Peritoneal dialysis and inflammation

Velloso, Marina Souza Silva; Otoni, Alba; Sabino, Adriano de Paula; Castro, Whocely Victor de; Pinto, Sérgio Wyton Lima; Marinho, Maria Aparecida Silva; Rios, Danyelle Romana Alves

doi:10.1016/j.cca.2013.12.003

Cited by 29 publications

(23 citation statements)

References 30 publications

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“…However, long-term PD therapy promotes progressive peritoneal membrane damage and subsequently leads to peritoneal fibrosis [3,4]. The progression of peritoneal fibrosis causes ultrafiltration failure and encapsulating peritoneal sclerosis, which limits the lifelong use of PD therapy [3,5].…”

Section: Itraconazole Attenuates Peritoneal Fibrosis Through Its Effementioning

confidence: 99%

Itraconazole Attenuates Peritoneal Fibrosis Through Its Effect on the Sonic Hedgehog Signaling Pathway in Mice

et al. 2018

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Background: Peritoneal fibrosis is a devastating complication of peritoneal dialysis. However, its precise mechanism is unclear, and specific treatments have not yet been established. Recent evidence suggests that the sonic hedgehog (SHH) signaling pathway is involved in tissue fibrogenesis. Drugs that inhibit this pathway are emerging in the field of anti-fibrosis therapy. Itraconazole, an anti-fungal agent, was also recently recognized as an inhibitor of the SHH signaling pathway. In this study, we used a mouse model to investigate whether the SHH signaling pathway is involved in the development of peritoneal fibrosis and the effects of itraconazole on peritoneal fibrosis. Methods: Peritoneal fibrosis was induced by intraperitoneal (IP) injection of 0.1% chlorhexidine gluconate (CG) solution every other day for 4 weeks, with or without itraconazole treatment (20 mg/kg, IP injection on a daily basis). Male C57BL/6 mice were divided into 4 groups: saline group, saline plus itraconazole group, CG group, and CG plus itraconazole group. Isotonic saline was administered intraperitoneally to the control group. The peritoneal tissues were evaluated for histological changes, expression of fibrosis markers, and the main components of the SHH signaling pathway. Results: Peritoneal thickening was evident in the CG group and was significantly decreased by itraconazole administration (80.4 ± 7.7 vs. 28.2 ± 3.8 µm, p < 0.001). The expression of the following SHH signaling pathway components was upregulated in the CG group and suppressed by itraconazole treatment: SHH, patched, smoothened, and glioma-associated oncogene transcription factor 1. The IP injection of CG solution increased the expression of fibrosis markers such as α-smooth muscle actin and transforming growth factor-β1 in the peritoneal tissues. Itraconazole treatment significantly decreased the expression of these markers. Conclusion: Our study provides the first evidence that the SHH signaling pathway may be implicated in peritoneal fibrosis. It also demonstrates that itraconazole treatment has protective effects on peritoneal fibrosis through the regulation of the SHH signaling pathway. These findings suggest that blockage of the SHH signaling pathway is a potential therapeutic strategy for peritoneal fibrosis.

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Section: Itraconazole Attenuates Peritoneal Fibrosis Through Its Effementioning

confidence: 99%

Itraconazole Attenuates Peritoneal Fibrosis Through Its Effect on the Sonic Hedgehog Signaling Pathway in Mice

et al. 2018

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“…Research on biocompatibility focuses both on technical progress, thereby improving the quality of materials [2,3,4], and on exploration of mechanisms underlying CKD- and dialysis-related complications [5,6,7,8]. However, ideal dialyzers, peritoneal fluids or markers of biocompatibility have not been found so far.…”

Section: Introductionmentioning

confidence: 99%

“…Both hemodialysis (HD) and peritoneal dialysis (PD) influence a variety of phenomena, such as inflammation, matrix remodeling, apoptosis or oxidative stress [1,5,6,7,9,10]. Among these, the endothelial activation, chronic inflammatory process and matrix remodeling form a combination that is responsible for accelerated atherosclerosis, which is one of the CKD hallmarks, aggravated by dialysis commencement.…”

Section: Introductionmentioning

confidence: 99%

The Impact of Dialysis Modality on Novel Markers of Stress Reaction, Matrix Remodeling and Endothelial Damage in Children on Chronic Dialysis

Musiał

Zwołińska²

2014

Blood Purif

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Background/Aims: Dialysis triggers stress reaction, matrix remodeling and endothelial damage, but little is known about the changes it induces on selected heat shock proteins (Hsp90α), adhesion molecules (E-cadherin, sE-selectin), metalloproteinases (MMP-8) and their extracellular inducer (EMMPRIN). The aim of this study was to assess serum concentrations of the above-mentioned parameters in children on chronic dialysis. Methods: 19 patients on hemodialysis (HD), 22 children on peritoneal dialysis (PD) and 30 age-matched controls were examined. Serum concentrations of parameters were assessed by ELISA. Results: Hsp90α, MMP-8, EMMPRIN and E-cadherin concentrations were significantly increased in children on dialysis vs. controls and higher levels were in HD than PD patients. There was no difference in the level of sE-selectin between HD and PD modalities. A single HD session diminished Hsp90α, MMP-8, EMMPRIN and E-cadherin values, but had no impact on sE-selectin levels. Conclusions: Hemodialysis evokes stress reaction, matrix and endothelium destruction, to a greater extent than peritoneal dialysis. Single hemodialysis influences circulating cells rather than endothelial cells.

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“…A series of studies have focused on its mechanisms, however, the cause of systematic inflammation in PD is not completely understood [64]. Patients undergoing CAPD have increased levels of pro-inflammatory cytokines, including IL-1 β , IL-6, TNF-α, and TGF-β, in both PD effluent and plasma [65]. The serum leptin level increases during acute infection, and even after apparent remission of peritonitis, in response to IL-1 and TNF-α [66].…”

Section: Introductionmentioning

confidence: 99%

Angiogenesis and Inflammation in Peritoneal Dialysis: The Role of Adipocytes

Shi

Sheng³

2017

Kidney Blood Press Res

984

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Chronic inflammation and angiogenesis are the most common complications in patients undergoing maintenance peritoneal dialysis (PD), resulting in progressive peritoneum remolding and, eventually, utrafiltration failure. Contributing to the deeper tissue under the peritoneal membrane, adipocytes play a neglected role in this process. Some adipokines act as inflammatory and angiogenic promoters, while others have the opposite effects. Adipokines, together with inflammatory factors and other cytokines, modulate inflammation and neovascularization in a coordinated fashion. This review will also emphasize cellular regulators and their crosstalk in long-term PD. Understanding the molecular mechanism, targeting changes in adipocytes and regulating adipokine secretion will help extend therapeutic methods for preventing inflammation and angiogenesis in PD.

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Peritoneal dialysis and inflammation

Cited by 29 publications

References 30 publications

Itraconazole Attenuates Peritoneal Fibrosis Through Its Effect on the Sonic Hedgehog Signaling Pathway in Mice

Itraconazole Attenuates Peritoneal Fibrosis Through Its Effect on the Sonic Hedgehog Signaling Pathway in Mice

The Impact of Dialysis Modality on Novel Markers of Stress Reaction, Matrix Remodeling and Endothelial Damage in Children on Chronic Dialysis

Angiogenesis and Inflammation in Peritoneal Dialysis: The Role of Adipocytes

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