Résumé
Peritoneal ultrafiltration failure is a common reason for peritoneal dialysis (PD) withdrawal as well as mortality in PD patients. Based on the three-pore system, inter-cellular small pores and trans-cellular ultra-small pores (aquaporin-1) are mainly responsible for water transfer across the peritoneum. Both small and ultra-small pores-dependent water (free water) transport decline accompanied with time on PD, with more significant decrease in free water, resulting in peritoneal ultrafiltration failure. The reduction of free water transport is associated with fast peritoneal solute transfer, reduced crystalloid osmotic gradient due to increased interstitial glucose absorption, and declined osmotic conductance to glucose resulted from impaired aquaporin-1 function and peritoneal interstitial fibrosis. The decline of small pore-based water is mainly because of fast loss of crystalloid osmotic gradient, decrease of hydrostatic pressure mediated by peritoneal vasculopathy, as well as reduced absolute number of small pores. The current review discusses the advance on pathogenesis of acquired peritoneal ultrafiltration failure in long-term PD.
Sujets)
Humains , Péritoine , Ultrafiltration , Solutions de dialyse , Dialyse péritonéale/méthodes , Eau , GlucoseRésumé
Objective·To explore the changes of pyruvate dehydrogenase (PDH) activity and pyruvate dehydrogenase kinase 4 (PDK4) expression in the end-stage renal disease (ESRD) patients' skeletal muscles. Methods·Skeletal muscle samples were collected from non-chronic kidney disease (non-CKD) patients and ESRD patients. PDH activity was detected by ELISA assay. Real-time qPCR was performed to examine gene transcription levels of PDK1-PDK4 and PDH subunits.Western blotting analysis was used to detect protein expression levels of PDK1 and PDK4. Results·There were no demographic differences between two groups of patients. Plasma creatinine and urea nitrogen were significantly elevated in ESRD group (both P<0.05), while estimated glomerular filtration rate, hemoglobin and plasma albumin in ESRD group were significantly lower than those in non-CKD group (all P<0.05).Skeletal muscle PDH activity in ESRD group was markedly lower than that in non-CKD group(P=0.014).There were no differences in PDK1-PDK4 and PDH subunits mRNA transcription levels between ESRD and non-CKD group.PDK4 protein expression was significantly higher than that in non-CKD group (P=0.000). Conclusion·The decreased PDH activity in ESRD patients' skeletal muscle may be related to up-regulation of PDK4.
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Objective·To investigate the mechanism of fructose-induced monocyte chemoattratant protein-1(MCP-1) production in HK-2 cells.Methods·The HK-2 cells were divided into fructose incubated (1,5 and 10 mmol/L) group,fructose and ketohexo-kinase inhibitor (KHK-IN) coincubation (fructose 5 mmol/L,KHK-IN was 12,100 and 1 000 nmol/L,respectively) group,uric acid incubation (5,15 and 50 mg/dL) group,fructose and allopurinol co-incubation (fructose 5 mmol/L,allopurinol were 0.01,0.1 and 0.5 mmol/L) group,uric acid and allopurinol co-incubation (uric acid 50 mg/dL,allopttrinol respectively 0.01,0.1and 0.5 mmol/L) group,H2O2 incubation (0.1 and 0.3 mmol/L) group,fructose and N-acetylcysteine (NAC) coincubation (fructose 5 mmol/L,NAC respectively 5,10 and 50 mmol/L) group,and uric acid and NAC co-incubation (uric acid 50 mg/dL,NAC was 5,10and 50 mmol/L,respectively) group.The quantitative PCR method and Western blotting method were used to observe the expression ofMCP-1 mRNA and protein.The effects of fructose and uric acid on the production of ROS in HK-2 cells were observed by using a fluorescent probe.Results·Fructose doseand time-dependently induced MCP-1 gene transcription and protein production in HK-2 cells,which could be blocked by the ketohexo-kinase blockers.Exogenous uric acid induced MCP-1 production in HK-2 cells.Allopurinol inhibited fructose,but not exogenous uric acid-induced MCP-1 expression.Both fructose and uric acid induced ROS generation.Incubation with H2O2promoted MCP-1 production in HK-2 cells.NAC completely inhibited MCP-1production induced by fructose and H2O2.Conclusion·Catalyzed by the ketohexo-kinase,fructose resultes the production of MCP-1 through uric acid and reactive oxygen species.
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Objective · To assess volume status in maintenance hemodialysis (MHD) patients.Methods · Body composition analysis was performed on 128 MHD patients from Renji Hospital,Shanghai Jiao Tong University School of Medicine.The volume status was assessed based on body composition data and predialysis systolic blood pressure (preBPsys),edema grade,brain natriuretic peptide (BNP).Patients were divided into hyperhydrated group (percentage of hydration status,HS%> 15%) or normohydrated group (HS% ≤ 15%).Body composition data were compared,including lean tissue index (LTI) and fat tissue index (FTI).The blood pressure,edema grade,serum calcium,serum phosphate,intact parathyroid hormone (iPTH),hemoglobin,albumin,pre-albumin,hypersensitive C-reactive protein (hs-CRP),serum sodium,and urea clearance Kt/V were compared between two groups.Results · Sixtynine patients were normohydrated and preBPsys reached target;10 patients were overhydrated with higher preBPsys;18 patients had overhydration but preBPsys was in target range.Compared to normohydraed group,patients in hyperhydmted group had more obvious edema,higher BNP level,significantly lower LTI,serum albumin and pre-albumin levels,while serum sodium was significantly higher (P<0.05).Conclusion· Volume status of hemodialysis patients can be objectively and accurately assessed by body composition analysis using bioimpedance technique with blood pressure,edema grade and biochemical parameters.Hyperhydrated patients may have higher serum sodium level,lower serum albumin,lower hemoglobin,and less lean tissue mass concomitantly.Sodium intake control,nutrition status improvement,and anemia correction may be useful to reduce hyperhydration.