Long-term Peritoneal Dialysis Treatment Research Articles

Role of endothelial hyaluronan in peritoneal membrane transport and disease conditions during peritoneal dialysis

Peritoneal membrane dysfunction in peritoneal dialysis (PD) is primarily attributed to angiogenesis; however, the integrity of vascular endothelial cells can affect peritoneal permeability. Hyaluronan, a component of the endothelial glycocalyx, is reportedly involved in preventing proteinuria in the normal glomerulus. One hypothesis suggests that development of encapsulating peritoneal sclerosis (EPS) is triggered by protein leakage due to vascular endothelial injury. We therefore investigated the effect of hyaluronan in the glycocalyx on peritoneal permeability and disease conditions. After hyaluronidase-mediated degradation of hyaluronan on the endothelial cells of mice, macromolecules, including albumin and β2 microglobulin, leaked into the dialysate. However, peritoneal transport of small solute molecules was not affected. Pathologically, hyaluronan expression was diminished; however, expression of vascular endothelial cadherin and heparan sulfate, a core protein of the glycocalyx, was preserved. Hyaluronan expression on endothelial cells was studied using 254 human peritoneal membrane samples. Hyaluronan expression decreased in patients undergoing long-term PD treatment and EPS patients treated with conventional solutions. Furthermore, the extent of hyaluronan loss correlated with the severity of vasculopathy. Hyaluronan on endothelial cells is involved in the peritoneal transport of macromolecules. Treatment strategies that preserve hyaluronan in the glycocalyx could prevent the leakage of macromolecules and subsequent related complications.

Rapid Initiation of Peritoneal Dialysis by Automated Peritoneal Dialysis or Hemodialysis: A Randomized Clinical Trial

Introduction: It is still controversial whether automated peritoneal dialysis (APD) or hemodialysis (HD) is a more favorable choice for the rapid initiation of peritoneal dialysis (PD). Methods: A pilot randomized prospective controlled trial was carried out in Shanghai Ruijin Hospital. Sixty-seven patients who chose long-term PD treatment and needed unplanned dialysis were enrolled and randomized into HD-CAPD group (33 cases) or APD-CAPD group (34 cases) based on the dialysis modality during the transition period (within 14 days from the day PD catheter was implanted). Continuous ambulatory PD started after the transition period. The primary outcome was the decline rates of residual glomerular filtration rate (GFR). Secondary outcomes included the rates of mechanical complications, the rates of infectious complications, and complications of end-stage renal disease. Results: We found residual GFR decline was faster in HD-CAPD group than in APD-CAPD group (0.06 mL/min/w vs. 0.03 mL/min/w, p < 0.01). The incidences of mechanical complications were similar in APD-CAPD group comparing with HD-CAPD group, including hernia (2.9% vs. 3.0%, p = 1.00), catheter malposition (0.02 episodes/patient-months vs. 0.02 episodes/patient-months, p = 0.70), leakage (5.9% vs. 6.1%, p = 1.00), and omental wrap (0 episode vs. 3 episodes, p = 0.368). Though the 1-year overall infection rates were similar (0.03 episodes/patient-months vs. 0.05 episodes/patient-months, p = 0.10), APD-CAPD group had lower rate of bacteremia compared to HD-CAPD group (0 episodes/patient-months vs. 0.02 episodes/patient-months, p < 0.01). Conclusions: Both APD and HD could be used for patients who need to start dialysis in an unplanned manner. APD may have the advantage in protecting residual renal functions among these patients.

Astragaloside IV Alleviates Intestinal Barrier Dysfunction via the AKT-GSK3β-β-Catenin Pathway in Peritoneal Dialysis.

Background and aims: Long-term peritoneal dialysis (PD) causes intestinal dysfunction, including constipation, diarrhea, or enteric peritonitis. However, the etiology and pathogenesis of these complications are still unclear and there are no specific drugs available in the clinic. This study aims to determine whether Astragaloside IV (AS IV) has therapeutic value on PD-induced intestinal epithelial barrier dysfunction in vivo and in vitro. Methods: We established two different long-term PD treatment mice models by intraperitoneally injecting 4.25% dextrose-containing peritoneal dialysis fluid (PDF) in uremia mice and normal mice, which were served as controls. In addition, PDF was applied to T84 cells in vitro. The therapeutic effects of AS IV on PD-induced intestinal dysfunction were then examined by histopathological staining, transmission electron microscopy, western blotting, and reverse transcription polymerase chain reaction. The protein levels of protein kinase B (AKT), glycogen synthase kinase 3β (GSK-3β) and β-catenin were examined after administration of AS IV. Results: In the present study, AS IV maintained the intestinal crypt, microvilli and desmosome structures in an orderly arrangement and improved intestinal epithelial permeability with the up-regulation of tight junction proteins in vivo. Furthermore, AS IV protected T84 cells from PD-induced damage by improving cell viability, promoting wound healing, and increasing the expression of tight junction proteins. Additionally, AS IV treatment significantly increased the levels of phosphorylation of AKT, inhibited the activity GSK-3β, and ultimately resulted in the nuclear translocation and accumulation of β-catenin. Conclusion: These findings provide novel insight into the AS IV-mediated protection of the intestinal epithelial barrier from damage via the AKT-GSK3β-β-catenin signal axis during peritoneal dialysis.

Inhibition of PI3K/AKT/mTOR Signalling Pathway Activates Autophagy and Suppresses Peritoneal Fibrosis in the Process of Peritoneal Dialysis.

Peritoneal dialysis (PD) is an important part of replacement therapy for kidney failure. However, long-term PD treatment can cause peritoneal fibrosis. Autophagy may be involved in the pathological mechanism of peritoneal fibrosis (PF). Although autophagy is currently known to be involved in course of PF, its specific effects still lack in-depth research. In this experiment, a high-glucose (HG)-induced peritoneal fibrosis rat model was successfully established via intraperitoneal injection of HG peritoneal dialysate, and the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 and the mechanistic target of rapamycin (mTOR) inhibitor rapamycin were used to treat peritoneal fibrosis rats. In addition, in vitro studies of high glucose-induced peritoneal fibrosis were performed using rat peritoneal mesothelial cells (PMCs). In vivo and in vitro experiments showed that LY294002 and rapamycin effectively inhibited the process of PF induced by high glucose. In addition, LY294002 and rapamycin were found to alleviate fibrosis by eliminating intracellular reactive oxygen species (ROS) levels, promoting the expression of the epithelial mesenchymal transdifferentiation proteins zonula occludens-1 (ZO-1) and E-cadherin, and inhibiting the expression of p-PI3K, PI3K, p-mTOR, mTOR, the fibroblast-specific proteins ferroptosis suppressor protein 1 (FSP1), and alpha-smooth muscle actin (α-SMA). Moreover, LY294002 and rapamycin promoted expression of autophagy-related proteins LC3-II/I, p62, and beclin-1. The current data indicated that inhibition of PI3K/AKT/mTOR signalling pathway activated autophagy and suppressed PF in the process of PD. Therefore, intervention in this signalling pathway may become a research goal for the prevention and treatment of PF, which has important clinical significance.

STAT3/HIF-1\u03b1 signaling activation mediates peritoneal fibrosis induced by high glucose

BackgroundEpithelial-mesenchymal transition (EMT) of mesothelial cells is a key step in the peritoneal fibrosis (PF). Recent evidence indicates that signal transducer and activator of transcription 3 (STAT3) might mediate the process of renal fibrosis, which could induce the expression of hypoxia-inducible factor-1α (HIF-1α). Here, we investigated the effect of STAT3 activation on HIF-1α expression and the EMT of mesothelial cells, furthermore the role of pharmacological blockade of STAT3 in the process of PF during peritoneal dialysis (PD) treatment.MethodsFirstly, we investigated the STAT3 signaling in human peritoneal mesothelial cells (HPMCs) from drained PD effluent. Secondly, we explored the effect of STAT3 signaling activation on the EMT and the expression of HIF-1α in human mesothelial cells (Met-5A) induced by high glucose. Finally, peritoneal fibrosis was induced by daily intraperitoneal injection with peritoneal dialysis fluid (PDF) so as to explore the role of pharmacological blockade of STAT3 in this process.ResultsCompared with the new PD patient, the level of phosphorylated STAT3 was up-regulated in peritoneal mesothelial cells from long-term PD patients. High glucose (60 mmol/L) induced over-expression of Collagen I, Fibronectin, α-SMA and reduced the expression of E-cadherin in Met-5A cells, which could be abrogated by STAT3 inhibitor S3I-201 pretreatment as well as by siRNA for STAT3. Furthermore, high glucose-mediated STAT3 activation in mesothelial cells induced the expression of HIF-1α and the profibrotic effect of STAT3 signaling was alleviated by siRNA for HIF-1α. Daily intraperitoneal injection of high-glucose based dialysis fluid (HG-PDF) induced peritoneal fibrosis in the mice, accompanied by the phosphorylation of STAT3. Immunostaining showed that phosphorylated STAT3 was expressed mostly in α-SMA positive cells in the peritoneal membrane induced by HG-PDF. Administration of S3I-201 prevented the progression of peritoneal fibrosis, angiogenesis, macrophage infiltration as well as the expression of HIF-1α in the peritoneal membrane induced by high glucose.ConclusionsTaken together, these findings identified a novel mechanism linking STAT3/HIF-1α signaling to peritoneal fibrosis during long-term PD treatment. It provided the first evidence that pharmacological inhibition of STAT3 signaling attenuated high glucose-mediated mesothelial cells EMT as well as peritoneal fibrosis.

Experimental models in peritoneal dialysis (Review).

Peritoneal dialysis (PD) is one of the most commonly used dialysis methods and plays an important role in maintaining the quality of life of patients with end-stage renal disease. However, long-term PD treatment is associated with adverse effects on the structure and function of peritoneal tissue, which may lead to peritoneal ultrafiltration failure, resulting in dialysis failure and eventually PD withdrawal. In order to prevent the occurrence of these effects, the important issues that need to be tackled are improvement of ultrafiltration, protection of peritoneal function and extension of dialysis time. In basic PD research, a reasonable experimental model is key to the smooth progress of experiments. A good PD model should not only simulate the process of human PD as accurately as possible, but also help researchers to understand the evolution process and pathogenesis of various complications related to PD treatment. To better promote the clinical application of PD technology, the present review will summarize and evaluate the in vivo PD experimental models available, thus providing a reference for relevant PD research.

Relationship between plasminogen activator inhibitor-1 gene alterations and fibrosis in peritoneal dialysis patients.

Peritoneal fibrosis (PF) is a pathological change that occurs mostly long-term peritoneal dialysis (PD) patients, as a result of triggering the inflammatory response. Plasminogen activator inhibitor-1 (PAI-1) is an important molecule featured in the development of fibrosis. It has been shown in literature that PAI-1 gene alterations are associated with fibrosis in many tissues and organs. However, PAI-1 gene alterations in long-term PD patients have not yet been investigated. In this study, PAI-1 4G/5G polymorphism was examined by reverse hybridization, and all coding exons of the PAI-1 gene were examined by sequence analysis to provide treatment modification in patients with predisposition before fibrosis develops. The patients were divided into two groups according to ultrafiltration failure test and duration of PD treatment: those with suspected PF or a high probability of developing PF (36%) and those with a low probability of developing PF (64%). There was no significant difference between the two groups in findings such as peritoneal equilibration test (PET), Kt/V, the content of the PD solution used, peritonitis, and PAI-1 4G/5G polymorphism (P > .05). A total of eight gene alterations (rs2227660, rs2227668, rs2854233, rs41281004, rs61553169, rs368413856, rs2227684) were detected by sequence analysis, one of which was exonic (rs6092). When the genotype distributions of these variants were examined, no significant difference was found between the two groups. PAI-1 gene changes were not detected in patients with the probability of developing PF. There is a need for further studies involving other molecules responsible for predisposing to PF with larger patient populations in patients undergoing long-term PD treatment.

Molecular hydrogen regulates PTEN-AKT-mTOR signaling via ROS to alleviate peritoneal dialysis-related peritoneal fibrosis.

As a convenient, effective and economical kidney replacement therapy for end-stage renal disease (ESRD), peritoneal dialysis is available in approximately 11% of ESRD patients worldwide. However, long-term peritoneal dialysis treatment causes peritoneal fibrosis. In recent years, the application potential of molecular hydrogen in the biomedicine has been well recognized. Molecular hydrogen selectively scavenges cytotoxic reactive oxygen species (ROS) and acts as an antioxidant. In this experiment, a high glucose-induced peritoneal fibrosis mouse model was successfully established by intraperitoneal injection of high glucose peritoneal dialysate, and peritoneal fibrosis mice were treated with hydrogen-rich peritoneal dialysate. In addition, in vitro studies of high glucose-induced peritoneal fibrosis were performed using MeT-5A cells. In vitro and in vivo experiments show that molecular hydrogen could inhibit peritoneal fibrosis progress induced by high glucose effectively. Furthermore, it has been found that molecular hydrogen alleviate fibrosis by eliminating intracellular ROS and inhibiting the activation of the PTEN/AKT/mTOR pathway. The present data proposes that molecular hydrogen exerts the capacity of anti-peritoneal fibrosis through the ROS/PTEN/AKT/mTOR pathway. Therefore, molecule hydrogen is a potential, safe, and effective treatment agent, with peritoneal protective property and great clinical significance.

Effects of long-term treatment with low-GDP, pH-neutral solutions on peritoneal membranes in peritoneal dialysis patients.

The morphological changes induced by bio-incompatible peritoneal dialysis (PD) solutions are well known. However, the morphological damage induced by long-term low-glucose degradation product (GDP), pH-neutral solutions has not been reported in detail. The aim of this study was to investigate the long-term effects of pH-neutral PD solutions on morphological and functional changes in the peritoneal membrane. We assessed peritoneal membrane biopsy samples from PD patients treated with acidic (Conventional group) or pH-neutral solutions (pH-neutral group) using pathology and immunopathology techniques. Analyses of 54 Conventional and 73 pH-neutral group samples showed that the peritoneal membrane was thicker (P < 0.001), the ratio of luminal diameter to vessel diameter (L/V ratio) was significantly smaller (P < 0.001), and advanced glycation end-product (AGE) accumulation was higher in the Conventional than in the pH-neutral group (P < 0.001). Comparison of samples from patients in the Conventional (n = 33) and pH-neutral groups (n = 33) who were treated for 4-10years also showed significant differences in peritoneal thickness, L/V ratio and AGE score. Furthermore, the L/V ratio in the Conventional group significantly decreased over time (P < 0.01); however, no such change was seen in the pH-neutral group. Peritoneal membrane thickness was not associated with PD duration in both groups. Dialysate-to-plasma ratio of creatinine and L/V ratio negatively correlated with PD treatment duration in the Conventional group, but not in the pH-neutral group. These findings suggest that pH-neutral solutions prevent the morphological and functional peritoneal changes induced by long-term PD treatment.

Hyperbranched polyglycerol is superior to glucose for long-term preservation of peritoneal membrane in a rat model of chronic peritoneal dialysis.

BackgroundReplacing glucose with a better biocompatible osmotic agent in peritoneal dialysis (PD) solutions is needed in PD clinic. We previously demonstrated the potential of hyperbranched polyglycerol (HPG) as a replacement for glucose. This study further investigated the long-term effects of chronic exposure to HPG as compared to a glucose-based conventional PD solution on peritoneal membrane (PM) structure and function in rats.MethodsAdult male Wistar rats received once-daily intraperitoneal injection of 10 mL of HPG solution (1 kDa, HPG 6%) compared to Physioneal™ 40 (PYS, glucose 2.27%) or electrolyte solution (Control) for 3 months. The overall health conditions were determined by blood chemistry analysis. The PM function was determined by ultrafiltration, and its injury by histological and transcriptome-based pathway analyses.ResultsHere, we showed that there was no difference in the blood chemistry between rats receiving the HPG and the Control, while PYS increased serum alkaline phosphatase, globulin and creatinine and decreased serum albumin. Unlike PYS, HPG did not significantly attenuate PM function, which was associated with smaller change in both the structure and the angiogenesis of the PM and less cells expressing vascular endothelial growth factor, α-smooth muscle actin and MAC387 (macrophage marker). The pathway analysis revealed that there were more inflammatory signaling pathways functioning in the PM of PYS group than those of HPG or Control, which included the signaling for cytokine production in both macrophages and T cells, interleukin (IL)-6, IL-10, Toll-like receptors, triggering receptor expressed on myeloid cells 1 and high mobility group box 1.ConclusionsThe results from this experimental study indicate the superiority of HPG to glucose in the preservation of the peritoneum function and structure during the long-term PD treatment, suggesting the potential of HPG as a novel osmotic agent for PD.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-1098-z) contains supplementary material, which is available to authorized users.

MicroRNA Regulation of Peritoneal Cavity Homeostasis in Peritoneal Dialysis

Preservation of peritoneal cavity homeostasis and peritoneal membrane function is critical for long-term peritoneal dialysis (PD) treatment. Several microRNAs (miRNAs) have been implicated in the regulation of key molecular pathways driving peritoneal membrane alterations leading to PD failure. miRNAs regulate the expression of the majority of protein coding genes in the human genome, thereby affecting most biochemical pathways implicated in cellular homeostasis. In this review, we report published findings on miRNAs and PD therapy, with emphasis on evidence for changes in peritoneal miRNA expression during long-term PD treatment. Recent work indicates that PD effluent- (PDE-) derived cells change their miRNA expression throughout the course of PD therapy, contributing to the loss of peritoneal cavity homeostasis and peritoneal membrane function. Changes in miRNA expression profiles will alter regulation of key molecular pathways, with the potential to cause profound effects on peritoneal cavity homeostasis during PD treatment. However, research to date has mainly adopted a literature-based miRNA-candidate methodology drawing conclusions from modest numbers of patient-derived samples. Therefore, the study of miRNA expression during PD therapy remains a promising field of research to understand the mechanisms involved in basic peritoneal cell homeostasis and PD failure.

Alterations in proteoglycan components and histopathology of the peritoneum in uraemic and peritoneal dialysis (PD) patients

Proteoglycans (PGs) are dominant extracellular matrices (ECMs) in the peritoneal tissues. Human peritoneal mesothelial cells synthesize small proteoglycans including decorin. Peritonitis and long-term peritoneal dialysis (PD) cause fibrotic changes in the peritoneum that result in ECM remodelling and PG synthesis. Twenty-five peritoneal tissues from eight patients at initiation of PD, five long-term PD (>6 years) patients with severe peritonitis lasting for almost 1 month, nine patients after long-term PD (>6 years) without peritonitis and three normal subjects were included in the present study. Expressions of decorin, versican, hyaluronan, MMP-2, alfa smooth muscle actin (alphaSMA) and CD68 for macrophages in these specimens were examined by immunohistochemical staining. Although expression of decorin was detected in normal subjects, it was markedly decreased with long-term PD treatment. In long-term PD patients, the expression of versican was observed in their fibrotic-thickened peritoneum. Versican was present in fibrous regions, elastic lamina of the peritoneum, vascular walls and perivascular regions. Hyaluronan was observed in the whole thickened peritoneum, but its distribution differed in part from that of versican. MMP-2 was mainly observed around the blood vessels. Alfa SMA-positive cells, namely 'myofibroblasts' and CD68-positive cells, i.e. macrophages, were observed in the fibrotic-thickened peritoneum of long-term PD patients. Expressions of MMP-2, hyaluronan, SMA and CD68 in the peritoneum were marked in long-term PD patients' samples, which were strongly immunostained by versican, and were especially high in peritonitis patients. It appears that alterations in PGs, including marked induction of versican with peritonitis and disappearance of decorin, are involved in peritoneal remodelling in PD patients. Versican expression was closely related to the appearance of myofibroblasts and macrophages. These observations suggest that the alteration in PG components following PD therapy and severe inflammation contribute to fibrous thickening of the peritoneum.

The “Heart” of Peritoneal Dialysis: Residual Renal Function

The CANUSA study originally reported the importance of total small-solute clearance in predicting survival of peritoneal dialysis (PD) patients. However, subsequent reanalysis of data from the CANUSA study clearly demonstrated that the predictive power for mortality in PD patients was largely attributable to residual renal function (RRF) and not to the dose of PD. While this should not lead to the assumption that the dose of PD is unimportant, it does clearly indicate that the contribution of residual renal clearance and PD clearance to the overall survival of PD cannot be considered equivalent. In a previous study, we also demonstrated the importance of loss of RRF in predicting a heightened risk of mortality and cardiovascular death in PD patients. In this review, we focus our discussion on the different potential mechanisms that explain the important link between RRF and cardiovascular disease and survival of PD patients. We provide evidence to explain why RRF is so important to patients receiving long-term PD treatment and why it should be regarded as the "heart" of PD.

The Plasma Leak–to–Response Hypothesis: A Working Hypothesis on the Pathogenesis of Encapsulating Peritoneal Sclerosis after Long-Term Peritoneal Dialysis Treatment

Encapsulating peritoneal sclerosis (EPS) is one of the most serious complications of long-term peritoneal dialysis (PD). Long-term PD therapy has been suggested as a risk factor for EPS development among patients in Japan and Australia. Although the primary mechanism of EPS development has not been clarified, histologic changes of the peritoneum associated with prolonged PD are postulated to be causally related. The present article proposes a working hypothesis--the plasma leak-to-response hypothesis--that vascular alterations in the peritoneum of long-term PD patients play a crucial role in the initiation and development of EPS.

Beyond the membrane—The role of new PD solutions in enhancing global biocompatibility

Since the introduction of continuous ambulatory peritoneal dialysis (CAPD) during the late 1970s as a form of home-based, self-care renal replacement therapy, peritoneal dialysis (PD) has become an appealing alternative for the treatment of patients with end-stage renal disease (ESRD). A significant amount of research over the last 25 years has resulted in continuous improvements in the quality of PD treatment. Survival of patients on PD is now at least as good as with hemodialysis, especially during the first years of treatment, and results are gradually improving. Considerable progress has been made in understanding the nature of the interactions between the dialysis solution and the peritoneal membrane, how these interactions may result in structural alterations to the membrane, and how peritoneal solute and fluid transport are influenced by these alterations. During recent years, as PD technique survival has improved and peritonitis rates declined, PD researchers have focused more attention on ways to improve the biocompatibility of dialysis solutions with the goal of extending the life of the peritoneum as a dialyzing membrane, which may improve and extend the life of the PD patient. The reason for this research focus is the observation that the characteristic structural and functional alterations to the peritoneal membrane during long-term PD treatment may be the consequence of the continuous exposure to solutions with high concentrations of glucose, glucose degradation products (GDPs), and lactate, low pH, and high osmolality. It is now clear that these alterations to the peritoneal membrane may have a profound effect on the well-being of the patient on long-term PD therapy. According to the Consensus Conference on Biocompatibility held in 1994 [1], biocompatibility is “the ability of a material, device or system to perform without a clinically significant host response in a specific application.” When applied to PD, biocompatibility refers to the ability

Association between an Increased Surface Area of Peritoneal Microvessels and a High Peritoneal Solute Transport Rate

The peritoneal solute transport rate (PSTR) often increases, especially for small solutes, during long-term peritoneal dialysis (PD) treatment. Although the mechanism by which PSTR increases in PD patients is not known, it is likely that an increased PSTR reflects an increased surface area of the peritoneal capillary and post-capillary venules (microvessels), but this has not previously been investigated. The aim of this study was to clarify the relationship between PSTR and peritoneal microvessel alterations in biopsy specimens of peritoneum obtained from PD patients after various times on PD, and the possible contribution of the duration of PD in relation to these alterations. Tissue from the parietal peritoneum was obtained from 22 PD patients (age 48.5 +/- 9.0 years, duration of PD 66.3 +/- 46.6 months, incidence of peritonitis 0.3/patient-year). The patients were subdivided into three groups according to duration of PD: zero months (group 0, n = 4), less than 60 months (group I, n = 7), and more than 60 months (group II; n = 11). For each specimen, the relative microvessel area (RVA) calculated as total area of microvessels/total area of peritoneal field, and the relative microvessel number (RVN), calculated as number of microvessels/total area of peritoneal field, were determined. The ratio RVA/RVN was used to assess the average area of microvessels. The PSTR was evaluated for creatinine, glucose, beta2-microglobulin, and albumin using the peritoneal equilibration test. The dialysate-to-plasma concentration ratio (D/P) for creatinine showed a significant positive correlation with both RVA (rho = 0.77, p < 0.001) and RVA/RVN (rho = 0.51, p = 0.01), but not with RVN. The D/P for beta2-microglobulin correlated with RVA (rho = 0.51, p = 0.015) but not with RVN or RVA/RVN. No differences were found between the three groups in the values for RVN, whereas there was an apparent significant increase in RVA with time on PD (p < 0.001 for group 0 vs both groups I and II). Furthermore, in high transporters, RVA tended to be higher in group II than in group I. The present study demonstrates for the first time that an increased peritoneal solute transport rate (for both creatinine and beta2-microglobulin) is associated with an increased surface area of peritoneal microvessels, especially in patients on long-term PD treatment. This indicates that increased vascularization and/or dilatation of peritoneal microvessels may play a key role in the development of a high PSTR.

Body composition in patients treated with peritoneal dialysis.

Malnutrition is a common complication in uremia and during maintenance dialysis. Several factors contribute to its development. Different modes of dialysis treatment may differ in their effects on nutritional status. In order to analyse the nutritional consequences of peritoneal dialysis (PD), body composition analyses were performed in PD patients between February 1993 and March 1996. Body cell mass (BCM) was estimated from measurements of total body potassium (TBK) in a whole-body counter. Total body water (TBW) was determined by measurement of tritiated water. Body fat (BF) was calculated from body weight (BW), TBK and TBW. Observed values were related to predicted (o/p) derived from local population studies. Sixty patients were repeatedly investigated during the study period. Of these, 34 were investigated during the first year of PD. At the start of dialysis, TBK o/p was 0.94 and BF o/p 0.76. No change in body composition was seen during the observation period in the group as a whole. However, within the group individual changes in BW were strongly correlated with individual changes in BF (r=0.66, P=0.0001). Twenty-six patients were examined during the second and third year of PD. In this group, BW o/p remained constant over time. However, there was a small but significant decline of TBK o/p and a concomitant increase of BF o/p (P<0.05). No correlation was observed between changes in TBK and changes in serum albumin. The results of this study indicate, that there may be a risk for further reduction of body cell mass during long-term PD treatment, while body energy stores are maintained or even increased.

Recent developments in peritoneal dialysis.

Significant developments over the past 10 years have established continuous ambulatory peritoneal dialysis as a successful kidney-replacement treatment. Peritonitis rates have fallen, and investigators are attempting to establish objective criteria for adequacy of dialysis. Malnutrition is a serious concern, but short-term experience with intraperitoneal amino acids promises success in the management of this complication. A significant improvement in the well-being of patients with end-stage renal disease was produced by recombinant human erythropoietin, and use of recombinant human growth hormone promises catch-up growth for children receiving long-term peritoneal dialysis treatment. As increasing numbers of patients are maintained on continuous ambulatory peritoneal dialysis over longer periods, we will begin to encounter beta 2-microglobulin-related amyloidosis possibly at the same rate in these patients as in those receiving long-term hemodialysis treatment.