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Journal articles on the topic 'Peritoneal dialysis'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 August 2024

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1

Nakamoto, Hidetomo, Hiroe Imai, Yuji Ishida, Yasuhiro Yamanouchi, Tsutomu Inoue, Hirokazu Okada, and Hiromichi Suzuki. "New Animal Models for Encapsulating Peritoneal Sclerosis—Role of Acidic Solution." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 21, no. 3_suppl (December 2001): 349–53. http://dx.doi.org/10.1177/089686080102103s64.

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Objective Encapsulating peritoneal sclerosis (EPS), in which all or part of the intestine is enveloped in a fibrous ball resembling a cocoon, is a serious complication of peritoneal dialysis (PD). The aim of the present study was to investigate whether pH-neutral or acidic dialysis solutions induce peritoneal fibrosis. Design We divided 18 male Wistar–Kyoto (WKY) rats into three groups and dialyzed them with various solutions as follows: group I, 10 mL acidic dialysis solution (pH 3.8, containing 1.35% glucose), n = 6; group II, 10 mL pH 5.0 dialysis solution, n = 6; and group III, 10 mL neutral dialysis solution (pH 7.0), n = 6. Peritoneal catheters were inserted, and dialysis solution was injected every day for 40 days. At the end of the experiment, a peritoneal equilibration test (PET) was performed. Expression of mRNA of aquaporins 1 and 4 (AQP-1 and AQP-4) in the peritoneum were studied by semiquantitative reverse-transcriptase polymerase chain reaction (RT-PCR). Results In rats treated with pH 3.8 dialysis solution, necropsy findings revealed features identical to those of EPS. The typical appearance was of granulation tissue or fibrotic tissue (or both) covering multiple surfaces. Multiple adhesions were present. In microscopic examinations, peritoneal fibrosis and loss of mesothelium were found. In rats treated with pH 7.0 dialysis solution, no signs of EPS were seen. In rats treated with pH 5.0 dialysis solution, milder changes (subserosal thickening and partial adhesion of the peritonea) were observed. The mRNA of AQP-1 and AQP-4 were expressed in the peritonea of the rats. The expression of the AQPs was significantly suppressed in rats treated with pH 3.8 dialysis solution. Conclusions In rats, long-term intraperitoneal injection of acidic dialysis solution produced features typical of EPS in humans. Newly developed neutral dialysis solutions protected the against the development of EPS during peritoneal dialysis in rats.

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2

Andreoli, Maria Claudia Cruz, and Claudia Totoli. "Peritoneal Dialysis." Revista da Associação Médica Brasileira 66, suppl 1 (2020): s37—s44. http://dx.doi.org/10.1590/1806-9282.66.s1.37.

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SUMMARY Peritoneal dialysis (PD) is a renal replacement therapy based on infusing a sterile solution into the peritoneal cavity through a catheter and provides for the removal of solutes and water using the peritoneal membrane as the exchange surface. This solution, which is in close contact with the capillaries in the peritoneum, allows diffusion solute transport and osmotic ultrafiltration water loss since it is hyperosmolar to plasma due to the addition of osmotic agents (most commonly glucose). Infusion and drainage of the solution into the peritoneal cavity can be performed in two ways: manually (continuous ambulatory PD), in which the patient usually goes through four solution changes throughout the day, or machine-assisted PD (automated PD), in which dialysis is performed with the aid of a cycling machine that allows changes to be made overnight while the patient is sleeping. Prescription and follow-up of PD involve characterizing the type of peritoneal transport and assessing the offered dialysis dose (solute clearance) as well as diagnosing and treating possible method-related complications (infectious and non-infectious).

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Lu, Jingyuan, Danye Shi, Xinhui Zhao, Minhui Xi, Hualin Qi, and Qiang He. "Crocin ameliorates peritoneal fibrosis in rat induced by peritoneal dialysis via Wnt5a/β-Catenin pathway." Quality Assurance and Safety of Crops & Foods 14, no. 4 (September 1, 2022): 36–44. http://dx.doi.org/10.15586/qas.v14i4.1151.

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Peritoneal dialysis is used in the treatment of patients with kidney diseases. Long-term peritoneal dialysis could result in peritoneal fibrosis and recurrent peritonitis, thus leading to failure of ultrafiltration. Crocin is a bioactive carotenoid and isolated from stigma of Crocus sativus, and ameliorates pulmonary and myocardial fibrosis. The role of crocin in peritoneal fibrosis was assessed. Firstly, rats model with peritoneal dialysis was treated with 4.25% peritoneal dialysate. Results showed that injection with peritoneal dialysate induced obvious hyperplasia and increased thickness in peritoneum structure. Rats with peritoneal dialysis were injected with increasing concentrations of crocin at 10, 20, or 40 mg/kg. Crocin ameliorated the pathological changes in the peritoneum of peritoneal dialysate-induced rats. Secondly, crocin attenuated peritoneal dialysate-induced decrease of E-cadherin, increase of fibronectin, α-smooth muscle actin (α-SMA), and collagen I. Moreover, crocin enhanced ultrafiltration volume and reduced glucose transport in rats model with peritoneal dialysis. Thirdly, crocin also reduced levels of Interleukin (IL)-1β, Tumor Necrosis Factor-α (TNF –α), and IL-6 in peritoneal tissues of rats model with peritoneal dialysis. Lastly, protein expression of Wnt5a and β-Catenin in rats model with peritoneal dialysis were also downregulated by crocin. In conclusion, crocin exerted anti-inflammatory and anti-fibrotic effects on rats model with peritoneal dialysis through inactivation of Wnt5a/β-Catenin pathway.

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4

Sulowicz, Wladyslaw, Tadeusz Cichocki, and Zygmunt Hanicki. "Changes in Activity of Selected Lysosomal Enzymes in Peritoneal Macrophages of Renal Failure Patients on Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 9, no. 4 (October 1989): 313–17. http://dx.doi.org/10.1177/089686088900900417.

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Activity of acid phosphatase (AP), beta-glucuronidase (GR), N-acetyl-beta-D-glucosaminidase (GZ), and peroxidase (P) was assessed using a semiquantitative cytochemical method in peritoneal macro phages of 30 patients with end-stage renal failure treated by intermittent peritoneal dialysis and of 30 control patients with normal renal function. The dialysed patients showed a significantly higher activity of GR and P at the beginning of the treatment as compared with the respective activities observed in the control group and a further significant rise of these activities after 4 months of dialysis. Activity of AP at the beginning of the treatment was insignificantly lower than in the control group and the difference became significant at the end of the investigated period. There was no significant difference between the dialysed patients and the control group in the activity of GZ assessed at the beginning of the dialytic treatment and after 4 months of dialysis. A significant decrease in that activity was, however, observed in the course of dialysis.

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5

Wieczorowska-Tobis, K., K. Korybalska, A. Polubinska, M. Radkowski, A. Breborowicz, and D. G. Oreopoulos. "In Vivo Model to Study the Biocompatibility of Peritoneal Dialysis Solutions." International Journal of Artificial Organs 20, no. 12 (December 1997): 673–77. http://dx.doi.org/10.1177/039139889702001203.

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This study was designed to analyze the complex morphologic and functional effects of dialysis solutions on peritoneum in a rat model on chronic peritoneal dialysis. Peritoneal catheters were inserted into 10 male, Wistar rats and the animals were dialyzed twice daily for 4 weeks with 4.25% Dianeal. During the study we observed two opposite effects: healing of the peritoneum after catheter implantation - decreased cell count in dialysate, decreased permeability of the peritoneum to glucose and total protein, increased volume of drained dialysate; and damage to the membrane due to its exposure to peritoneal dialysis solution - increased hyaluronic acid levels in dialysate, a tendency of the peritoneum to thicken when compared to non-dialyzed animals. Our rat model of CAPD may be used for quantitative and qualitative assessment of the effects of peritoneal dialysis solution on the peritoneum during chronic dialysis

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Wu, George, Katarzyna Wieczorowska Tobis, Alicja Polubinska, Katarzyna Korybalska, Violetta Filas, Paul Tam, Ian French, and Andrzej Breborowicz. "N-Acetylglucosamine Changes Permeability of Peritoneum during Chronic Peritoneal Dialysis in Rats." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 18, no. 2 (March 1998): 217–24. http://dx.doi.org/10.1177/089686089801800212.

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Objective To evaluate the effect of supplementation of dialysis fluid with N-acetylglucosamine (NAG) on the permeability of peritoneum during chronic peritoneal dialysis in rats. Design Experiments were performed on rats with surgically implanted peritoneal catheters. Dialysis solution [DianeaI1.5% (Baxter, Deerfield, IL, U.S.A.) supplemented with either NAG 50 mmol/L or glucose 50 mmol/L (control)] was infused intraperitoneally twice, every day, for 8 weeks. Peritoneal equilibration tests (PET) were performed in all animals at the beginning of the study and after 8 weeks of dialysis. Additionally, at the end of each week, dialysis solution infused in the morning was drained after 4 hours of intraperitoneal dwell. White blood cell count, creatinine, and total protein concentrations were measured in the effluent dialysate. After 8 weeks of dialysis, the morphology of the peritoneum was studied. Results In rats exposed to dialysis fluid supplemented with NAG, peritoneal permeability to creatinine and proteins was reduced when compared to animals dialyzed with glucose solution. In NAG treated animals, staining with alcian blue for polyanions in the peritoneal interstitium was significantly stronger than in rats dialyzed with glucose solution. Conclusions Chronic peritoneal dialysis with dialysis solution supplemented with N-acetylglucosamine causes accumulation of glycosaminoglycans in the peritoneal interstitium, which results in a change of peritoneal permeability.

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7

Kostović, Milica, Milica Cvetkovic, and Dejan Petrovic. "Gastrointestinal Non-Infectious Complications in Patients on Peritoneal Dialysis." Serbian Journal of Experimental and Clinical Research 17, no. 2 (June 1, 2016): 153–60. http://dx.doi.org/10.1515/sjecr-2015-0039.

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Abstract Gastrointestinal complications are common among patients on peritoneal dialysis. Risk factors for the development of gastrointestinal complications in this patient population include: toxic effects of uremic toxins, frequent use of nonsteroidal anti-inflammatory drugs, Helicobacter pylori infection, angiodysplasia, increased intra-abdominal pressure, use of bioincompatible solution for peritoneal dialysis, increased glucose in solutions for peritoneal dialysis, secondary hyperparathyroidism (hypercalcemia), a disorder of lipid metabolism (hypertriglyceridemia), and the duration of peritoneal dialysis treatment. The most important non-infectious gastrointestinal complications in patients on peritoneal dialysis are: gastrointestinal bleeding, herniation and leaking of the dialysate from the abdomen (increased intra-abdominal pressure), impaired lung function (intra-abdominal hypertension), acute pancreatitis, and encapsulating sclerosis of the peritoneum. Intra-abdominal hypertension is defined as IAP ≥ 12 mmHg. Pouring the peritoneal dialysis solution leads to increased intra-abdominal pressure, which results in the development of hernias, pleuro-peritoneal dialysate leakage (hydrothorax), and restrictive pulmonary dysfunction. Risk factors for the development of acute pancreatitis in this patient population include: uraemia, secondary hyperparathyroidism with hypercalcemia, hypertriglyceridemia, features of the peritoneal dialysis solution (osmolarity, acidity, glucose, chemical irritation, and calcium in the solution for peritoneal dialysis lead to “local hypercalcemia”), toxic substances from the dialysate, the bags and tubing, and peritonitis and treatment of peritonitis with antibiotics and anticoagulants. Encapsulating sclerosis of the peritoneum is rare and is the most serious complication of long-term peritoneal dialysis. It is characterized by thickening of the peritoneum, including cancer, and signs and symptoms of obstructive ileus. Diagnosis is based on clinical, laboratory and radiological parameters. Encapsulating sclerosis of the peritoneum can be indicated by an AR-CA-125 concentration of less than 33 U/min and a concentration of AR-IL-6 greater than 350 pg/min in the effluent of patients with ultrafiltration weakness. Treatment consists of stopping peritoneal dialysis, using anti-inflammatory (corticosteroids) and anticicatricial drugs (tamoxifen), while surgical treatment includes enterolysis and adhesiolysis.

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Djurdjevic-Mirkovic, Tatjana. "Peritoneal dialysis - experiences." Medical review 63, no. 11-12 (2010): 753–57. http://dx.doi.org/10.2298/mpns1012753d.

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Peritoneal dialysis is the method of treatment of terminal-stage chronic kidney failure. Nowadays, this method is complementary to haemodialysis. It is based on the principles of the diffusion of solutes and ultrafiltration of fluids across the peritoneal membrane, which acts as a filter. The dialysate is introduced into the peritoneum via the previously positioned peritoneal catheter. The peritoneal dialysis is carried out on daily basis, at home by the patient, and the ?exchange? is repeated 4-5 times during the 24 hours. The first steps in peritoneal dialysis at the Department for Haemodialysis of the Clinical Centre of Vojvodina date back to 1973. Until 1992, the patients were subjected to this program only sporadically. Since 1998 the peritoneal dialysis method has been performed at the Clinic for Nephrology and Clinical Immunology. In the period 1998-2008 ninety nine peritoneal catheters were placed. Chronic glomerulonephritis, nephroangiosclerosis and diabetes were identified as the most common causes of chronic renal failure. Two methods of catheter placement were applied: the standard open surgery method (majority of patients) and laparoscopy. Most of the patients were subjected to continuous ambulatory peritoneal dialysis, whereas four patients received automatic dialysis. Transplantation was performed in 10 patients, i.e. cadaveric transplantation and living-related donor transplantation, each in 5 patients. Peritoneal dialysis was available as a service outside our institution as well. A ten-year experience in peritoneal dialysis gained at our Centre has proved the advantages and qualities of this method, strongly supporting its wider application in the treatment of terminal-stage chronic kidney failure.

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Kowalewska, Paulina M., Peter J. Margetts, and Alison E. Fox-Robichaud. "Peritoneal Dialysis Catheter Increases Leukocyte Recruitment in the Mouse Parietal Peritoneum Microcirculation and Causes Fibrosis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 36, no. 1 (January 2016): 7–15. http://dx.doi.org/10.3747/pdi.2014.00211.

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♦BackgroundThe objective of this study was to examine the effects of a conventional dialysis solution and peritoneal catheter on leukocyte- endothelial cell interactions in the microcirculation of the parietal peritoneum in a subacute peritoneal dialysis (PD) mouse model.♦MethodsAn intraperitoneal (IP) catheter with a subcutaneous injection port was implanted into mice and, after a 2-week healing period, the animals were injected daily for 6 weeks with a 2.5% dextrose solution. Intravital microscopy (IVM) of the parietal peritoneum microcirculation was performed 4 hours after the last injection of the dialysis solution. Leukocyte-endothelial cell interactions were quantified and compared with catheterized controls without dialysis treatment and naïve mice.♦ ResultsThe number of rolling and extravascular leukocytes along with peritoneal fibrosis and neovascularization were significantly increased in the catheterized animals compared with naïve mice but did not significantly differ between the 2 groups of catheterized animals with sham injections or dialysis solution treatment.♦ConclusionThe peritoneal catheter implant increased leukocyte rolling and extravasation, peritoneal fibrosis and vascularization in the parietal peritoneum independently from the dialysis solution treatment.

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10

Hirahara, Ichiro, Eiji Kusano, Satoru Yanagiba, Yukio Miyata, Yasuhiro Ando, Shigeaki Muto, and Yasushi Asano. "Peritoneal Injury by Methylglyoxal in Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 26, no. 3 (May 2006): 380–92. http://dx.doi.org/10.1177/089686080602600317.

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Background Peritoneal dialysis (PD) is a common treatment for patients with reduced or absent renal function. Long-term PD leads to peritoneal injury with structural changes and functional decline, such as ultrafiltration loss. At worst, peritoneal injury leads to encapsulating peritoneal sclerosis, a serious complication of PD. Glucose degradation products contained in PD fluids contribute to the bioincompatibility of conventional PD fluids. Methylglyoxal (MGO) is an extremely toxic glucose degradation product. The present study examined the injurious effect of MGO on peritoneum in vivo. Methods Male Sprague–Dawley rats ( n = 6) were administered PD fluids (pH 5.0) containing 0, 0.66, 2, 6.6, or 20 mmol/L MGO every day for 21 days. On day 22, peritoneal function was estimated by the peritoneal equilibration test. Drained dialysate was analyzed for type IV collagen-7S, matrix metalloproteinase (MMP), and vascular endothelial growth factor (VEGF). Histological analysis was also performed. Results In rats receiving PD fluids containing more than 0.66 mmol/L MGO, peritoneal function decreased significantly and levels of type IV collagen-7S and MMP-2 in drained dialysate increased significantly. In the 20-mmol/L MGO-treated rats, loss of body weight, expression of VEGF, thickening of the peritoneum, and formation of abdominal cocoon were induced. MMP-2 and VEGF were produced by infiltrating cells in the peritoneum. Type IV collagen was detected in basement membrane of microvessels. Conclusion MGO induced not only peritoneal injury but also abdominal cocoon formation in vivo. The decline of peritoneal function may result from reconstitution of microvessel basement membrane or neovascularization.

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RADULESCU, Daniela, Dragos Adrian GEORGESCU, Andrei ANGELESCU, and Bogdan Florin GEAVLETE. "Abdominal Pseudocyst in the Vicinity of Calcified Renal Allograft in a Patient with Peritoneal Dialysis - Case Report." Medicina Moderna - Modern Medicine 27, no. 3 (September 26, 2020): 237–40. http://dx.doi.org/10.31689/rmm.2020.27.3.237.

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Abdominal pseudocysts are rarely reported in peritoneal dialysis and usually arise secondary to repeated dialysisrelated peritonitis. We present the case of a patient with end-stage renal disease treated for 9 years by continuous ambulatory peritoneal dialysis that developed an abdominal pseudocyst in the vicinity of the non-functional and calcifi ed renal graft. Because the adequacy of peritoneal dialysis was optimal, surgical removal of the invaginated peritoneum and closure of the breach allowed the patient to continue peritoneal dialysis treatment.

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Catalan, Marina Penélope, Jaime Esteban, Dolores Subirá, Jesús Egido, and Alberto Ortiz. "Inhibition of Caspases Improves Bacterial Clearance in Experimental Peritonitis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 23, no. 2 (March 2003): 123–26. http://dx.doi.org/10.1177/089686080302300205.

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Background Inhibition of caspases improves the antibacterial capacity of leukocytes cultured with peritoneal dialysis solutions, and improves the prognosis of septic, polymicrobial experimental peritonitis. Objective To test whether inhibition of caspases alters the evolution of peritonitis in the presence of peritoneal dialysis solution. Design 32 mice were assigned to therapy with either the pan-caspase inhibitor zVAD or vehicle for 48 hours following infection with Staphylococcus aureus, in the presence of lactate-buffered, 4.25% glucose peritoneal dialysis solution. 16 mice received vehicle in phosphate-buffered saline. Main Outcome Measure Number of bacteria recovered from the peritoneum at 48 hours. Results Peritoneal dialysis solution accelerated leukocyte apoptosis. zVAD decreased the number of apoptotic peritoneal leukocytes and the number of bacteria recovered from the peritoneum at 48 hours (zVAD 2.8 ± 0.3 vs vehicle 3.9 ± 0.2 log colony forming units of S. aureus, p = 0.007). Conclusions Inhibition of caspases accelerates peritoneal bacterial clearance in the presence of peritoneal dialysis solutions in vivo in the experimental setting. Inhibition of caspases should be explored as a mean to accelerate recovery following peritonitis in the clinical setting.

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Akimoto, Tetsu, Tomoyuki Yamazaki, Marina Kohara, Saki Nakagawa, Yoshihiko Kanai, Sayoko Izawa, Hisashi Yamamoto, et al. "Pleuroperitoneal Communication and Ovarian Cancer Complicating Peritoneal Dialysis: A Case Report of a Patient with End-Stage Kidney Disease." Clinical Medicine Insights: Case Reports 10 (January 1, 2017): 117954761773581. http://dx.doi.org/10.1177/1179547617735818.

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Peritoneal dialysis has been a widely accepted modality for treating end-stage kidney disease, but a regular dialysis schedule can be seriously disrupted by various comorbid conditions requiring surgical intervention. A 40-year-old woman who had been receiving peritoneal dialysis was sequentially but separately complicated by pleuroperitoneal communication and ovarian cancer. Despite the need for temporary interruption of her peritoneal dialysis schedule, it was successfully resumed after the relevant surgeries for each disease. Several concerns regarding overall postoperative dialytic management strategies, including how to deal with the peritoneal dialysis catheter during the postoperative period as well as how long peritoneal dialysis should be interrupted, which remain an unresolved issue in the field of nephrology, are also discussed.

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Dinarvand, Peyman, Seyed Mahdi Hassanian Mehr, and Alireza R. Rezaie. "Activated Protein C Prevents Peritoneal Fibrosis." Blood 124, no. 21 (December 6, 2014): 4229. http://dx.doi.org/10.1182/blood.v124.21.4229.4229.

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Abstract Patients with chronic kidney disease require dialysis (hemodialysis or peritoneal dialysis) for treatment. Peritoneal dialysis is an alternative to hemodialysis for the treatment of end-stage renal disease and is based on the use of the peritoneum as a permeable membrane where ultrafiltration and diffusion between dialysate and blood can take place across the peritoneum. Peritoneal fibrosis is one of the main complications of peritoneal dialysis and affects up to 20% of patients undergoing continuous ambulatory peritoneal fibrosis. The exact mechanism of this process has yet to be elucidated and no effective therapy for the problem has been established. APC is a natural vitamin-K dependent anticoagulant protease, which also has potent antiinflammatory activity. We hypothesized that the antiinflammatory function of APC may inhibit dialysis-mediated peritoneal fibrosis. To test this hypothesis, we generated a chlorhexidine gluconate (CG)-induced peritoneal fibrosis model by injecting CG to male C57BL/6 mice for 21 days with or without intraperitoneal administration of a low dose of recombinant APC (50 µg/kg/day bodyweight) one hour before injecting CG. At 10 and 21 days after injection, the mice were sacrificed and the parietal peritoneum and omentom were dissected for histological evaluation and for analysis of expression of inflammatory molecules. Strikingly, we discovered that APC inhibits the thickness of peritoneal fibrosis and potently inhibits the mRNA expression of TGF-b1, cytokeratins, a2-integrin, MMP-2 and 9 and also significantly increases the mRNA expression of TIMP-2 in peritoneal tissues of the experimental animals. We also discovered that APC significantly decreases the concentration of TGF-b1 and dramatically increases the concentration of tPA in peritoneal fluids. Taken together, our findings suggest that APC may have therapeutic potential in ameliorating dialysis-mediated peritoneal fibrosis. Disclosures No relevant conflicts of interest to declare.

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Mushahid, Ali, Farooq Aadil, Ghosh Soumyodhriti, Nagpure Amit, Sharma Deendayal, Mujalde Vikram Singh, Gupta Shilpi, and Mathur Praveen. "Peritoneal Dialysis Cannulations-Our Experience." Scholars Journal of Applied Medical Sciences 4, no. 6 (June 2016): 1878–80. http://dx.doi.org/10.21276/sjams.2016.4.6.2.

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Slobodan, Krstić, Trbojević-Stanković Jasna, Žunić Snežana, Jovanović Nataša, and Stojimirović Biljana. "Surgical Technique Using An Improvised Peritoneal Catheter In An Experimental Non-Uremic Rabbit Model Of Peritoneal Dialysis." Acta Veterinaria 65, no. 3 (September 1, 2015): 319–27. http://dx.doi.org/10.1515/acve-2015-0026.

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AbstractExperimental models have strongly contributed to the comprehension of the processes of peritoneal damage that take place during peritoneal dialysis treatment in human patients. A variety of peritoneal dialysis models have been developed, mostly using rats and rabbits.In this study we present the successful development of a custom-made improvised peritoneal catheter for an experimental non-uremic rabbit model of peritoneal dialysis.A detailed description of the surgical technique of peritoneal catheter implantation, care and removal is provided.This innovative approach to constructing a peritoneal catheter in rabbit animal model of peritoneal dialysis is easy, reproducible and inexpensive. The surgical technique applied provided adequate tissue samples for both light and electron microscopy.

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Santoboni, Alberto. "Peritoneal dialysis: Marginal dialysis?" Giornale di Tecniche Nefrologiche e Dialitiche 26, no. 5_suppl (January 2014): 46–47. http://dx.doi.org/10.5301/gtnd.2014.11915.

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Gabella, Paolo, Francesca Bermond, Cristiana Bagnis, and Martino Marangella. "Peritoneal dialysis: Marginal dialysis." Giornale di Tecniche Nefrologiche e Dialitiche 26, no. 5_suppl (January 2014): 44–45. http://dx.doi.org/10.5301/gtnd.2014.11966.

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Krishnan, Rajesh G., Milos V. Ognjanovic, Jean Crosier, and Malcolm G. Coulthard. "Acute Hydrothorax Complicating Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 27, no. 3 (May 2007): 296–99. http://dx.doi.org/10.1177/089686080702700315.

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Aim To determine whether gradually increasing the peritoneal dialysate fill volume from 10 to 40 mL/kg over 6 days, rather than commencing at 40 mL/kg, prevents hydrothorax in children and reverses it if present. Methods A review of children peritoneally dialyzed in a single center. Results During the 20 years beginning June 1985, 416 children were peritoneally dialyzed, of which 327 (79%) had acute and 89 had end-stage renal failure. Among 253 children who had gradually increasing fill volumes, none developed acute hydrothoraces, but 13/163 (8%) who began with 40 mL/kg cycles did ( p < 0.000, Fisher's exact test). These were diagnosed after a median (range) of 48 (6 – 72) hours and were predominantly right sided. Initially, we readily abandoned peritoneal dialysis; 2 were changed to hemodialysis. Subsequently, we found that peritoneal dialysis could be continued by using small volumes with the patients sitting up; cycle volumes were then gradually increased again. One pre-term baby died soon after developing an acute hydrothorax. One patient on chronic peritoneal dialysis developed an acute hydrothorax after forceful vomiting, but recovered after being dialyzed sitting up with low fills. Conclusion Acute hydrothorax can be prevented and treated using graduated cycle volumes, and is not a contraindication for peritoneal dialysis.

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Breborowicz, Andrzej, and Dimitrios G. Oreopoulos. "Is Normal Saline Harmful to the Peritoneum?" Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 25, no. 4_suppl (April 2005): 67–70. http://dx.doi.org/10.1177/089686080502504s09.

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♦ Background Normal saline (0.9% NaCl) is used during various abdominal surgical interventions and during peritoneal dialysis to rinse the peritoneal cavity. Although no clear clinical evidence exists for the bioincompatibility of normal saline, various experimental studies have suggested that 0.9% NaCl solution can initiate fibrosis of peritoneum. ♦ Material and Methods We review the data derived from in vitro and in vivo experimental studies demonstrating the cytotoxic effect of 0.9% NaCl and its ability to initiate peritoneal adhesions. ♦ Results Normal saline reduces the viability and fibrinolytic activity of peritoneal mesothelial cells. Use of normal saline to wash the peritoneal cavity during abdominal operations or after chronic peritoneal dialysis is more likely to produce adhesions than is no irrigation at all. Chronic exposure of the peritoneum to normal saline causes overgrowth of the connective tissue and formation of new blood vessels within that tissue. Conclusion ♦ Normal saline is a bioincompatible solution that predisposes to the formation of peritoneal adhesions and fibrosis of the peritoneum. A 0.9% NaCl solution should therefore not be used to rinse the peritoneal cavity after interruption of peritoneal dialysis.

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Gaggiotti, E., A. Arduini, M. Bonomini, G. Valentini, G. Sacchi, E. Sansoni, D. Salvo, and N. Di Paolo. "Prevention of Peritoneal Sclerosis: A New Proposal to Substitute Glucose with Carnitine Dialysis Solution (Biocompatibility Testing in Vitro and in Rabbits)." International Journal of Artificial Organs 28, no. 2 (February 2005): 177–87. http://dx.doi.org/10.1177/039139880502800215.

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Aim Commercial glucose peritoneal dialysis solutions expose the peritoneum to hyperosmolar glucose containing variable amounts of non-enzymic breakdown products of glucose. These solutions are toxic for the peritoneum. The aim of the present study is to compare in vitro and in vivo characteristics of a new dialysis solution containing carnitine, a naturally occurring compound, as substitute of glucose. Material and Methods We compared in vitro and in the rabbit a new peritoneal dialysis solution containing carnitine, with two standard bicarbonate glucose peritoneal dialysis solutions and a solution containing icodextrin. Results In vitro and in vivo the solution containing carnitine seems to be more biocompatible than standard glucose solutions and those containing icodextrin. Conclusions In our study the peritoneal dialysis solution containing carnitine seems to prevent the mesothelial changes observed with solutions containing glucose. Since carnitine has been extensively studied and seems to be well tolerated by hemodialysis patients, even at high doses for long periods, clinical trials in humans may be planned in the near future.

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Nakamoto, Hidetomo, Hiroe Imai, Rie Fukushima, Yuji Ishida, Yasuhiro Yamanouchi, and Hiromichi Suzuki. "Role of the Renin–angiotensin System in the Pathogenesis of Peritoneal Fibrosis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 28, no. 3_suppl (June 2008): 83–87. http://dx.doi.org/10.1177/089686080802803s17.

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⋄ Background Although the effects of angiotensin type 1 receptor blocker (ARB) have been studied, little is known about ARBs in hypertensive patients undergoing dialysis. In the present study, we evaluated the effect of an ARB, olmesartan medoxomil (CS866), on the progression of peritoneal fibrosis in peritoneal dialysis by examining its effect in a model of peritoneal fibrosis in hypertensive rats. ⋄ Materials and Methods W e all ocated 40 male Wistar rats with 2-kidney, 1-clip renovascular hypertension (2K1C-RVH) to 4 groups (each n = 10) that were dialyzed using various solutions for 42 days as follows: • Group I—10 mL pH 3.5 dialysis solution containing 1.35% glucose • Group II—10 mL pH 3.5 dialysis solution, plus oral administration of CS866 5 mg/kg daily • Group III—10 mL pH 3.5 dialysis solution, plus oral administration of the calcium channel blocker (CCB) amlodipine 3 mg/kg daily • Group IV—10 mL pH 7.0 dialysis solution Dialysis solution was injected every day for 42 days. ⋄ Results Treatment with CS866 and amlodipine induced a significant reduction of blood pressure in 2K1C-RVH rats. In rats treated with pH 3.5 dialysis solution, necropsy findings revealed features identical to those of encapsulating peritoneal sclerosis (EPS). The typical appearance was multiple surfaces covered with granulation tissue or fibrosic tissue or both. Multiple adhesions were present. Microscopic findings revealed that acidic dialysis solution induced peritoneal fibrosis and loss of mesothelium. Treatment with CS866 prevented the progression of peritoneal fibrosis and adhesions. However amlodipine did not improve the progression of peritoneal fibrosis and peritoneal adhesions. In CS866-treated rats, no signs of EPS were present. ⋄ Conclusions Long-term intraperitoneal exposure to acidic dialysis solution produced features typical of EPS. Acidic dialysis solution induces activation of the peritoneal renin– angiotensin system and progression of peritoneal fibrosis. For the peritoneum undergoing peritoneal dialysis, ARB protects against progression of peritoneal fibrosis and peritoneal adhesions.

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Korybalska, Katarzyna, Katarzyna Wieczorowska–Tobis, Alicja Polubinska, Justyna Wisniewska, James Moberly, Leo Martis, Andrzej Breborowicz, and Dimitrios G. Oreopoulos. "L-2-Oxothiazolidine-4-Carboxylate: An Agent that Modulates Lipopolysaccharide-Induced Peritonitis in Rats." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 22, no. 3 (May 2002): 293–300. http://dx.doi.org/10.1177/089686080202200301.

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Objective L-2-Oxothiazolidine-4-carboxylate (OTZ), a cysteine precursor, is a substrate for intracellular glutathione synthesis. As shown previously, OTZ prevents free-radical induced cellular damage during in vitro simulation of peritoneal dialysis. In the present study, we examined the effect of adding OTZ to peritoneal dialysis solution on peritoneal function and structure during lipopolysaccharide (LPS)-induced peritonitis in rats. In addition, we studied the effects of pretreatment with OTZ (given orally) on the effects of LPS-induced peritonitis in rats. Methods Peritonitis was induced in rats by adding LPS (5 μg/mL) to the dialysis fluid. For acute experiments, rats were exposed to a single infusion of dialysis solution containing LPS or to LPS plus 5 mmol/L OTZ; peritoneal cell counts and permeability were determined after 4 hours. Alternatively, rats were pretreated with OTZ added to the drinking water (0.1%) for 10 days prior to infusion of LPS. For chronic experiments, peritoneal dialysis was performed over a 3-week period in rats with implanted peritoneal catheters. On days 8, 9, and 10 of the experiment, the rats were infused intraperitoneally with solution containing LPS (5 μg/mL), or LPS plus 5 mmol/L OTZ, to induce acute peritonitis. At the end of dialysis (10 days after the episodes of peritonitis), peritoneal function was assessed using a peritoneal equilibration test (PET), and peritoneal biopsies were taken to assess effects on peritoneal morphology. Results In the acute experiments, exposure to LPS led to increased peritoneal cell counts (+61% vs control, p < 0.05) and enhanced permeability of the peritoneum, leading to a loss in ultrafiltration (–63%, p < 0.0005). The glutathione concentration in peritoneal leukocytes also decreased during acute peritonitis (–31%, p < 0.05). During LPS-induced peritonitis, OTZ prevented the increase in dialysate cell count and the decrease in cellular glutathione content. Simultaneous administration of OTZ did not prevent the increased peritoneal permeability induced by LPS. However, in rats pretreated with OTZ, LPS-induced permeability to protein was significantly lower than in the nontreated animals (0.049 ± 0.011 vs 0.087 ± 0.034, p < 0.05). In the chronic experiments, LPS-induced peritonitis did not lead to any functional differences in peritoneal transport at the end of 3 weeks of dialysis. However, LPS-induced peritonitis led to increased thickness of the peritoneum and neovascularization within peritoneal interstitium compared to peritonitis-free animals. In contrast to the LPS-treated animals, the peritoneum of the rats exposed to LPS in the presence of OTZ was of a thickness similar to that in the control rats. Conclusion Supplementation of dialysis fluid with OTZ prevented changes in cellular glutathione levels and dialysate cell counts during acute peritonitis in rats. During chronic dialysis in rats exposed to intermittent peritonitis episodes, OTZ prevented increased thickening and neovascularization of the peritoneum. Our results suggest this may help to protect the peritoneal membrane during episodes of peritonitis.

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ITO, TAKAFUMI, NORIAKI YORIOKA, MASAO YAMAMOTO, KATSUKO KATAOKA, and MICHIO YAMAKIDO. "Effect of Glucose on Intercellular Junctions of Cultured Human Peritoneal Mesothelial Cells." Journal of the American Society of Nephrology 11, no. 11 (November 2000): 1969–79. http://dx.doi.org/10.1681/asn.v11111969.

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Abstract. During continuous ambulatory peritoneal dialysis, the peritoneum is directly and continuously exposed to unphysiologic peritoneal dialysis fluid; the resulting mesothelial damage has been suggested to cause loss of ultrafiltration and dialysis efficacy. The present study investigated the effect of a high glucose concentration on cultured human peritoneal mesothelial cells to clarify the cause of decreased dialysis efficacy during prolonged peritoneal dialysis. High glucose caused a concentration-dependent decrease in cell proliferation, damage to the intercellular junctions, and excess production of transforming growth factor-β (TGF-β). The levels of intercellular junctional proteins (ZO-1, E-cadherin, and β-catenin) were decreased, and immuno-staining by anti—ZO-1 and anti— β-catenin antibodies became weaker and often discontinuous along the cell contour. Mannitol had similar but weaker effects at the same osmolality, and an anti—TGF-β neutralizing antibody reduced the effects of high glucose. Therefore, these effects were induced not only by glucose itself but also by hyperosmolality and by a glucose-induced increase of TGF-β. These findings suggest that the peritoneal mesothelium is damaged by prolonged peritoneal dialysis using high glucose dialysate and that impairment of the intercellular junctions of peritoneal mesothelial cells by high glucose dialysate induces peritoneal hyperpermeability and a progressive reduction in dialysis efficacy.

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Pérez-Díaz, Vicente, Alfonso Pérez-Escudero, Sandra Sanz-Ballesteros, Guadalupe Rodríguez-Portela, Susana Valenciano-Martínez, Sofía Palomo-Aparicio, Esther Hernández-García, Luisa Sánchez-García, Raquel Gordillo-Martín, and Hortensia Marcos-Sánchez. "A New Method to Increase Ultrafiltration in Peritoneal Dialysis: Steady Concentration Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 36, no. 5 (September 2016): 555–61. http://dx.doi.org/10.3747/pdi.2016.00007.

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Background Peritoneal dialysis (PD) has limited power for liquid extraction (ultrafiltration), so fluid overload remains a major cause of treatment failure. Methods We present steady concentration peritonal dialysis (SCPD), which increases ultrafiltration of PD exchanges by maintaining a constant peritoneal glucose concentration. This is achieved by infusing 50% glucose solution at a constant rate (typically 40 mL/h) during the 4-hour dwell of a 2-L 1.36% glucose exchange. We treated 21 fluid overload episodes on 6 PD patients with high or average-high peritoneal transport characteristics who refused hemodialysis as an alternative. Each treatment consisted of a single session with 1 to 4 SCPD exchanges (as needed). Results Ultrafiltration averaged 653 ± 363 mL/4 h — twice the ultrafiltration of the peritoneal equilibration test (PET) (300 ± 251 mL/4 h, p < 0.001) and 6-fold the daily ultrafiltration (100 ± 123 mL/4 h, p < 0.001). Serum and peritoneal glucose stability and dialysis efficacy were excellent (glycemia 126 ± 25 mg/dL, peritoneal glucose 1,830 ± 365 mg/dL, D/P creatinine 0.77 ± 0.08). The treatment reversed all episodes of fluid overload, avoiding transfer to hemodialysis. Ultrafiltration was proportional to fluid overload ( p < 0.01) and inversely proportional to final peritoneal glucose concentration ( p < 0.05). Conclusion This preliminary clinical experience confirms the potential of SCPD to safely and effectively increase ultrafiltration of PD exchanges. It also shows peritoneal transport in a new dynamic context, enhancing the influence of factors unrelated to the osmotic gradient.

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Tomo, Tadashi. "Peritoneal Dialysis Solutions Low in Glucose Degradation Products—evidence for Clinical Benefits." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 28, no. 3_suppl (June 2008): 123–27. http://dx.doi.org/10.1177/089686080802803s23.

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In Japan, two types of new peritoneal dialysis fluid (PDF) are ordinarily used: two-chambered PDF, and icodextrin PDF. Two-chambered PDF has several biocompatible characteristics, one being low glucose degradation products (GDPs). Of the several GDPs in PDF, 3,4-dideoxyglucosone-3-ene (3,4-DGE) is thought to be strongly associated with the cytotoxicity of standard PDF. Using a PDF low in GDPs may reduce exposure of the peritoneum to 3,4-DGE, helping to preserve peritoneal function in PD patients. Additionally, use of a PDF low in GDPs may reduce plasma levels of advanced glycosylation end-products in PD patients, a change that may help to preserve vascular function in PD patients. Peritoneal rest for 24 hours after exposure to a PDF with low GDPs improves the activity of human peritoneal mesothelial cells. As compared with the use of standard PDF, the use of low-GDP PDF in combination therapy (peritoneal dialysis plus hemodialysis) may more effectively preserve peritoneal function. The new PDF low in GDPs has bio-compatible characteristics relative to peritoneum and system that may help to preserve peritoneal function or reduce complications such as atherosclerosis or dialysis-related amyloidosis in dialysis patients.

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Kazancioglu, Rumeyza. "Peritoneal Defense Mechanisms—the Effects of New Peritoneal Dialysis Solutions." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 29, no. 2_suppl (February 2009): 198–201. http://dx.doi.org/10.1177/089686080902902s40.

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It remains to be determined whether the peritoneal dialysis procedure induces abnormalities in the normal host defenses of the abdominal cavity and whether these perturbations are important in the pathogenesis of peritonitis. The peritoneum is a smooth membrane that lines the abdominal cavity and participates in the diffusion of water and solutes during peritoneal dialysis. The diaphragmatic lymphatic uptake and the opsonization of micro-organisms, with phagocytosis and killing by peritoneal macrophages, mesothelial cells, lymphocytes, polymorphonuclear leukocytes, and newly defined proteins such as defensins, play a combined role in the peritoneal host defense. Because the composition of earlier peritoneal dialysis fluids is clearly non-physiologic, continuous exposure of peritoneal cells to these solutions may result in an impairment of the local peritoneal host defense mechanisms. However, with the newer solutions, it has been shown that peritoneal defense mechanisms may improve.

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Redmond, Avril, and Elizabeth Doherty. "Peritoneal dialysis." Nursing Standard 19, no. 40 (June 15, 2005): 55–66. http://dx.doi.org/10.7748/ns.19.40.55.s55.

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Redmond, Avril, and Elizabeth Doherty. "Peritoneal dialysis." Nursing Standard 19, no. 40 (June 15, 2005): 55–65. http://dx.doi.org/10.7748/ns2005.06.19.40.55.c3893.

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Gould, Caroline. "Peritoneal dialysis." Nursing Standard 20, no. 3 (September 28, 2005): 67–68. http://dx.doi.org/10.7748/ns.20.3.67.s73.

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Gokal, Ram. "Peritoneal Dialysis." Drugs & Aging 17, no. 4 (October 2000): 269–82. http://dx.doi.org/10.2165/00002512-200017040-00003.

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Teitelbaum, Isaac. "Peritoneal Dialysis." New England Journal of Medicine 385, no. 19 (November 4, 2021): 1786–95. http://dx.doi.org/10.1056/nejmra2100152.

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Fung, Winston Wing-Shing, Jack Kit-Chung Ng, and Philip Kam-Tao Li. "Peritoneal Dialysis." Nephrology Self-Assessment Program 20, no. 1 (August 2021): 19–34. http://dx.doi.org/10.1681/nsap.2021.20.1.2.

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Taskapan, Hulya, Olof Heimburger, Cengiz Utas, and Paul Tam. "Peritoneal Dialysis." International Journal of Nephrology 2011 (2011): 1. http://dx.doi.org/10.4061/2011/218974.

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Twardowski, Zbylut J. "Peritoneal dialysis." Postgraduate Medicine 85, no. 5 (April 1989): 161–82. http://dx.doi.org/10.1080/00325481.1989.11700663.

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Lum, Gary M. "Peritoneal dialysis." Critical Care Medicine 27, no. 11 (November 1999): 2595–96. http://dx.doi.org/10.1097/00003246-199911000-00058.

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Kratochwill, K., M. Boehm, R. Herzog, L. Kuster, A. Gleiss, C. Aufricht, A. Vychytil, et al. "PERITONEAL DIALYSIS." Nephrology Dialysis Transplantation 29, suppl 3 (May 1, 2014): iii16—iii18. http://dx.doi.org/10.1093/ndt/gfu114.

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HATHAWAY, LISA. "Peritoneal dialysis." Nursing Made Incredibly Easy! 2, no. 5 (September 2004): 55–58. http://dx.doi.org/10.1097/00152258-200409000-00011.

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Chaimovitz, Cidio. "Peritoneal dialysis." Kidney International 45, no. 4 (April 1994): 1226–40. http://dx.doi.org/10.1038/ki.1994.163.

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&NA;. "PERITONEAL DIALYSIS." ASAIO Journal 42, no. 2 (April 1996): 102–4. http://dx.doi.org/10.1097/00002480-199642020-00022.

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Choi, Peter, and Edwina A. Brown. "Peritoneal Dialysis." Medicine 31, no. 6 (June 2003): 70–73. http://dx.doi.org/10.1383/medc.31.6.70.28314.

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Burkart, John M. "Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 17, no. 3_suppl (June 1997): 5–7. http://dx.doi.org/10.1177/089686089701703s01.

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These presentations highlighted some of the current research needs in peritoneal dialysis. They are not meant to eclipse other important issues, such as adequacy and nutrition. These needs have become apparent as the therapy has evolved and progressed. They in fact are a testament to the increasing acceptance, use, and development of the therapy and suggest that there is potential for even further advancement for the therapy of peritoneal dialysis in the future.

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&NA;. "PERITONEAL DIALYSIS." ASAIO Journal 43, no. 2 (March 1997): 79–81. http://dx.doi.org/10.1097/00002480-199743020-00014.

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&NA;. "PERITONEAL DIALYSIS." ASAIO Journal 44, no. 2 (March 1998): 78A. http://dx.doi.org/10.1097/00002480-199803000-00291.

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&NA;. "PERITONEAL DIALYSIS." ASAIO Journal 44, no. 2 (March 1998): 78A. http://dx.doi.org/10.1097/00002480-199803000-00292.

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&NA;. "PERITONEAL DIALYSIS." ASAIO Journal 44, no. 2 (March 1998): 78A. http://dx.doi.org/10.1097/00002480-199803000-00293.

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&NA;. "PERITONEAL DIALYSIS." ASAIO Journal 44, no. 2 (March 1998): 79A. http://dx.doi.org/10.1097/00002480-199803000-00294.

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&NA;. "PERITONEAL DIALYSIS." ASAIO Journal 44, no. 2 (March 1998): 79A. http://dx.doi.org/10.1097/00002480-199803000-00295.

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&NA;. "PERITONEAL DIALYSIS." ASAIO Journal 44, no. 2 (March 1998): 79A. http://dx.doi.org/10.1097/00002480-199803000-00296.

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&NA;. "PERITONEAL DIALYSIS." ASAIO Journal 44, no. 2 (March 1998): 79A. http://dx.doi.org/10.1097/00002480-199803000-00297.

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