Water transport across the peritoneal membrane

Devuyst, Olivier; Rippe, Bengt

doi:10.1038/ki.2013.250

Cited by 81 publications

(76 citation statements)

References 50 publications

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“…44,45 The loss of AQP1-mediated free-water transport has been suggested as a potential cause of UF failure in long-term PD patients. 46,47 Admittedly, this study does not allow ruling out a dysfunction or biochemical modification of AQP1.…”

Section: Discussionmentioning

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

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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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Section: Discussionmentioning

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

Self Cite

105

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“…Water flux across the endothelium occurs mainly via paracellular pathways accounted for by small pores permeable to water and small solutes and by large pores permeable to water and macromolecules and by a transcellular pathway accounted for by aquaporin 1 (AQP1) (17). To estimate the contribution of these two pathways, we measured water fluxes before and after inhibition of AQP1 with mercury chloride.…”

Section: Nephrotic Syndrome (Ns)mentioning

confidence: 99%

Oxidative Stress and Nuclear Factor κB (NF-κB) Increase Peritoneal Filtration and Contribute to Ascites Formation in Nephrotic Syndrome

Udwan

Brideau

Fila

et al. 2016

Journal of Biological Chemistry

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Water accumulation in the interstitium (edema) and the peritoneum (ascites) of nephrotic patients is classically thought to stem from the prevailing low plasma albumin concentration and the decreased transcapillary oncotic pressure gradient. However, several clinical and experimental observations suggest that it might also stem from changes in capillary permeability. We addressed this hypothesis by studying the peritoneum permeability of rats with puromycin aminonucleosideinduced nephrotic syndrome. The peritoneum of puromycin aminonucleoside rats displayed an increase in the water filtration coefficient of paracellular and transcellular pathways, and a decrease in the reflection coefficient to proteins. It also displayed oxidative stress and subsequent activation of NF-B. Scavenging of reactive oxygen species and inhibition of NF-B prevented the changes in the water permeability and reflection coefficient to proteins and reduced the volume of ascites by over 50%. Changes in water permeability were associated with the overexpression of the water channel aquaporin 1, which was prevented by reactive oxygen species scavenging and inhibition of NF-B. In conclusion, nephrotic syndrome is associated with an increased filtration coefficient of the peritoneum and a decreased reflection coefficient to proteins. These changes, which account for over half of ascite volume, are triggered by oxidative stress and subsequent activation of NF-B. Nephrotic syndrome (NS)3 is a multifactorial glomerular disease defined by massive proteinuria and hypoalbuminemia. Irrespective of its etiology, NS is commonly associated with renal retention of sodium leading to the generation of ascites and/or edema (1, 2). Association of sodium retention with edema rather than with hypertension suggests that fluid flux across the capillary endothelium increases, and accordingly the capillary filtration capacity is 2-fold higher in nephrotic patients (3). Classically, this increase is thought to stem from hypoalbuminemia and a decreased oncotic gradient across the capillary wall. However, several observations militate against this theory: 1) the transcapillary gradient of oncotic pressure is almost unchanged in nephrotic patients (4, 5); 2) during steroid-induced remission of nephrotic syndrome, natriuresis resumes and edema decreases before normalization of serum albumin levels (6); and 3) diuretic treatments reduce edema without significantly changing the oncotic pressure gradient (5). Consequently, a new concept has emerged according to which the asymmetry of volume expansion in NS results from alterations of the intrinsic properties of the endothelial filtration barrier, i.e. its water permeability and/or its reflection coefficient to proteins. However, this hypothesis has not been demonstrated experimentally, and neither the molecular basis of these capillary alterations nor their connection to proteinuria and/or hypoalbuminemia is elucidated. Several studies have highlighted the pathophysiological importance of reactive oxygen species (ROS) in ...

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“…Conversely, excessive activation of this pathway causes inappropriate antidiuresis (1), and excessive production of cAMP downstream of the V2 receptor has been associated with cyst progression in autosomal dominant polycystic kidney disease (2). Although AVP is not primarily involved in the peritoneal membrane, the osmotic transport of water through aquaporins is essential in mediating ultrafiltration in peritoneal dialysis (3).…”

Section: Martin Wilkie Editor-in-chiefmentioning

confidence: 99%

Classification, Measurement, and Debate—The Science of Peritoneal Dialysis

Wilkie¹

2013

Perit Dial Int

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Water transport across the peritoneal membrane

Cited by 81 publications

References 50 publications

Interstitial Fibrosis Restricts Osmotic Water Transport in Encapsulating Peritoneal Sclerosis

Interstitial Fibrosis Restricts Osmotic Water Transport in Encapsulating Peritoneal Sclerosis

Oxidative Stress and Nuclear Factor κB (NF-κB) Increase Peritoneal Filtration and Contribute to Ascites Formation in Nephrotic Syndrome

Classification, Measurement, and Debate—The Science of Peritoneal Dialysis

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