Long-term peritoneal dialysis is associated with a decrease in body weight.
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ABSTRACT:
SUBMITTER: Imam TH
PROVIDER: S-EPMC7857837 | biostudies-literature | 2021 Jan
REPOSITORIES: biostudies-literature
Publications
Long-term peritoneal dialysis is associated with a decrease in body weight.
Imam Talha H TH Shi Jiaxio M JM Yi David K DK Yang Su-Jau SJ
Clinical kidney journal 20191206 1
Similar Datasets
Project description:Encapsulating peritoneal sclerosis (EPS) is the most serious complication of long-term peritoneal dialysis (PD), with a mortality rate that exceeds 30%. There have been many reports of the incidence of EPS being strongly correlated to the duration of PD. Patients on PD for longer than 5 years, and especially those receiving this treatment for more than 8 years, should undergo careful and repeated surveillance for risk factors associated with the development of EPS. The development of ultrafiltration failure, a high dialysate/plasma creatinine ratio, as determined by the peritoneal equilibration test, peritoneal calcification, a persistently elevated C-reactive protein level, and severe peritonitis in patients on PD for longer than 8 years are signals that should prompt the clinician to consider terminating PD as a possible means of preventing the development of EPS. The impact of the newer, biocompatible PD solutions on the incidence of EPS has not yet been determined.
| S-EPMC2778779 | biostudies-other
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-11-22 | GSE246102 | GEO
Project description:Bacterial infections and the concurrent inflammation have been associated with increased long-term cardiovascular (CV) risk. In patients receiving peritoneal dialysis (PD), bacterial peritonitis is a common occurrence, and each episode further increases late CV mortality risk. However, the underlying mechanism(s) remains to be elucidated before safe and efficient anti-inflammatory interventions can be developed. Damage-Associated Molecular Patterns (DAMPs) have been shown to contribute to the acute inflammatory response to infections, but a potential role for DAMPs in mediating long-term vascular inflammation and CV risk following infection resolution in PD, has not been investigated. We found that bacterial peritonitis in mice that resolved within 24h led to CV disease-promoting systemic and vascular immune-mediated inflammatory responses that were maintained up to 28 days. These included higher blood proportions of inflammatory leukocytes displaying increased adhesion molecule expression, higher plasma cytokines levels, and increased aortic inflammatory and atherosclerosis-associated gene expression. These effects were also observed in infected nephropathic mice and amplified in mice routinely exposed to PD fluids. A peritonitis episode resulted in elevated plasma levels of the DAMP Calprotectin, both in PD patients and mice, here the increase was maintained up to 28 days. In vitro, the ability of culture supernatants from infected cells to promote key inflammatory and atherosclerosis-associated cellular responses, such as monocyte chemotaxis, and foam cell formation, was Calprotectin-dependent. In vivo, Calprotectin blockade robustly inhibited the short and long-term peripheral and vascular consequences of peritonitis, thereby demonstrating that targeting of the DAMP Calprotectin is a promising therapeutic strategy to reduce the long-lasting vascular inflammatory aftermath of an infection, notably PD-associated peritonitis, ultimately lowering CV risk.
2023-11-22 | GSE246101 | GEO
Project description:Bacterial infections and the concurrent inflammation have been associated with increased long-term cardiovascular (CV) risk. In patients receiving peritoneal dialysis (PD), bacterial peritonitis is a common occurrence, and each episode further increases late CV mortality risk. However, the underlying mechanism(s) remains to be elucidated before safe and efficient anti-inflammatory interventions can be developed. Damage-Associated Molecular Patterns (DAMPs) have been shown to contribute to the acute inflammatory response to infections, but a potential role for DAMPs in mediating long-term vascular inflammation and CV risk following infection resolution in PD, has not been investigated. We found that bacterial peritonitis in mice that resolved within 24h led to CV disease-promoting systemic and vascular immune-mediated inflammatory responses that were maintained up to 28 days. These included higher blood proportions of inflammatory leukocytes displaying increased adhesion molecule expression, higher plasma cytokines levels, and increased aortic inflammatory and atherosclerosis-associated gene expression. These effects were also observed in infected nephropathic mice and amplified in mice routinely exposed to PD fluids. A peritonitis episode resulted in elevated plasma levels of the DAMP Calprotectin, both in PD patients and mice, here the increase was maintained up to 28 days. In vitro, the ability of culture supernatants from infected cells to promote key inflammatory and atherosclerosis-associated cellular responses, such as monocyte chemotaxis, and foam cell formation, was Calprotectin-dependent. In vivo, Calprotectin blockade robustly inhibited the short and long-term peripheral and vascular consequences of peritonitis, thereby demonstrating that targeting of the DAMP Calprotectin is a promising therapeutic strategy to reduce the long-lasting vascular inflammatory aftermath of an infection, notably PD-associated peritonitis, ultimately lowering CV risk.
2023-11-22 | GSE246100 | GEO
Project description:Bacterial infections and the concurrent inflammation have been associated with increased long-term cardiovascular (CV) risk. In patients receiving peritoneal dialysis (PD), bacterial peritonitis is a common occurrence, and each episode further increases late CV mortality risk. However, the underlying mechanism(s) remains to be elucidated before safe and efficient anti-inflammatory interventions can be developed. Damage-Associated Molecular Patterns (DAMPs) have been shown to contribute to the acute inflammatory response to infections, but a potential role for DAMPs in mediating long-term vascular inflammation and CV risk following infection resolution in PD, has not been investigated. We found that bacterial peritonitis in mice that resolved within 24h led to CV disease-promoting systemic and vascular immune-mediated inflammatory responses that were maintained up to 28 days. These included higher blood proportions of inflammatory leukocytes displaying increased adhesion molecule expression, higher plasma cytokines levels, and increased aortic inflammatory and atherosclerosis-associated gene expression. These effects were also observed in infected nephropathic mice and amplified in mice routinely exposed to PD fluids. A peritonitis episode resulted in elevated plasma levels of the DAMP Calprotectin, both in PD patients and mice, here the increase was maintained up to 28 days. In vitro, the ability of culture supernatants from infected cells to promote key inflammatory and atherosclerosis-associated cellular responses, such as monocyte chemotaxis, and foam cell formation, was Calprotectin-dependent. In vivo, Calprotectin blockade robustly inhibited the short and long-term peripheral and vascular consequences of peritonitis, thereby demonstrating that targeting of the DAMP Calprotectin is a promising therapeutic strategy to reduce the long-lasting vascular inflammatory aftermath of an infection, notably PD-associated peritonitis, ultimately lowering CV risk.
| S-EPMC10716465 | biostudies-literature
Project description:IntroductionInternationally, peritoneal dialysis (PD) is increasingly being commenced within 2 weeks of catheter insertion. Studies are warranted to evaluate outcomes of this strategy.MethodsThis study examines outcomes of early-start PD (ESPD) and conventional-start PD (CSPD), commencing at ≤14 days and >14 days after catheter insertion, respectively. All adults with kidney failure within a large metropolitan PD unit initiating PD through a new catheter, inserted using laparoscopic or modified Seldinger technique, between August 2019 and August 2022, were included in this retrospective observational study. Demographic data and episodes of infectious and mechanical complications were collected using electronic medical records. Analysis was conducted using analysis of variance and Chi-square testing. A P-value < 0.05 was significant with Bonferroni correction performed where relevant. Kaplan-Meier and competing risks analyses were performed for time to PD-related peritonitis and transfer to hemodialysis.ResultsA total of 297 patients (70% male, mean age 58.7 years) were included, with 130 (43.8%) patients undertaking ESPD. Most patients had laparoscopically inserted catheters (65.3%) and 65 patients (22.0%) received prior hemodialysis. When compared to CSPD, ESPD was associated with a higher number of pericatheter leaks (6.9% vs. 0.6%, P = 0.003), with otherwise similar complication episodes and no significant difference with respect to time to PD-related peritonitis or transfer to hemodialysis. Catheter insertion technique or prior hemodialysis treatment did not significantly influence outcomes.ConclusionESPD is associated with increased pericatheter leaks when compared to CSPD, with an otherwise similar complication profile.
| S-EPMC11403086 | biostudies-literature
Project description:Peritoneal hyalinizing vasculopathy (PHV) represents the cornerstone of long-term peritoneal dialysis (PD), and especially characterizes patients associated with encapsulating peritoneal sclerosis. However, the mechanisms of PHV development remain unknown. A cross sectional study was performed in 100 non-selected peritoneal biopsies of PD patients. Clinical data were collected and lesions were evaluated by immunohistochemistry. In selected biopsies a microRNA (miRNA)-sequencing analysis was performed. Only fifteen patients (15%) showed PHV at different degrees. PHV prevalence was significantly lower among patients using PD fluids containing low glucose degradation products (GDP) (5.9% vs. 24.5%), angiotensin converting enzyme inhibitors (ACEIs) (7.5% vs. 23.4%), statins (6.5% vs. 22.6%) or presenting residual renal function, suggesting the existence of several PHV protective factors. Peritoneal biopsies from PHV samples showed loss of endothelial markers and induction of mesenchymal proteins, associated with collagen IV accumulation and wide reduplication of the basement membrane. Moreover, co-expression of endothelial and mesenchymal markers, as well as TGF-β1/Smad3 signaling activation were found in PHV biopsies. These findings suggest that an endothelial-to-mesenchymal transition (EndMT) process was taking place. Additionally, significantly higher levels of miR-7641 were observed in severe PHV compared to non-PHV peritoneal biopsies. Peritoneal damage by GDPs induce miRNA deregulation and an EndMT process in submesothelial vessels, which could contribute to collagen IV accumulation and PHV.
| S-EPMC7461593 | biostudies-literature
Project description:ObjectiveThis report presents a method quantitatively analyzing abnormalities of body water and monovalent cations (sodium plus potassium) in patients on peritoneal dialysis (PD) with true hyponatremia.MethodsIt is well known that in the face of euglycemia serum sodium concentration is determined by the ratio between the sum of total body sodium plus total body potassium on the one hand and total body water on the other. We developed balance equations that enabled us to calculate excesses or deficits, relative to the state of eunatremia and dry weight, in terms of volumes of water and volumes of isotonic solutions of sodium plus potassium when patients presented with hyponatremia. We applied this method retrospectively to 5 episodes of PD-associated hyponatremia (serum sodium concentration 121-130 mEq/L) and compared the findings of the method with those of the clinical evaluation of these episodes.ResultsEstimates of the new method and findings of the clinical evaluation were in agreement in 4 of the 5 episodes, representing euvolemic hyponatremia (normal total body sodium plus potassium along with water excess) in 1 patient, hypovolemic hyponatremia (deficit of total body sodium plus potassium along with deficit of total body water) in 2 patients, and hypervolemic hyponatremia (excess of total body sodium along with larger excess of total body water) in 1 patient. In the 5(th) patient, in whom the new method suggested the presence of water excess and a relatively small deficit of monovalent cations, the clinical evaluation had failed to detect the cation deficit.ConclusionsEvaluation of imbalances in body water and monovalent cations in PD-associated hyponatremia by the method presented in this report agrees with the clinical evaluation in most instances and could be used as a guide to the treatment of hyponatremia. Prospective studies are needed to test the potential clinical applications of this method.
| S-EPMC4033325 | biostudies-literature
Project description:BackgroundBody weight in lower animals and humans is highly stable despite a very large flux in energy intake and expenditure over time. Conversely, the existence of higher-than-average variability in weight may indicate a disruption in the mechanisms responsible for homeostatic weight regulation.ObjectiveIn a sample chosen for weight-gain proneness, we evaluated whether weight variability over a 6-mo period predicted subsequent weight change from 6 to 24 mo.DesignA total of 171 nonobese women were recruited to participate in this longitudinal study in which weight was measured 4 times over 24 mo. The initial 3 weights were used to calculate weight variability with the use of a root mean square error approach to assess fluctuations in weight independent of trajectory. Linear regression analysis was used to examine whether weight variability in the initial 6 mo predicted weight change 18 mo later.ResultsGreater weight variability significantly predicted amount of weight gained. This result was unchanged after control for baseline body mass index (BMI) and BMI change from baseline to 6 mo and for measures of disinhibition, restrained eating, and dieting.ConclusionsElevated weight variability in young women may signal the degradation of body weight regulatory systems. In an obesogenic environment this may eventuate in accelerated weight gain, particularly in those with a genetic susceptibility toward overweight. Future research is needed to evaluate the reliability of weight variability as a predictor of future weight gain and the sources of its predictive effect. The trial on which this study is based is registered at clinicaltrials.gov as NCT00456131.
| S-EPMC4625595 | biostudies-literature
Project description:The microenvironmental changes in peritoneal dialysis effluent (PDE) after long-term vintage (LV) of PD in patients with ultrafiltration failure (LV_UF) are unclear. Single-cell sequencing revealed that peritoneal neutrophils were elevated in LV_UF patients, while MRC1-macrophage subcluster decreased compared with PD patients with short vintage (SV) and LV without ultrafiltration failure (LV_NOT_UF). Compared with the LV_NOT_UF group, the upregulated differentially expressed genes (DEGs) of monocytes/macrophages in the LV_UF group were involved in inflammatory response and EMT progress. LV_UF patients had a higher proportion of epithelial-like mesothelial cells (E-MCs), which were characterized by autophagy activation, inflammation, and upregulation of neutrophil- and autophagy-related DEGs compared to the LV_NOT_UF group. Additionally, mesenchymal-like MCs and AQP1 expression were reduced in the LV_UF group compared with the other groups. Both neutrophils and monocytes/macrophages interacted with MCs. Our study provides insights into the roles of peritoneal mesothelial cells and inflammatory cells in PD patients with UF.
| S-EPMC11647153 | biostudies-literature