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Icodextrin-induced peritonitis: study of five cases and comparison with bacterial peritonitis.

BACKGROUND: An epidemic of aseptic peritonitis related to the presence of peptidoglycan contaminant in some batches of icodextrin solution (Extraneal, Baxter Healthcare Corporation) occurred in Europe in the first six months of 2002. METHODS: By case-control study we examined the clinical and biologic features of 5 patients with icodextrin-induced peritonitis (group AP) and compared them with 7 patients with bacterial peritonitis (group BP) recruited in our clinical center between January and June 2002. RESULTS: Diagnosis of icodextrin-induced peritonitis was confirmed in all cases by a positive reintroduction test with contaminated batches of icodextrin. No recurrence was observed on re-exposure to icodextrin free of peptidoglycan. Skin tests were positive with contaminated icodextrin in 2 of 5 patients, while they were negative with icodextrin solution free of peptidoglycan (<0.6 ng/mL). During peritonitis, serum level of C-reactive protein (CRP) was lower in group AP (42.4 +/- 34 mg/L) than in group BP (135 +/- 59 mg/L) (P= 0.01). Leukocyte number in peritoneal dialysis effluent was lower in group AP (284 +/- 101/mm3), with a lower neutrophil/monocyte ratio (N/M = 0.67) than in group BP (1410 +/- 973/mm3; N/M = 4) (P < 0.05). A low number of peritoneal fluid eosinophilia (11 +/- 8%) was detected in group AP. CONCLUSION: Icodextrin-induced peritonitis was associated with a burst of intraperitoneal cytokines. The phenotype of peritoneal neutrophils was different between aseptic and bacterial peritonitis, indicating that inflammatory stimuli that activate neutrophils in both types of peritonitis are clearly distinct. Finally, peritoneal injury measured by weight gain, peritoneal permeability, and CA125 concentration seemed to be less severe during icodextrin-induced peritonitis than during bacterial peritonitis.

Aged↗

Lymphatic versus nonlymphatic fluid absorption from the peritoneal cavity as related to the peritoneal ultrafiltration capacity and sieving properties.

In this article we discuss the role of capillary fluid absorption via Starling mechanisms (the transcapillary hydrostatic pressure gradient opposed by the colloid osmotic pressure gradient as multiplied by the capillary UF coefficient) vs. lymphatic fluid absorption as determinants of the total fluid loss from the peritoneal cavity during continuous ambulatory peritoneal dialysis (CAPD). We also mention that, under nonsteady state conditions, there is in addition some net absorption of fluid into the interstitium of tissues surrounding the peritoneal cavity. Support for the contention that nonlymphatic fluid absorption directly into the capillaries is the major mode of fluid transport from the peritoneal cavity to the blood is given by measurements of the peritoneal-to-blood clearance of tracer albumin (or other proteins). Such measurements yield clearance values of the order of 0.2-0.3 ml/min in CAPD. This represents only about 20% of the total peritoneal fluid loss rate (1.2-1.3 ml/min) in ordinary CAPD dwells. Indirect support for a relatively low lymph flow is also derived from capillary physiology. Like continuous capillary walls, the peritoneal membrane shows a bimodal selectivity towards molecules of graded molecular size. Thus, small solute transport can be described as occurring by diffusion through numerous 'small' (approximately 50 A radius) pores, whereas large solute transport is consistent with blood-peritoneal convection through smaller numbers of 'large' (radius approximately 250 A) pores. Furthermore, peritoneal sieving data are compatible with the notion that large crystalloid osmotic pressure gradients cause fluid flow through a water-exclusive ('ultra-small' pore) pathway. A three-pore model of peritoneal selectivity can explain why small solute sieving coefficients are only 0.5-0.6, even though small solute reflection coefficients are close to zero. Another important implication of the three-pore concept is that the peritoneal UF-coefficient is much higher than previously thought, emphasizing the role of capillary absorption in the fluid loss from the peritoneal cavity in CAPD. It is concluded that fluid loss from the peritoneal cavity is dominated by capillary fluid absorption. Hence, lymphatic absorption accounts for just a small fraction of the peritoneal-to-blood absorption of fluid in peritoneal dialysis.

Absorption↗

Serial changes of interleukin-6 and interleukin-8 levels in drain dialysate of uremic patients with continuous ambulatory peritoneal dialysis during peritonitis.

In this study, we investigated whether peritoneal dialysate interleukin-6 (IL-6) and IL-8 levels were elevated during peritonitis in continuous ambulatory peritoneal dialysis (CAPD) patients, with special reference to the high peritonitis occurrence (HPO) group. Serial measurements of IL-6 and IL-8 levels in dialysate before, during and after resolution of peritonitis were done in 13 CAPD patients with 15 episodes of peritonitis. Based on the peritonitis occurrence, 7 patients were assigned to the low peritonitis occurrence (LPO) and 6 patients to the HPO group. Marked elevation of IL-6 and IL-8 in drain dialysate occurred in the early period of peritonitis especially on the first 2 days in both groups. However, there were no significant differences between the groups in the levels of IL-6 and IL-8 in drain dialysate on the first day of peritonitis. However, the disappearance of peritoneal dialysate IL-8 level was faster in the LPO than in the HPO group. The decrease in IL-8 levels during peritonitis was faster than that of IL-6. Marked elevation of IL-6 and IL-8 in drain dialysate was found in the patient with peritonitis caused by Staphylococcus epidermidis and mixed gram-negative bacilli. Therefore, we hypothesize that when peritonitis occurs too frequently in a short period in the HPO group, more IL-6 and IL-8 have been produced in the peritoneum contributing to the ongoing peritoneal injury and/or fibrosis.

Adolescent↗

Continuous cycler therapy, manual peritoneal dialysis therapy, and peritonitis.

An increasing number of patients are prescribed a continuous-cycling regimen because standard manual peritoneal-dialysis exchanges alone are not sufficient in achieving adequate dialysis as defined by the Dialysis Outcome Quality Initiative. Consequently, the number of patients on continuous-cycler therapy is increasing. There is controversy as to whether there are differences in the development of peritonitis between patients maintained on manual therapy and those on continuous cycling therapy. As a result, we retrospectively reviewed the charts of all cycler peritoneal dialysis (CPD) patients maintained on either manual peritoneal dialysis (Baxter UltraBag; Group I) or continuous cycler peritoneal dialysis (Baxter HomeChoice Cycler; Group II) between 1 June 1994 and 31 December 1996. A total of 239 patients were in Group I and 106 in Group II. Both groups were similar in age, race, gender, and presence of diabetes mellitus, coronary artery disease, peripheral vascular disease, and gastrointestinal disease. There was no difference in the overall rate of peritonitis between the two groups of patients [1 episode in 10.4 patient-months (Group I) vs. 1 in 10.0 patient-months (Group II); -0.01843 to 0.02619]. The rates of Staphylococcus aureus peritonitis [1 episode in 48.5 patient-months (Group I) vs. 1 in 141.8 patient months (Group II); -0.06152 to -1.1689]; polymicrobial peritonitis [1 episode in 278.8 patient-months (Group I) vs. 1 in 1134 patient months (Group II): -0.0079 to -0.0478], and fungal peritonitis (1 episode in 202.7 patient-months (Group I) vs. no episodes (Group II); 0.00202 to 0.00785] were significantly lower among patients maintained on the Baxter HomeChoice Cycler. The rate of gram-negative peritonitis was higher among patients maintained on the Baxter HomeChoice Cycler, but this difference was not statistically significant [1 episode in 82.6 patient-months (Group I) vs. 1 episode in 45.4 patient months (Group II); 0.4723 to -0.0248]. We conclude that individual rates of peritonitis were different for patients maintained on either manual or continuous CPD therapy, while the overall rate of peritonitis was found to be similar for both groups of patients. The finding that there may be a difference with the gram-negative peritonitis rate is important since gram-negative peritonitis has been shown to have a more severe outcome in terms of morbidity, mortality, and patient dropout from CPD therapy. A larger, randomized, multicenter study comparing the rates of gram-positive, gram-negative, fungal, and polymicrobial peritonitis is warranted.

Female↗

[Fungal peritonitis episodes in a peritoneal dialysis centre during a 10-year period: a report of 11 cases].

Fungal peritonitis is a rare cause of peritonitis, but it is associated to poorer prognosis and higher mortality than bacterial peritonitis. Until now, predisposing factors and treatment have not been well established. We retrospectively reviewed all the cases of fungal peritonitis diagnosed for ten years in 218 patients undergoing continuous ambulatory peritoneal dialysis. In all we detected 11 episodes of fungal peritonitis in 11 patients, that means the 4% of continuous ambulatory peritoneal dialysis peritonitis. All the cases of fungal peritonitis were caused by Candida species. As a result of fungal peritonitis 36% of the patients died, 55% had to change to long-term hemodialysis because of failure in peritoneal dialysis technique. Only one case (9%) managed to continue peritoneal dialysis. The factors associated with the development of fungal peritonitis were: the presence of antibiotic use within 1 month before fungal peritonitis, patient older than 70 years old, low levels in albumine plasmatic and long permanence in continuous ambulatory peritoneal dialysis. The treatment consisted in intraperitoneal fluconazol combined with oral 5-flucytosine for 4 to 6 weeks. In the two last cases we associated intravenous caspofungine too. Given that no improvement was seen within 72 hours of treatment, the catheter must be removed in all the cases.

Administration, Oral↗

Analysis of inflammatory mediators and peritoneal permeability to macromolecules shortly before the onset of overt peritonitis in patients treated with CAPD.

OBJECTIVE: To investigate whether changes in peritoneal membrane characteristics and inflammatory mediators in dialysate precede the onset of overt infection during continuous ambulatory peritoneal dialysis (CAPD)-related peritonitis. DESIGN: CAPD patients with a high peritonitis incidence stored every night bag at 4 degrees C. Routinely, each bag was thrown away after two days. Only if patients developed peritonitis, all bags were delivered for study. Thus, two night bags immediately prior to the first peritonitis bag were available for analysis. A control study was done 14 days after recovery. Dialysate samples were measured for TNF alpha, IL-6, PGE2, 6-keto-PGF1 alpha, TxB2, and serum proteins. The clearance of beta 2-microglobulin was used as an indicator of the effective peritoneal surface area. The intrinsic peritoneal permeability was characterized by the restriction coefficient. RESULTS: Eight episodes occurred in 5 patients. The night dwells available prior to the first peritonitis effluent were drained maximally nine dwells and minimally one dwell before the first peritonitis bag. Dialysate leukocyte counts exceeded 100 x 10(6)/L only on the day of manifest infection. However, bacterial cultures were already positive at least one day before overt infection in four episodes and in three of these cases two days before. No changes were observed prior to peritonitis for the clearance of beta 2-microglobulin or the restriction coefficient. In contrast to these permeability characteristics, the cytokines, TNF alpha and, though less significant, also IL-6, were increased in dialysate one day prior to overt infection, when compared to the values obtained at the control investigation. This was especially evident in effluents drained no longer than two dwells before the first peritonitis bag. Prostaglandin concentrations in dialysate were not different before the onset of manifest peritonitis from the values measured after recovery. CONCLUSION: In this study, the increased effective peritoneal surface area and intrinsic peritoneal permeability during acute infection appeared to be preceded by elevations in the cytokines TNF alpha and, to a lesser extent, IL-6. These increments occurred only very shortly before the onset of clinical symptoms.

6-Ketoprostaglandin F1 alpha↗

A scanning electron microscopy study of peritoneal stomata in different peritoneal regions.

Peritoneal stomata constitute the principal pathways for the drainage of intraperitoneal contents from the peritoneal cavity to the lymphatic system and have been claimed to be exclusively restricted to the peritoneal surface of the diaphragm. This concept has been revised by the demonstration of peritoneal stomata in the omental, mesenteric, ovaric and pelvic peritoneum. Therefore, the aim of this study was to further assess peritoneal surfaces of several other abdominal organs and of the abdominal wall with special reference to the occurrence of peritoneal stomata. The peritoneum covering the spleen, stomach, intestine, liver, diaphragm and anterior abdominal wall obtained from rats was examined by scanning electron microscopy. Whereas the splenic and hepatic peritoneal surfaces were composed of uniformly distributed cuboidal mesothelial cells, the gastric and intestinal peritoneal surfaces were arranged in parallel folds composed of prominent mesothelial cells with elongated finger-like cytoplasmic processes. In addition to diaphragmatic peritoneal stomata, mesothelial openings were also found on the peritoneal surfaces covering the anterior abdominal wall and the liver. The parietal peritoneal stomata were arranged in clusters, oval in shape and delimited by flattened mesothelial cells exposing the underlying submesothelial connective tissue. The hepatic mesothelial openings formed by deep channel-like gaps of adjacent cuboidal mesothelial cells were almost completely occluded by a dense microvillous coat. As the submesothelial connective tissue was not identifiable with certainty, the mesothelial openings were regarded as corresponding to stoma-like structures. These findings yield further evidence that peritoneal stomata are obviously not confined to the diaphragmatic area but extend to other peritoneal regions. It is therefore suggested that these extra-diaphragmatic parietal and visceral peritoneal surfaces contribute to the absorption capacity of the entire peritoneum and are subsequently involved in either therapeutic procedures or pathological processes affecting the peritoneal cavity.

Animals↗

Effect of indomethacin on peritoneal protein loss in a rabbit model of peritonitis.

BACKGROUND: Although various inflammatory mediators have been previously shown to be released into the peritoneal cavity during peritonitis in peritoneal dialysis patients, those that are involved in governing changes in peritoneal permeability to small solutes and protein remain incompletely defined. METHODS: We determined the importance of prostanoid production in the enhanced protein loss observed during acute peritonitis by inhibition experiments using indomethacin, an inhibitor of cyclooxygenase activity. The association between changes in peritoneal permeability and the generation of inflammatory mediators after adding Escherichia coli to peritoneal dialysate was first examined in series 1 experiments. Series 2 experiments then determined the effect of intraperitoneal administration of indomethacin (75 microg/mL) on changes in peritoneal permeability after adding E. coli to peritoneal dialysate. All experiments were performed in male New Zealand White rabbits (2.6 to 3.4 kg body weight) using an eight-hour dwell of dialysate containing 2.5% glucose. Peritoneal permeability to creatinine and protein was assessed by time-dependent changes in the dialysate to plasma concentration ratios of these solutes. RESULTS: Series 1 experiments showed enhanced leukocyte migration into the peritoneal cavity and increased peritoneal permeability to protein during bacterial challenge that was accompanied by an increase in the dialysate concentrations of prostaglandin E2 (PGE2), 6-keto-PGF1alpha, and interleukin-8, but not nitrate + nitrite (a measure of local nitric oxide production). Inhibition of prostanoid production by intraperitoneal administration of indomethacin in series 2 experiments resulted in lower dialysate concentrations of PGE2 and 6-keto-PGF1alpha and in lower peritoneal permeability to protein, both to control levels. No effect of indomethacin on transperitoneal migration of leukocytes or the generation of interleukin-8 was observed. CONCLUSIONS: Enhanced production of prostanoids likely plays an important role in governing the increase in peritoneal permeability to protein during acute, bacterial peritonitis in the rabbit.

6-Ketoprostaglandin F1 alpha↗

Genetic polymorphism of VEGF: Impact on longitudinal change of peritoneal transport and survival of peritoneal dialysis patients.

BACKGROUND: Vascular endothelial growth factor (VEGF) plays a pivotal role in the peritoneal angiogenesis and hyperpermeability in patients on peritoneal dialysis. We hypothesis that VEGF genetic polymorphism may affect the longitudinal change of peritoneal transport and clinical outcome of peritoneal dialysis patients. METHODS: We studied 135 consecutive new peritoneal dialysis patients. VEGF genetic polymorphism at -1154 and -2578 positions were determined by polymerase chain reaction (PCR) methodologies. Standard peritoneal test and dialysis adequacy and transport test (DATT) were performed at the initiation of peritoneal dialysis. After 12 months, DATT was repeated in 83 patients. In 35 patients, VEGF production in vivo was determined by its levels in serum and peritoneal dialysis effluent, and mRNA expression in peritoneal dialysis effluent. Patients were followed for 19.4 +/- 8.5 months for survival study. RESULTS: There was no relation between VEGF genotype and baseline peritoneal transport group. The changes in 24-hour dialysate-to-plasma (D/P) creatinine after 12 months were 0.028 +/- 0.159, -0.013 +/- 0.137, and 0.141 +/- 0.231 for CC, CA, and AA genotype at -2578 position, respectively [one-way analysis of variance (ANOVA), P= 0.028]. The AA genotype had significantly higher increase in 24-hour D/P creatinine than the other genotypes. Similar results were found with the genotype at -1154 position, which had marked linkage disequilibrium with the genotype at -2578 position. Actuarial patient survival was 90.3% and 74.9% at 24 months for CC and CA/AA genotypes at -2578 position, respectively (P= 0.036). After correcting for confounding covariates, the adjusted hazard ratio of death was 3.04 (95% CI, 1.10 to 8.36) for the CA/AA group as compared to CC group. Although baseline serum VEGF level was higher in patients with CC genotype than those with CA/AA genotype at -2578 position (541.5 +/- 322.8 pg/mL vs. 298.8 +/- 209.4 pg/mL, P= 0.012), VEGF mRNA expression in peritoneal dialysis effluent was significantly lower in patients with CC genotype (1.82 +/- 2.77 vs 4.48 +/- 3.28, P= 0.021). VEGF protein level in peritoneal dialysis effluent was also marginally lower in patients with CC genotype, although the difference was not significant. Genotype at -1154 position was not associated with VEGF production in vivo or patient survival. CONCLUSION: We conclude that in peritoneal dialysis patients, the AA genotype of VEGF promoter at -2578 position was associated with progressive increase in peritoneal transport. The CA/AA genotype at -2578 position was also associated with an excess mortality. Our finding also suggests that systemic and local peritoneal VEGF production may be differentially regulated.

Adult↗

Peritoneal lymphatic absorption and solute exchange during zymosan-induced peritonitis in the rat.

Lymph flow is elevated in most inflammatory conditions. However, a few previous studies have indicated that peritoneal lymph flow may actually fall during acute peritonitis. This study was performed to explore this issue further and to study the pathophysiology of peritoneal exchange during peritonitis. Therefore, we wanted to assess the total peritoneal clearance (Cl) and the clearance from peritoneum to plasma (Cl --> P) of 125I-labeled albumin (125I-albumin) as well as plasma-to-dialysate clearance (Cl --> D) of Evans blue-labeled albumin together with peritoneal ultrafiltration (UF) profiles and mass transfer area coefficients of 51Cr-EDTA and glucose in rats after acute peritonitis induced by zymosan. Zymosan incubation of the peritoneal cavity (120 mg) for 4 h generally led to a 4- to 10-fold increase in peritoneal fluid white blood cell count, indicating that acute peritonitis had been induced. Then 16 ml of 3.86% Dianeal and 125I-albumin were instilled intraperitoneally, whereas Evans blue-labeled albumin and 51Cr-EDTA were given as infusions intravenously. Compared with control, mass transfer area coefficients for glucose and 51Cr-EDTA increased markedly from 0.43 +/- 0.06 and 0.25 +/- 0.04 to 0.91 +/- 0.06 and 0.59 +/- 0.05 (SE) ml/min, respectively, during peritonitis, whereas Cl and Cl --> D increased from 32.8 +/- 5.6 and 8.6 +/- 1.6 to 74.5 +/- 7.3 and 12.9 +/- 1.0 microl/min, respectively. The UF profile in peritonitis indicated type I loss of UF (resulting from the increases in permeability-surface area product for glucose). However, the Cl --> P declined to 5.9 +/- 1.0 microl/min from 7.9 +/- 0.8 microl/min (P < 0.05) in control. In conclusion, despite marked effects on peritoneal solute transport and on UF, conceivably resulting from vasodilatation and increases in capillary permeability, zymosan-induced peritonitis did not cause any acute increases in direct peritoneal lymphatic absorption.

Animals↗

Analysis of the peritoneal cellular immune system during CAPD shortly before a clinical peritonitis.

We analysed the peritoneal cellular immune system 24-48 h before the onset of a clinical peritonitis. Peritoneal cells were obtained from the overnight dialysis effluents 1 or 2 days (day-1 and day-2) preceding the day of peritonitis, the last overnight effluent before the peritonitis effluent (day P), and the first peritonitis effluent. Nine peritonitis episodes of six patients were studied. The number of Fc receptor positive cells, the chemotactic activity, and immunophenotype of the peritoneal cell population at day-2 and day-1 were similar to the postperitonitis control effluent. However, immunophagocytosis and phagocytosis capacity of the peritoneal macrophages was decreased in five of six episodes at day-2 and -1 compared to control peritoneal macrophages. The overnight effluents of day P revealed a moderate influx of neutrophilic granulocytes and an increase of bacterial killing capacity and chemotactic activity. Activation of the peritoneal T cells at day P was shown by the increase in MHC class II positive T cells and an increase in the CD4/CD8 ratio. Bacterial cell cultures of the effluents were positive in three episodes 24-48 h before peritonitis, and of all overnight effluents at day P. These results indicate that malfunctioning of phagocytosis by peritoneal macrophages may contribute to the development of a CAPD peritonitis.

Adult↗

Serial peritoneal macrophage function studies in CAPD patients with peritonitis.

Continuous ambulatory peritoneal dialysis, peritoneal macrophage, IL-1, IFN-r, TNF, phagocytosis. Peritoneal macrophages (PM) perform first-line defense activity against peritonitis, the most important complication in CAPD therapy. Our longitudinal study compared the PM function in 14 patients in a low peritonitis occurrence group (LPOG) and 6 in a high peritonitis occurrence group (HPOG) before and during peritonitis; all started CAPD therapy after January 1988. The results show that at the onset of peritonitis, PM function including bactericidal killing (BA) activity, phagocytosis index (PI), H2O2 release, interleukin-1 (IL-1) and tumor necrosis factor (TNF) secretion can increase rapidly in the LPOG. However, this was absent in the HPOG. Both groups had a decrease of PM immunological function in the initial 7 to 10 days after onset of peritonitis, then PM functions began to return toward their pre-peritonitis state. However, in the HPOG, the recovery of PM function was very slow, resulting in significantly lower PM functions. In vitro, when normal PM were put into peritonitis dialysate, IL-1, TNF production and PI, BA activity of PM were decreased. This suppressor activity was absent in the peritonitis-free dialysate. These results suggest a suppressor factor(s) in the HPOG peritoneal dialysate may decrease the function of PM rather than cause easy peritonitis development.

Bacterial Infections↗

Risks of peritoneal membrane failure in children undergoing long-term peritoneal dialysis.

Children undergoing long-term peritoneal dialysis are at risk for membrane injury, necessitating conversion to hemodialysis. We analyzed the incidence and risk factors for membrane failure (inadequate ultrafiltration with or without peritoneal adhesions and decreased peritoneal surface area) in 68 children maintained with peritoneal dialysis for more than 3 months at our institution. The overall incidence of membrane failure was 16.2% (11/68). Kaplan-Meier estimates of peritoneal membrane survival were 88% at 24 months, 72% at 36 months, 65% at 48 months, and 52% at 60 months. Logistic regression analysis demonstrated that the risk of membrane failure increased with the number of episodes of peritonitis (odds ratio 1.61). The rate of peritonitis was 1 per 7.02 patient months in children who developed membrane failure compared with 1 per 9.18 patient months in children without membrane failures but the rate of peritonitis was not predictive of membrane failure (P = 0.09). Multiple logistic regression analysis demonstrated that peritonitis caused by Pseudomonas aeruginosa or alpha streptococcal organisms were independent predictors of membrane failure. We conclude that peritoneal membrane survival declines substantially with time on peritoneal dialysis and that membrane failure is associated with peritonitis, particularly peritonitis caused by Pseudomonas aeruginosa and alpha streptococcal organisms. The mechanism(s) of membrane injury are unknown but may be related to the inflammatory response initiated during peritonitis.

Adolescent↗

Fungal peritonitis in children on peritoneal dialysis.

Fungal peritonitis is a rare but serious complication in children on peritoneal dialysis (PD). In this study, risk factors were evaluated, and therapeutic measures were reviewed. A retrospective, multi-centre study was performed in 159 Dutch paediatric PD patients, between 1980 and 2005 (3,573 months). All peritonitis episodes were reviewed. Fungal peritonitis episodes were evaluated based on possible risk factors and treatment strategy. A total of 321 episodes of peritonitis occurred, with 9 cases of fungal peritonitis (2.9%). Candida peritonitis occurred most frequently (78%). Seven patients (78%) had used antibiotics in the prior month. Fungal peritonitis patients had a higher previous bacterial peritonitis rate compared to the total study population (0.13 versus 0.09 episodes/patient*month), with twice as many gram negative organisms. In all fungal peritonitis patients, the PD catheter was removed. In four patients restart on PD was possible. Fungal peritonitis is a rare complication of PD in children, but is associated with high technique failure. The most important risk factors are a high bacterial peritonitis rate, prior use of antibiotics, and previous bacterial peritonitis with gram negative organisms. The PD catheter should be removed early, but in children, peritoneal lavage with fluconazole before removal may be useful to prevent technique failure.

Antifungal Agents↗

Fungal peritonitis in patients on continuous ambulatory peritoneal dialysis.

The purpose of this study was to analyze the microbiological and clinical features of fungal peritonitis in patients with endstage renal failure treated with continuous ambulatory peritoneal dialysis (CAPD). The diagnosis of peritonitis was based on abdominal discomfort or pain, cloudy peritoneal effluent with an elevated leukocyte count and isolation of fungi from the peritoneal effluent. Amphotericin B, flucytosine, ketoconazole, miconazole and more recently fluconazole were used for antifungal therapy. From 1983 to 1997 13 patients experienced 14 episodes of fungal peritonitis, comprising 3.1% of all episodes of peritonitis in the dialysis centre. Isolates from the peritoneal effluent comprised Candida tropicalis in two cases, Candida parapsilosis in two cases, Candida albicans in one case, Candida lusitaniae in one case,Cephalosporium spp. in three cases, Aspergillus fumigatus in two cases, and an Aspergillus sp., a Trichoderma sp. and a yeast in one case each. In eight cases bacterial infection shortly before the episode of fungal peritonitis was documented. In 12 (86%) cases the peritoneal catheter had to be removed. Four patients died during the treatment, and one patient died 2 months after the end of treatment due to intra-abdominal bleeding from peritoneal adhesions. Only two patients continued CAPD later; the other patients were switched to hemodialysis. It is concluded that fungal peritonitis is a rare but serious complication in CAPD patients with high rates of morbidity, mortality and drop-out from the CAPD programme (85%). The most frequent isolates were Candida spp. A predisposing factor for fungal peritonitis could be a recent bacterial infection treated with antibiotics. Early peritoneal catheter removal is recommended.

Adult↗

Response of chronic renal failure mice to peritoneal Staphylococcus epidermidis challenge: impact of repeated peritoneal instillation of dialysis solution.

The effect of repeated instillation of peritoneal dialysis (PD) solution on the peritoneal clearance of a Staphylococcus epidermidis challenge was investigated in a mouse model of surgically induced chronic renal failure. For periods of up to 2 weeks, mice bearing peritoneal catheter implants underwent daily (3 mL) or twice daily (1.5 mL) peritoneal instillation of PD solution (4.25% dextrose) by transcutaneous injection into the catheter lumen. Peritoneal instillation of PD solution did not have a significant influence on the microbiological status of peritoneal structures of renal failure or sham-operated mice following experimental intracatheter S epidermidis inoculation with 10(6) colony-forming units (CFU) (assessment 48 hours after inoculation) or 10(8) CFU (assessment 1 week after inoculation). Microbiological and scanning electron microscopy (SEM) assessments of recovered peritoneal catheters demonstrated that S epidermidis remained associated with the catheter site after other peritoneal structures had become culture negative. SEM of the parietal peritoneum revealed striking morphologic alterations of the mesothelial surface as a consequence of daily PD solution infusion. In the absence of S epidermidis inoculation, repeated instillation of PD solution caused a marked acute peritoneal inflammation without evidence of a concomitant systemic inflammatory response. Furthermore, peritoneal inflammatory response to S epidermidis challenge was augmented by the infusion procedure. Concurrent assessments of inflammatory response and microbiological status revealed that, in spite of heightened peritoneal inflammatory response with peritoneal infusion, bacterial clearance from the catheter site was not improved. Although the animal preparation was limited to peritoneal infusion without drainage, the influence of repeated peritoneal instillation of hyperosmolar, acidic PD solution on the response of mice to S epidermidis challenge was successfully addressed.

Animals↗

Factors increasing severity of peritonitis in long-term peritoneal dialysis patients.

Peritonitis is the most frequent complication and a leading cause of discontinuation of peritoneal dialysis (PD). Intact epithelial lining, sufficient blood flow, and adequate immunologic responses are vital to eradicate infection. In long-term PD, various pathological changes such as denudation of peritoneal mesothelial cells, duplication of submesothelial and/or capillary basement membranes, submesothelial fibrin deposit, and peritoneal fibrosis have been reported. Causes of these changes of the peritoneum are multifactorial. Commonly used dialysis solutions that are acidic, hypertonic, containing high concentrations of glucose and lactate, contaminated by glucose and/or plastic degradation products are not biocompatible and may induce chronic immune reactions in the peritoneal cavity. Long-term exposure of the peritoneum to dialysis solutions, the peritoneal catheter, and recurrent episodes of peritonitis all contribute to peritoneal injury. In addition, long-term exposure of peritoneal cells such as macrophages, mesothelial cells, and fibroblasts to dialysis solutions may also alter the normal immunologic reactions against bacteria. Peritoneal concentrations of opsonins such as Ig, complement, and protease are approximately 1% of the serum levels and far below the level sufficient to eradicate bacteria due to continuous peritoneal lavage and dilution with dialysis solutions. Furthermore, glycation of IgG induces chronic activation of macrophages and decreases normal opsonic activities against bacteria. Fibrin deposits, collagen accumulation, and cellular desert of the peritoneum observed in long-term peritoneal dialysis patients may serve as a safe shelter for bacteria from contact with inflammatory cells and opsonin and delay eradication of bacteria. In conclusion, peritonitis is often more severe in patients on long-term PD. In this setting, peritonitis needs special attention to prevent life-threatening infection and further damage of the peritoneum.

Collagen↗

A comparison of peritonitis rates from the United States Renal Data System database: CAPD versus continuous cycling peritoneal dialysis patients.

BACKGROUND: Previous comparisons of peritonitis rates between continuous ambulatory peritoneal dialysis (CAPD) and continuous cycling peritoneal dialysis (CCPD) have produced varying results. METHODS: Using United States Renal Data System data, the authors evaluated peritonitis rates in 1994 through 1997 incident CAPD (n = 9,190) and CCPD (n = 2,785) Medicare patients. Patients were characterized during a 6-month entry period (months 4 through 9) and followed for a maximum of 2 years (months 10 through 33). Medicare claims data provided the date of the first peritonitis episode during the follow-up period. The time to first peritonitis after 9 months of PD was compared by the log-rank test, and then by Cox regression with adjustment for peritoneal dialysis modality, age, sex, race, primary end-stage renal disease (ESRD) diagnosis, number of entry-period hospital days, peritonitis during the entry period, hematocrit value, and congestive heart failure. RESULTS: For CAPD and CCPD, the adjusted average months to first peritonitis after 9 months of PD were 17.1 and 16.1, respectively. The probabilities of remaining without a peritonitis episode after 1 year of follow-up were 0.53 and 0.50, respectively ( P = 0.008). The risk of peritonitis was lower for CAPD than for CCPD (relative risk, 0.939; 95% confidence interval, 0.883 to 0.998). Other significant risk factors included age or=36% had lower risk of peritonitis. CONCLUSION: Compared with CCPD, CAPD is associated with a slightly but significantly lower risk for development of a first peritonitis episode after 9 months of peritoneal dialysis therapy.

Adolescent↗