The natural course of peritoneal membrane biology during peritoneal dialysis

Williams, Julie; Craig, Kathrine Jane; Ruhland, Christopher Von; Topley, Nicholas; Williams, Geraint T.

doi:10.1046/j.1523-1755.2003.08805.x

Cited by 109 publications

(103 citation statements)

References 39 publications

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“…1A) has a relatively large surface area (~1 m2) (3), a high degree of capillarization, and a relatively high blood flow (100-150 mL/min) in adults (4)(5)(6). The compact zone of the visceral peritoneum (that forms most of the peritoneal surface area) is about 20 m-thick in PD patients, whereas the parietal peritoneum can be thickened up to 500 m in long-term PD patients, compared to 50 m in controls (7). The blood capillaries are distributed in a thin interstitium where their density is relatively high: for 1 m2 of peritoneal surface area and 200 m tissue depth, the total available capillary surface area is <2 m2 (8).…”

Section: Structure Of the Peritoneal Membranementioning

confidence: 99%

Water transport across the peritoneal membrane

Devuyst

Rippe

2014

Kidney International

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Peritoneal dialysis involves diffusive and convective transports and osmosis through the highly vascularized peritoneal membrane. The capillary endothelium offers the rate-limiting hindrance for solute and water transport. It can be functionally described in terms of a three-pore model including transcellular, ultrasmall pores responsible for free-water transport during crystalloid osmosis. Several lines of evidence have demonstrated that the water channel aquaporin-1 (AQP1) corresponds to the ultrasmall pore located in endothelial cells. Studies in Aqp1 mice have shown that deletion of AQP1 is reflected by a 50% decrease in ultrafiltration and a disappearance of the sodium sieving. Haploinsufficiency in AQP1 is also reflected by a significant attenuation of water transport. Conversely, studies in a rat model and in PD patients have shown that the induction of AQP1 in peritoneal capillaries by corticosteroids is reflected by increased water transport and ultrafiltration, without affecting the osmotic gradient and small-solute transport. Recent data have demonstrated that a novel agonist of AQP1, predicted to stabilize the open-state conformation of the channel, modulates water transport and improves ultrafiltration. Whether increasing the expression of AQP1 or gating the already existing channels would be clinically useful in PD patients remains to be investigated. ABSTRACTPeritoneal dialysis involves diffusive and convective transports and osmosis through the highly vascularized peritoneal membrane. The capillary endothelium offers the rate-limiting hindrance for solute and water transport. It can be functionally described in terms of a threepore model including transcellular, ultrasmall pores responsible for free-water transport during crystalloid osmosis. Several lines of evidence have demonstrated that the water channel aquaporin-1 (AQP1) corresponds to the ultrasmall pore located in endothelial cells. Studies in Aqp1 mice have shown that deletion of AQP1 is reflected by a 50% decrease in ultrafiltration and a disappearance of the sodium sieving. Haplo-insufficiency in AQP1 is also reflected by a significant attenuation of water transport. Conversely, studies in a rat model and in PD patients have shown that the induction of AQP1 in peritoneal capillaries by corticosteroids is reflected by increased water transport and ultrafiltration, without affecting the osmotic gradient and small solute transport. Recent data have demonstrated that a novel agonist of AQP1, predicted to stabilize the open state conformation of the channel, modulates water transport and improves ultrafiltration. Whether increasing the expression of AQP1 or gating the already existing channels would be clinically useful in PD patients remains to be investigated.The development of peritoneal dialysis (PD) as a successful therapy for patients with end stage renal disease has been paralleled by the need to understand the transport mechanisms operating in the peritoneal membrane. Functional alterations in the dialysis capacity of the...

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Section: Structure Of the Peritoneal Membranementioning

confidence: 99%

Water transport across the peritoneal membrane

Devuyst

Rippe

2014

Kidney International

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“…[3][4][5] Prolonged exposure of the peritoneal membrane to nonphysiologic dialysis solutions leads to vascular proliferation, vasculopathy, and peritoneal fibrosis, with ensuing loss of ultrafiltration (UF) capacity resulting from enlarged vascular surface area, faster peritoneal solute transport rate, and early dissipation of the osmotic gradient. 3,4,[6][7][8][9] Encapsulating peritoneal sclerosis (EPS) is an exaggerated fibrogenic response of the peritoneal membrane, leading to encapsulation of the bowels and intestinal obstruction. This entity constitutes the most severe complication of PD (for review, see Korte et al 10 ).…”

mentioning

confidence: 99%

Interstitial Fibrosis Restricts Osmotic Water Transport in Encapsulating Peritoneal Sclerosis

Morelle

Sow

Hautem

et al. 2015

Journal of the American Society of Nephrology

105

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Encapsulating peritoneal sclerosis (EPS) is a rare but severe complication of peritoneal dialysis (PD) characterized by extensive fibrosis of the peritoneum. Changes in peritoneal water transport may precede EPS, but the mechanisms and potential predictive value of that transport defect are unknown. Among 234 patients with ESRD who initiated PD at our institution over a 20-year period, 7 subsequently developed EPS. We evaluated changes in peritoneal transport over time on PD in these 7 patients and in 28 matched controls using 3.86% glucose peritoneal equilibration tests. Compared with long-term PD controls, patients with EPS showed early loss of ultrafiltration capacity and sodium sieving before the onset of overt EPS. Multivariate analysis revealed that loss of sodium sieving was the most powerful predictor of EPS. Compared with long-term PD control and uremic peritoneum, EPS peritoneum showed thicker submesothelial fibrosis, with increased collagen density and a greater amount of thick collagen fibers. Reduced osmotic conductance strongly correlated with the degree of peritoneal fibrosis, but not with vasculopathy. Peritoneal fibrosis was paralleled by an excessive upregulation of vascular endothelial growth factor and endothelial nitric oxide synthase, but the expression of endothelial aquaporin-1 water channels was unaltered. Our findings suggest that an early and disproportionate reduction in osmotic conductance during the course of PD is an independent predictor of EPS. This functional change is linked to specific alterations of the collagen matrix in the peritoneal membrane of patients with EPS, thereby validating the serial three-pore membrane/fiber matrix and distributed models of peritoneal transport.

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“…Although the parietal peritoneal surface and the underlying microcirculation are major functional contributors to the dialysis membrane (14)(15)(16)(17) and greater pathological changes occur in the parietal peritoneum compared with the visceral peritoneum in the same PD patients (18), reports on the effects of PD fluids and catheter on leukocyte recruitment in this layer are lacking in the current literature. The objective of this study was to examine the effects of a conventional PD solution and the peritoneal catheter implant on leukocyte-endothelial cell interactions in the parietal peritoneum microcirculation.…”

Section: P Eritonitis Is a Major Problem In Peritoneal Dialysis (Pd)mentioning

confidence: 99%

Peritoneal Dialysis Catheter Increases Leukocyte Recruitment in the Mouse Parietal Peritoneum Microcirculation and Causes Fibrosis

2016

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ORIGINAL ARTICLES♦ Background: The 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. ♦ Methods: An 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.

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The natural course of peritoneal membrane biology during peritoneal dialysis

Cited by 109 publications

References 39 publications

Water transport across the peritoneal membrane

Water transport across the peritoneal membrane

Interstitial Fibrosis Restricts Osmotic Water Transport in Encapsulating Peritoneal Sclerosis

Peritoneal Dialysis Catheter Increases Leukocyte Recruitment in the Mouse Parietal Peritoneum Microcirculation and Causes Fibrosis

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