scholarly journals Glucose-Based Peritoneal dialysis solution suppresses adiponectin synthesis through oxidative stress in an experimental model of peritoneal dialysis

2012 ◽  
Vol 32 (1) ◽  
pp. 20-28 ◽  
Author(s):  
Joo Young Huh ◽  
Eun-Young Seo ◽  
Hi Bahl Lee ◽  
Hunjoo Ha

ObjectiveAccumulation of visceral fat is one of the major risk factors for the development of cardiovascular disease in peritoneal dialysis (PD) patients. Adiponectin, an adipokine commonly regarded as a negative indicator of metabolic disease, is reported to be downregulated in its gene level in end-stage renal disease patients. Since excessive fat deposit is involved in increased reactive oxygen species (ROS), PD solution (PDS) may contribute to ROS production, resulting in dysregulation of adiponectin. In this study, we tested our hypothesis that oxidative stress induced by PDS may play a role in the regulation of adiponectin.MethodsCommercial PDS containing 3.86% glucose (20 - 30 mL) was administered to SD rats for 12 weeks with and without N-acetylcysteine (NAC; 10 mmol/L). ELISA was used to quantify adiponectin in plasma and spent dialysate. For in vitro studies, fully differentiated 3T3-L1 adipocytes and adipocytes isolated from abdominal fat were treated with a high glucose solution, PDS, and H2O2. Adiponectin levels in the conditioned media were measured by ELISA and immunoblot assays. The mRNA levels of adiponectin in mature adipocytes were examined using real-time RT-PCR.ResultsThe levels of adiponectin in plasma and spent dialysate were significantly downregulated by PDS and this effect was suppressed by NAC. In 3T3-L1 adipocytes, adiponectin secretion was inhibited by 50 mmol/L glucose, PDS diluted 2-fold, and H2O2(200 μmol/L). In addition, H2O2downregulated expression of adiponectin mRNA and secretion of adiponectin oligomer complexes.ConclusionsOur data suggest that ROS induced by conventional glucose-based PDS may contribute to pathophysiological changes in abdominal fat and down regulate adiponectin secreted from adipocytes during long-term PD.

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Xueli Lai ◽  
Mingming Nie ◽  
Xiaodong Xu ◽  
Yuanjie Chen ◽  
Zhiyong Guo

Abstract Background Peritoneal dialysis (PD) is a safe and home-based treatment for end-stage renal disease (ESRD) patients. The direct thermal damage of abdominal organs is very rare. Case presentation We report a peritoneal dialysis patient presented abdominal pain and feculent effluent 3 weeks after he instilled hot dialysis solution. In spite of emergency exploratory laparotomy and active treatment, the patient died of septic shock. Biopsy revealed necrosis and perforation of the intestines. Conclusions Delayed bowel perforation by hot fluid is very rare. Standardized performance is of the first importance for peritoneal dialysis patients.


2021 ◽  
Vol 22 (12) ◽  
pp. 6196
Author(s):  
Anna Pieniazek ◽  
Joanna Bernasinska-Slomczewska ◽  
Lukasz Gwozdzinski

The presence of toxins is believed to be a major factor in the development of uremia in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD). Uremic toxins have been divided into 3 groups: small substances dissolved in water, medium molecules: peptides and low molecular weight proteins, and protein-bound toxins. One of the earliest known toxins is urea, the concentration of which was considered negligible in CKD patients. However, subsequent studies have shown that it can lead to increased production of reactive oxygen species (ROS), and induce insulin resistance in vitro and in vivo, as well as cause carbamylation of proteins, peptides, and amino acids. Other uremic toxins and their participation in the damage caused by oxidative stress to biological material are also presented. Macromolecules and molecules modified as a result of carbamylation, oxidative stress, and their adducts with uremic toxins, may lead to cardiovascular diseases, and increased risk of mortality in patients with CKD.


2005 ◽  
Vol 25 (4_suppl) ◽  
pp. 77-82 ◽  
Author(s):  
Akira Saito

Encapsulating peritoneal sclerosis (EPS) is a life-threatening complication of peritoneal dialysis (PD). The overall prevalence of EPS in Japanese PD patients is 2.3%. Among patients on PD for less than 5 years, the rate is 0.9%; among patients on PD for 5 – 10 years, the rate is 3.8%; and among patients on PD for >10 years, it is 11.5%. Thus, the longer the treatment duration, the higher the prevalence of EPS. Encapsulating peritoneal sclerosis does not result solely from the natural progression of peritoneal sclerosis. A “second hit” event, such as bacterial peritonitis, abdominal bleeding, or abdominal surgery may be needed to trigger the onset of EPS in the face of advanced peritoneal sclerosis. To prevent development of EPS, PD treatment is replaced by other treatments when patients reached high-transport status. Peritoneal lavage and prednisolone administration have been reported to be effective in preventing or stopping the progress of EPS. When bowel obstruction has occurred, total enterolysis to remove the fibrous capsule from the bowel is indicated. To maximize overall quality of life, patients with end-stage renal disease (ESRD) should have the choice to make use of all the treatment modalities available: PD, hemodialysis (HD), and transplantation. Furthermore, the development of truly biocompatible PD equipment—including peritoneal catheters, solutions, and systems—are desirable to extend PD treatment for the long term. The cost of individual products could decrease significantly if PD use were to increase to 30% from 10% among ESRD patients worldwide. As practitioners, we have to further improve the technical survival rate and functional duration of PD treatment so that adequate peritoneal function can be maintained for 10 years in at least 40% of PD patients. The goal is to place PD on par with HD using high-flux dialysis membranes and ultrapure dialysis solution.


2009 ◽  
Vol 32 (12) ◽  
pp. 872-882 ◽  
Author(s):  
Vassilis Filiopoulos ◽  
Dimitrios Hadjiyannakos ◽  
Lambrini Takouli ◽  
Polixeni Metaxaki ◽  
Vasilis Sideris ◽  
...  

Renal Failure ◽  
2007 ◽  
Vol 29 (3) ◽  
pp. 309-313 ◽  
Author(s):  
M. Kanbay ◽  
N. Bavbek ◽  
T. Delibasi ◽  
C. Koca ◽  
A. Kaya ◽  
...  

2004 ◽  
Vol 24 (3) ◽  
pp. 264-273 ◽  
Author(s):  
Naoko Yanagisawa ◽  
Dai-Qing Li ◽  
Åsa Ljungh

Background Deposition of proteins on surfaces of medical devices has been recognized to putatively relate to the process of regulation of biomaterial-associated complications by attachment of fibrin clots, eukaryotic cells, and microbes. The molecules adsorb to a varying extent, depending not only on the physicochemical properties of the biomaterial, but also on the composition of the host fluid. Objective Adsorption of proteins on catheters exposed both ex vivo and in vitro to dialysate of patients on peritoneal dialysis (PD) was studied. Methods Peritoneal dialysis effluent was collected from 5 patients with end-stage renal disease on continuous ambulatory PD. Tenckhoff catheters were obtained from 16 patients. Deposition of proteins on excised Tenckhoff catheters and tubing of different materials exposed to PD effluent in vitro was studied using 125iodine-labeled antibodies. Adhesion of Staphylococcus aureus and Staphylococcus epidermidis strains was quantified on tubing exposed to PD effluent in vitro. Results The presence of albumin, transferrin, immunoglobulin G, fibrinogen, fibronectin, von Willebrand factor, vitronectin, and thrombospondin was determined at various concentrations in PD effluent. All proteins analyzed were detected on PD catheters removed from patients. The extent of protein deposition on Tenckhoff catheters exposed to PD effluent, in vitro, rapidly reached a plateau and remained constant, as it did on polyvinyl chloride and polyethylene tubing. Adhesion of staphylococci was enhanced on Tenckhoff catheters exposed to PD effluent compared to unused PD solution. Conclusions The data identify surface exposed proteins that may serve as adhesion sites for microbes on peritoneal catheters indwelled in patients undergoing PD.


2020 ◽  
Vol 40 (05) ◽  
pp. 671-678
Author(s):  
Cenk Gokalp ◽  
Fatma Keklik Karadag ◽  
Matthias Christoph Braunisch ◽  
Christoph Schmaderer ◽  
Emrah Gunay ◽  
...  

Abstract Introduction Platelet dysfunction is not uncommon in patients with end-stage renal disease (ESRD). Type of renal replacement therapy may have an effect on platelet functions, which has not been well investigated. We evaluated in vitro closure time (CT) differences between peritoneal dialysis (PD) and hemodialysis (HD) patients using platelet function analyzer (PFA-100)and observed a significant difference between these renal replacement therapies. Methods Patients with ESRD undergoing PD (n = 24) or HD (n = 23) for more than 6 months were included. Blood samples for collagen/epinephrine (Col/EPI) and collagen/adenosine diphosphate (Col/ADP) measurements were obtained before HD at a mid-week session for HD patients and at an outpatient control time for PD patients. Results Three of 24 (12.5%) PD patients and 16 of 23 (69.5%) HD patients had prolonged PFA-100 Col/EPI, p< 0.001. Likewise, 4.2% of PD patients and 87.0% of HD patients had prolonged PFA-100 Col/ADP, p< 0.001. Moreover, the median times of PFA-Col/EPI and PFA-100 Col/ADP were significantly lower in PD patients compared with those of HD patients (p< 0.001). Multivariate analysis showed that the type of renal replacement was a risk factor for both elevated PFA-100 Col/ADP and PFA-100 Col/EPI after adjusted for platelets, hematocrit, and urea (p< 0.001). Conclusions The type of renal replacement therapy may have an effect on in vitro CTs; therefore, studies including more patients with long-term follow-up are needed to investigate if the difference has any impact on clinical outcomes.


2018 ◽  
Vol 19 (10) ◽  
pp. 3107 ◽  
Author(s):  
Abraham Arellano Buendía ◽  
Montserrat Tostado González ◽  
Omegar Sánchez Reyes ◽  
Fernando García Arroyo ◽  
Raúl Argüello García ◽  
...  

Diabetic nephropathy (DN) is presently the primary cause of chronic kidney disease and end-stage renal disease (ESRD). It has been suggested that inflammation and oxidative stress, in addition to or in concert with the metabolic changes, plays an important role in the maintenance and progression of the disease. Therefore, attenuating or blocking these mechanisms may be a therapeutic target to delay the progression of the disease. Diallyl thiosulfinate (allicin), a compound derived from garlic, inhibits free radical formation, increases glutathione synthesis and decreases the levels of proinflammatory molecules in vitro. This research aimed to assess the effect of allicin on oxidative stress and inflammation-induced diabetes. Animals were divided into control and diabetes (streptozotocin 50 mg/kg i.p.), and maintained for 30 days. After 30 days, the group of diabetic animals was subdivided into diabetes and allicin-treated diabetes (16 mg/kg/day oral gavage). The three experimental groups were maintained for another month. We analyzed the status of renal function, oxidative stress and proinflammatory cytokines. The untreated diabetic group showed hyperglycemia and increased diuresis, creatinine clearance, proteinuria, glycosuria and urinary excretion of N-acetyl-β-d-glucosaminidase (NAG), as well as increased oxidative stress and the expression of interleukin 1β (IL-1β), IL-6, nuclear factor kappa beta (NFκβ) and transforming growth factor-β1 (TGF-β1) in plasma and kidney. In contrast, the inhibitor of NFκβ (Iκβ) is decreased in the cortex. It has been demonstrated that the allicin treatment decreases hyperglycemia, polyuria, and NAG excretion. The oxidative stress and proinflammatory cytokines were also reduced by the allicin treatment. In conclusion, allicin delays the progression of diabetic nephropathy through antioxidant and anti-inflammatory mechanisms.


2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Elena Dozio ◽  
Federico Ambrogi ◽  
Massimo de Cal ◽  
Elena Vianello ◽  
Claudio Ronco ◽  
...  

End-stage renal disease patients on dialysis (CKD-G5D) have a high mortality rate due to cardiovascular diseases (CVD). In these patients, inflammation, oxidative stress, and uremia increase the production of glycation products (AGEs) which in turn accelerate CVD onset and progression. Recently, attention has been given to the soluble receptor for AGEs (sRAGE) as a marker of inflammation, oxidative stress, atherosclerosis, and heart failure in CKD-G5D. However, its association with patient outcomes is still under debate. Our aim is to explore whether sRAGE may be a predictor of mortality in CKD-G5D. We studied 123 CKD-G5D for 24 months. Of these patients, 56 were on hemodialysis (HD) and 67 on peritoneal dialysis (PD). Demographic, anthropometric, biochemical, and clinical data were recorded. sRAGE was quantified by enzyme-linked immunosorbent assay. sRAGE was a predictor of mortality at 2-year follow-up. Each increase of 100 pg/mL in sRAGE levels was associated with an approximately 7% increased risk of mortality. Furthermore, in the entire study group, as well as in PD and HD patient subgroups, sRAGE was positively correlated with brain natriuretic peptide (BNP) levels. Mortality rates as well as sRAGE levels in patients who died did not differ between PD and HD patients. In conclusion, the positive association observed with BNP levels suggests a role for sRAGE as a prognostic factor for mortality in CKD-G5D patients displaying an active process of cardiac remodeling.


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