Analysis of fluid transport pathways and their determinants in peritoneal dialysis patients with ultrafiltration failure

Paříková, Alena; Smit, Watske; Struijk, Dirk G.; Krediet, Raymond T.

doi:10.1038/sj.ki.5001861

Cited by 74 publications

(83 citation statements)

References 22 publications

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“…In addition, in the multivariate analysis of the peritonitis subgroups there was an association between membrane ultrafiltration capacity as well as PSTR in patients who had infections. Cause and effect cannot be inferred from this type of analysis, but this would be in line with more severe membrane injury causing reduced osmotic conductance and Pcl through more severe fibrosis (3,(20)(21)(22). This study's failure to detect a relationship between Pcl and comorbidity on multivariate analysis deserves comment.…”

Section: Discussionmentioning

confidence: 88%

“…This relative reduction in large-pore area could reflect many processes, including a resolution of the early inflammatory state of the membrane after the start of PD. Several studies have also shown that depending on when the initial membrane function tests are done, PSTR also decreases in the months after PD is established before the longer-term increase (10,(18)(19)(20)(21). Alternatively, it could mean that large pores are underrepresented in newly formed vessels (surprising because new vessel formation in diabetic nephropathy is associated with increased protein extravasation) or that interstitial and perivascular fibrosis, known to occur over time (1), is impeding large-pore leak through the interstitial structures.…”

Section: Discussionmentioning

confidence: 99%

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Longitudinal Study of Small Solute Transport and Peritoneal Protein Clearance in Peritoneal Dialysis Patients

Lambie

Davies

2014

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Peritoneal protein clearance (Pcl) is determined by both effective (small pores) membrane area and relative capillary leakiness (large pores). It is not known how these two components change with duration of peritoneal dialysis (PD) in the context of progressive membrane injury and differential attrition of patients with higher Pcl, which has been associated with increased mortality risk in several studies.Design, setting, participants, & measurements Patients treated continuously from 2000 to 2011 for a minimum of 4 years were selected from the longitudinal prospective Stoke PD Study. Pcl, membrane area (peritoneal solute transport rate [PSTR]), dialysis prescription, and residual renal function were measured every 6 months, along with comorbidity and peritonitis events. Multilevel multivariate analysis was used to determine associations with Pcl over time, taking into account within-subject correlations.Results From 280 incident patients, 335 datasets were analyzed from 49 patients receiving treatment for 4 years. Pcl correlated with PSTR at baseline (R=0.61; P,0.01), but over time there was progressive uncoupling of this relationship (year 4, R=0.28; P=0.05) with increasing PSTR (0.66-0.74; P,0.01) and stable Pcl (78.4-81.9 ml/d; P=0.7). Multivariate analysis found that age, PSTR, daily ultrafiltration, and sodium removal were significant predictors of Pcl when adjusted for sex, comorbidity, glucose exposure, and residual renal function. Peritonitis was associated with increased PSTR but a similar pattern of uncoupling. ConclusionThere is a progressive dissociation of the small-and large-pore pathways with time on PD, which would be in keeping with a switch from local inflammation early on to progressive fibrosis, combined with increased vascular surface area. Measuring longitudinal changes in Pcl may complement membrane function tests used to monitor progressive injury.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Longitudinal Study of Small Solute Transport and Peritoneal Protein Clearance in Peritoneal Dialysis Patients

Lambie

Davies

2014

Clinical Journal of the American Society of Nephrology

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“…Whether biochemical modifications of AQP1 (e.g. S-nitrosylation or abnormal glycation) may alter the integrity of the water pore and contribute to ultrafiltration failure remains unsolved (31,32). Similarly, the potential influence of variants in the AQP1 gene encoding AQP1 in the individual variability in free-water transport at the start of PD remains to be defined.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, overall, there is an increase, and not a reduction, in the abundance of AQP1 in the peritoneal membrane in typical ultrafiltration failure -as pointed in the detailed case study of Goffin et al (32). It is thus hypothesized that the interstitial fibrosis per se accounts for the reduction in transperitoneal UF, across both small and ultrasmall pores via a reduction in total LpS (31)(32)(33). One should stress, however, that mechanisms of ultrafiltration failure probably differ in shortvs.…”

Section: Aquaporin-1 In Ultrafiltration Failurementioning

confidence: 93%

“…By contrast, there seems to be an uncoupling between changes in the mass transfer area coefficient (MTAC) to glucose, and the changes occurring in LpS in these conditions (11). The unchanging, or even reduced, LpS in long-term PD has by some authors been attributed to reductions in AQP1-meditated water transport (31). However, a more likely explanation for these changes is that a combination of two processes, namely i) increases in the vascularization of the peritoneum; and ii) the production of fibrotic scar tissue in the peritoneum, have occurred in parallel (2).…”

Section: Aquaporin-1 In Ultrafiltration Failurementioning

confidence: 99%

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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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Ultrafiltration Failure

Mujais

Smit

2009

Nolph and Gokal’s Textbook of Peritoneal Dialysis

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Analysis of fluid transport pathways and their determinants in peritoneal dialysis patients with ultrafiltration failure

Cited by 74 publications

References 22 publications

Longitudinal Study of Small Solute Transport and Peritoneal Protein Clearance in Peritoneal Dialysis Patients

Longitudinal Study of Small Solute Transport and Peritoneal Protein Clearance in Peritoneal Dialysis Patients

Water transport across the peritoneal membrane

Ultrafiltration Failure

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