocytosis. Under hypertonic conditions, both phagocytosis and chemiluminescence were inhibited. We conclude that the currently available CAPD solutions are beyond the limits of acid and osmotic tolerance of human phagocytic cells, and may thus compromise the peritoneal defenses of CAPD patients.

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mentioning

confidence: 99%

Dialysis fluids and local host resistance in patients on continuous ambulatory peritoneal dialysis

Bronswijk

Verbrugh

Heezius

et al. 1988

Eur. J. Clin. Microbiol. Infect. Dis.

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“…Patients with EPS almost always have fast transport failure and ultrafi ltration failure: this was fi rst described by our team [29]. In one study, half of the patients on PD for > 2 years, who developed ultrafi ltration failure and continued PD developed EPS [62] Kidney transplantation and discontinuation of PD: In some studies, a high incidence of post-transplantation EPS has been reported [63].…”

Section: Ultrafi Ltration Failurementioning

confidence: 99%

“…Functional alterations of the peritoneum: Early studies described a decrease in ultrafi ltration and increased peritoneal permeability in patients with EPS [29]. Ultrafi ltration failure seemed to be the predominant early change in patients who are progressively developing EPS.…”

Section: Pathophysiology Of Epsmentioning

confidence: 99%

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Encapsulating Peritoneal Sclerosis: Case report and Current Status

Issad¹

2017

Arch Clin Nephrol

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Encapsulating peritoneal sclerosis (EPS), is a rare but devastating complication of long-term peritoneal dialysis (PD) with a high mortality rate. The incidence is between 0.5 and 3.3%, decreasing with time. EPS is defi ned as a clinical syndrome with major signs of gastrointestinal obstruction, infl ammatory parameters, radiological and macroscopic changes. Duration of treatment and cessation of PD are the main risk for development of EPS: about 75% of EPS occurred in patients transferred on hemodialysis or in the two years after kidney transplantation. Morphological alterations are disappearance of mesothelial layer, sub-mesothelial fi brosis, interstitial sclerosis and vasculopathy, ultrafi ltration failure, fast transport status of the peritoneal membrane, and loss of sodium sieving are the most predicting functional abnormalities. Some biomarkers could be found in the peritoneal effl uent. The pathophysiology is probably a consequence of a multiple-hit process in which expression of growth factors and cytokines play a role. Medical strategies (corticosteroids, immunosuppressive drugs, tamoxifen) in association with parenteral nutrition and/or surgery (enterolysis) are discussed. Prevention is the use of physiological peritoneal solutions, icodextrine instead of high glucose concentration solution, and peritoneal lavage after peritoneal dialysis cessation for any reason.

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“…2 The pathogenesis of EPS has not yet been elucidated, and several risk factors have been postulated. [3][4][5][6] The mechanism of fibroneogenesis in EPS is still unknown. Recently, we have reported that ascites obtained from patients with EPS (EPS ascites) showed significant fibroblast proliferative activity.…”

Section: Introductionmentioning

confidence: 99%

Multimeric vitronectin in ascites is involved in fibroblast spreading of EPS in patients on CAPD therapy

Masunaga

Asakura

Muto

et al. 2003

Clinical and Experimental Nephrology

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Sclerosing Encapsulating Peritonitis during CAPD. Evaluation of the Potential Risk Factors

Cited by 30 publications

References 14 publications

Dialysis fluids and local host resistance in patients on continuous ambulatory peritoneal dialysis

Dialysis fluids and local host resistance in patients on continuous ambulatory peritoneal dialysis

Encapsulating Peritoneal Sclerosis: Case report and Current Status

Multimeric vitronectin in ascites is involved in fibroblast spreading of EPS in patients on CAPD therapy

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