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Background Incremental peritoneal dialysis (iPD) can be useful in patients with residual renal function (RRF). RRF was well preserved and similar survival was shown in iPD compared to conventional PD (cPD) in previous study. However, the long-term survival of iPD remains unclear compared to cPD in diabetic patients. This study evaluated whether patient survival, hospitalization and peritonitis, and PD survival in iPD were lower than cPD or not. Methods We conducted a 12-year retrospective observational study of 303 PD patients (232 cPD and 71 iPD) using propensity score matching by age, gender, and diabetes mellitus (DM). Finally, 78 cPD patients and 39 iPD patients were included and 44 patients had DM. Incremental PD was defined as starting PD with two or three manual exchanges per day. Results The median duration of iPD was 24.1 months and iPD had higher RRF than cPD. Compared to cPD, the patient survival, PD survival and hospitalization benefits were not found in iPD but diabetic iPD patients had significantly longer survival and less hospitalization. Cumulative risk for peritonitis was lower iPD and PD duration of iPD was longer than those of cPD. The iPD was an independent factor associated with survival in patients with DM. Conclusions Incremental PD may be a safe PD modality to initiate and maintain PD in less uremic patients with tolerable RRF. Incremental PD would be a benefit for survival in diabetic patients. Further prospective studies are necessary to confirm the effectiveness of iPD in PD patients with similar RRF.

Aim: Stearoyl-CoA desaturase (SCD)-1 and elongase-6 (Elovl-6) are associated with fatty acid (FA) synthesis. We evaluated the effect of omega-3 FA on erythrocyte membrane FA contents through SCD-1 and Elovl-6 expression in the liver and kidney of a cyclosporine (CsA)-induced rat model. Methods: Male Sprague Dawley rats were divided into control, CsA, and CsA treated with omega-3 FA groups. We measured SCD-1 and Elovl-6 expression levels via western blot and immunohistochemistry analysis. Results: Erythrocyte membrane oleic acid content was lower in the CsA with omega-3 FA group compared to the CsA group. Compared to the control group, CsA-induced rats showed elevated SCD-1 expression in the kidney and liver, which omega-3 FA treatment reversed. Elovl-6 expression was increased in the liver, but decreased in the kidney in CsA group compared to control, which omega-3 FA treatment also reversed. Conclusions: Omega-3 FA supplementation decreased erythrocyte membrane oleic acid content by modulating SCD-1 and Elovl-6 expression in the kidney and liver of CsA-induced rats.

Background: Statin treatment has decreased the risk of cardiovascular events in patients with chronic kidney disease (CKD). Erythro-cyte membrane oleic acid level is higher in patients with acute coronary syndrome. This study aimed to evaluate the effect of pravas-tatin on the erythrocyte membrane fatty acid (FA) contents in patients with CKD. Methods: Sixty-two patients were enrolled from January 2017 to March 2019 (NCT02992548). Pravastatin was initially administered at a dose of 20 mg for 24 weeks. The pravastatin dose was increased to 40 mg after 12 weeks if it was necessary to control dyslipid-emia. The primary outcome was change in erythrocyte membrane FA, including oleic acid, after pravastatin treatment for 24 weeks. Results: Forty-five patients finished this study, and there was no adverse effect related to pravastatin. Compared with baseline, total cholesterol and low-density lipoprotein cholesterol levels were significantly decreased after pravastatin treatment. Compared with baseline, saturated FA, oleic acid, and arachidonic acid levels were significantly increased and polyunsaturated FA and linoleic acid (LA) levels were significantly decreased after pravastatin treatment. There was also a decrease in eicosapentaenoic acid after pravas-tatin treatment in CKD patients with estimated glomerular filtration rate < 60 mL/min/1.73㎡. Conclusion: Administration of pravastatin in patients with CKD leads to a decrease in FA known to be protective against the risk of CVD. Omega-3 FA or LA supplementation might be necessary to recover changes in erythrocyte membrane FA contents when pravas-tatin is used for treating dyslipidemia in patients with CKD.

Background and Aims Dyslipidemia is a major cause of cardiovascular disease (CVD) and CVD incidence is definitely increased according to peritoneal dialysis (PD) vintage. The PD solutions contained glucose may affect on dyslipidemia including hypertriglyceridemia. The oleic acid (OA) content in the erythrocyte membrane was increased in patients with acute coronary syndrome and is significantly higher in PD patients than hemodialysis patients. We conducted this trial for comparing effect of icodextrin or glucose PD solutions on triglyceride and oleic acid levels in PD patients. Method This EXIT trial is an open label, randomized, cross-over multi-center trial. Twenty-two patients were enrolled and 15 patients finished this trial. Glucose group was initially exposed to glucose PD solutions for 6 months and then exposed to icodextrin PD solution for 3 months. Extraneal group was initially exposed to icodextrin PD solution for 3 months and then exposed to glucose PD solutions for 6 months. Results The enrolled patients were aged 63.6 ± 9.5 years old and mean PD duration was 10.8 ± 5.9 months. There were no significant differences of baseline clinical and laboratory data between glucose group and extraneal group. There was no significant decrease of triglyceride levels, erythrocyte membrane OA and monounsaturated fatty acid (MUFA) contents after 3 months exposure of icodextrin PD solution compared to baseline. However, there was a tendency of triglyceride levels decrease (p=0.093) after 3 months exposure with icodextrin PD solution and there was a tendency of triglyceride levels increase (p=0.078) after 3 months exposure with glucose PD solutions compared to baseline levels. Continuous 6 months exposure with glucose PD solution significantly increased triglyceride levels (p=0.041), LDL cholesterol levels, erythrocyte membrane OA (p=0.009) and MUFA compared to baseline levels. Conclusion Continuous exposure of glucose PD solutions may negatively affect on triglyceride and erythrocyte membrane OA contents. Combined use of icodextrin and glucose PD solutions may prevent lipid derangement (ClinicalTrial.gov number, NCT NCT02166359).

Background and Aims Treatment with statin has been decreased the risk of cardiovascular events in patients with chronic kidney disease (CKD). Erythrocyte membrane oleic acid contents are significantly higher in patients with acute coronary syndrome than control subjects. Still, there is no report about the effect of statin on erythrocyte membrane fatty acid (FA) including oleic acid. The aim of this study was to evaluate the effect of pravastatin on the erythrocyte membrane FA in patients with CKD. Method Sixty two CKD patients were enrolled in this single arm randomized clinical trial and this trial was conducted at two centers from Jan 2017 to March 2019 (NCT02992548). Pravastatin with dose of 20mg was initially treated for 24 weeks. Pravastatin dose was increased to 40mg after 12 weeks, if it is necessary to control dyslipidemia. The primary outcome of this study was the change of erythrocyte membrane FA including oleic acid after pravastatin treatment for 24 weeks. We checked total cholesterol, triglyceride, LDL-cholesterol, HDL-cholesterol and adiponectin for secondary outcome at baseline and after 24 weeks. Erythrocyte membrane FA contents were measured by gas chromatography at baseline and after 24 weeks. Results Forty-five patients finished this study (age: 59.2±12.4 years, male: 42.2%, diabetes: 48.9%). There was no adverse effect related with pravastatin. Baseline serum creatinine was 1.5±0.7 mg/dL and estimated glomerular filtration rate was 54.2±27.3 ml/min/1.73 m2. Compared to baseline, total cholesterol (223.1±50.8 mg/dL vs. 168.4±32.5 mg/dL), LDL-cholesterol (149.1±35.3mg/dL vs. 100.1±25.4 mg/dL) and C-reactive protein were significantly decreased after pravastatin treatment. There were no significant changes in triglyceride, HDL-cholesterol, serum creatinine, amounts of proteinuria and adiponectin levels. Saturated FA, oleic acid and arachidonic acid contents of erythrocyte membrane were significantly increased after pravastatin treatment compared to baseline levels. Polyunsaturated FA (PUFA) and linoleic acid were significantly decreased after pravastatin treatment compared to baseline. Decreased tendency of eicosapentaenoic acid and omega-3 index were found after pravastatin treatment. Conclusion Linoleic acid or omega-3 FA supplementations may be necessary to recover erythrocyte membrane FA changes, when pravastatin is used for dyslipidemia treatment in CKD patients. Further study for reducing cardiovascular events are necessary by using combined PUFA and pravastatin treatment.

Minimal change disease (MCD) is a common cause of nephrotic syndrome and relatively well responds with steroid treatment. However, nearly half of patients with MCD experience recurrence of nephrotic syndrome. Thromboembolic events including renal vein thrombosis may occur in patients with MCD, but portal vein thrombosis rarely occurs. We experienced a case of frequent relapse/steroid dependent MCD with nephrotic syndrome progressed to steroid resistance associated with portal vein thrombosis. This patient showed complete remission of MCD and resolution of portal vein thrombosis after treatment with corticosteroid, cyclosporine, mycophenolate mofetil, and anticoagulant.

Elevated lactate levels are associated with acute illnesses, and the mortality is high. Here, we report a case of lactate-containing peritoneal dialysis (PD) solution inducing lactic acidosis corrected by changing to hemodialysis (HD). This 70-year-old female patient was treated with PD 8 months previously for end-stage renal disease caused by diabetes mellitus. She was admitted complaining of general weakness. Initial lactate level was 22.1 mg/dL and increased to 62.4 mg/dL showing high anion gap metabolic acidosis and compensatory hyperventilation. There are no definite causes of lactic acidosis besides the use of PD solutions containing a lactate component. The patient's lactate level was decreased after temporarily changing the dialysis modality to HD. Her lactate level was increased again after restarting PD, and decreased to normal after restarting HD. We report this case because physicians should consider lactate-containing PD solution as a possible cause of lactic acidosis.

Background: Previous studies have shown that a higher resistive index (RI) on renal duplex ultrasonography was related with renal progression and acute kidney injury, especially in patients with chronic kidney disease (CKD) using an angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor antagonist (ARB). We evaluated whether a RI value is a predictive factor for renal progression regardless of ACEI or ARB medication in patients with moderate renal dysfunction. Methods: We retrospectively analyzed 119 patients with moderate renal dysfunction that had been evaluated with renal duplex ultrasonography from February 2011 to April 2015. Moderate renal dysfunction was defined as a stage 3 to 4 CKD. Renal progression was defined as a doubling of the baseline serum creatinine (sCr), a decrease of baseline glomerular filtration rate by > 50%, or initiation of renal replacement therapy. Results: The mean age was 64.7 ± 11.0 years and sCr level was 2.1 ± 1.2 mg/dL. The RI ≥ 0.79 group showed a higher incidence of renal progression (P = 0.004, log-rank test) compared with the RI < 0.79 group, irrespective of ACEI or ARB usage. In the Cox proportional hazard model, RI ≥ 0.79 was an independent prognostic factor after adjusting for age, sex, diabetes mellitus, sCr, proteinuria, and use of ACEI or ARB (hazard ratio, 4.88; 95% confidence interval, 1.06-22.53; P = 0.043). Conclusion: RI ≥ 0.79 on the renal duplex ultrasonography can be a helpful predictor for renal progression in patients with moderate renal dysfunction, regardless of their ACEI or ARB usage.

Background : Serum myostatin levels are increased according to renal function decline and myostatin may be a main mediator of chronic kidney disease–related sarcopenia. A previous study reported that serum myostatin level was negatively associated with abdominal aortic calcification (AAC) in older males. The aim of this study was to assess the association between serum myostatin level and AAC among dialysis patients of both sexes. In addition, we analyzed the relationship between serum myostatin level, muscle mass, and bone mineral density (BMD).Methods : In this cross-sectional study, we evaluated AAC in the lateral lumbar spine using plain radiography and BMD in 71 patients undergoing dialysis. We classified patients into two groups according to the median value of myostatin as follows: those with high myostatin levels (≥ 5.0 ng/mL) and those with low myostatin levels (< 5.0 ng/mL).Results : The proportion of patients with an AAC score of five points or more was higher among those with low myostatin levels. Myostatin level was negatively associated with AAC scores on plain radiography and had a positive association with skeletal muscle mass and T-scores for BMD measured at the total hip and femur neck. Lower myostatin levels were independently associated with higher AAC scores following adjustment for age, sex, diabetes mellitus, dialysis vintage, dialysis modality, and osteoprotegerin level.Conclusion : Lower serum myostatin levels were associated with higher AAC scores, lower muscle mass, and lower BMD in dialysis patients. Further, prospective studies and those with larger cohorts are necessary to validate these findings.

Six transmembrane protein of prostate 2 (STAMP2) is a critical modulator of inflammation and metabolism in adipose tissue. There are no data on the expression of STAMP2 in chronic kidney disease, which is an inflammatory disease related to metabolic disorders. This study aimed to investigate STAMP2 expression in the kidney and heart in 5/6 nephrectomy (Nx) rats, and the effect of omega-3 fatty acid (FA) on STAMP2 expression. Male Sprague Dawley rats were divided into three groups: sham control (0.9% saline), 5/6 Nx (0.9% saline), and 5/6 Nx treated with omega-3 FA (300 mg per kg per day by gastric gavage). The expression of STAMP2 in the kidney and heart were examined by western blotting. Serum creatinine levels were higher in 5/6 Nx rats than in controls. Compared with sham controls, the expression of I&kappa, B, NF-&kappa, B, NOX4, SREBP-1, and LXR were upregulated and STAMP2 and phosphorylated-AMPK expression were downregulated in the kidney and heart of 5/6 Nx rats. Omega-3 FA supplementation prevented these changes in biomarkers related to inflammation and metabolic lipid disorders. Omega 3-FA supplementation induced the upregulation of STAMP2 protein in 5/6 Nx rats, which was associated with an attenuation of inflammation- and metabolic disease-related markers.

The firing process to bond an enamel frit onto a steel substrate is conducted under a high-temperature condition of approximately 830°ýC for 3min, which leads to the thermal deformation of the enameled steel product. This thermal deformation of the enameled steel is one of the main problems with the firing process. The thermal deformation is also affected by the residual stress of the enamel coating, which is generated by the mismatch between the thermal expansion coefficient of the enamel and that of the steel substrate. The objective of this study was to predict the deformation and residual stress of enameled steel using an analytical model and finite element analysis. To verify the results from the prediction methods, firing and cooling experiments were performed using the same conditions as such methods, and the experimental results were compared to those of the prediction methods. The residual stress was measured using a crack indentation technique based on a pyramidal diamond indenter. The magnitude of the residual stress could be determined by comparing the crack lengths in the unstressed and stressed specimens. The results of the prediction methods were in good agreement with the experimental results with respect to the deformation and residual stress.

The objective of this study is to design a stamping process for polymer-coated metal (PCM) sheets to prevent defects such as delamination and tearing. A defect diagram composed of the delamination limit curve and the tearing limit curve of the PCM sheet is developed for determining the safe region. Similar to the forming limit diagram, the defect diagram is constructed using the critical major and minor strains at which defects occur in various deformation modes. Experiments are performed for establishing the defect diagram of the PCM sheet by means of the limit dome height test and square cup deep-drawing test. A cross-hatched specimen is employed for estimating the delamination of the polymer layer from the steel substrate. Based on the defect diagram, a finite element analysis (FEA) of the stamping process is conducted to determine a forming condition without delamination and tearing. The effectiveness of the stamping process designed on the basis of the developed defect diagram is verified by a forming experiment. Comparison of the FEA results and experimental results reveals that the defect diagram is efficient and suitable for the design of the actual stamping process using PCM sheets.

The high incidence of cardiovascular disease and vitamin D deficiency in chronic kidney disease patients is well known. Vitamin D activation by omega-3 fatty acid (FA) supplementation may explain the cardioprotective effects exerted by omega-3 FA. We hypothesized that omega-3 FA and 25-hydroxyvitamin D (25(OH)D) supplementation may increase 1,25-dihydroxyvitamin D (1,25(OH)2D) levels compared to 25(OH)D supplementation alone in hemodialysis (HD) patients that have insufficient or deficient 25(OH)D levels. We enrolled patients that were treated for at least six months with 25(OH)D &lt, 30 ng/mL (NCT01596842). Patients were randomized to treatment for 12 weeks with cholecalciferol supplemented with omega-3 FA or a placebo. Levels of 25(OH)D and 1,25(OH)2D were measured after 12 weeks. The erythrocyte membrane FA contents were also measured. Levels of 25(OH)D were increased in both groups at 12 weeks compared to baseline. The 1,25(OH)2D levels at 12 weeks compared to baseline showed a tendency to increase in the omega-3 FA group. The oleic acid and monounsaturated FA content decreased, while the omega-3 index increased in the omega-3 FA group. Omega-3 FA supplementation may be partly associated with vitamin D activation, although increased 25(OH)D levels caused by short-term cholecalciferol supplementation were not associated with vitamin D activation in HD patients.

Background Modifications of erythrocyte membrane fatty acid (FA) contents may affect cellular function or transmembrane receptors. One cross-sectional study has shown that kidney transplant (KTP) recipients have lower erythrocyte membrane oleic acid content than dialysis patients do. Therefore, we prospectively tested whether erythrocyte membrane contents of FA including oleic acid change after KTP. Methods We recruited 23 KTP recipients (September 2011 through May 2014). Blood samples were obtained immediately before KTP and 6 months after. Erythrocyte membrane FA contents were measured by gas chromatography. Results Mean age of the enrolled KTP recipients was 45.3 ± 10.9 years, and men represented 66.7% of the cases. ABO-incompatible KTPs constituted 14.3% and cadaver donors 42.9% of the cases. Steroids, mycophenolate mofetil, and tacrolimus were used as immunosuppressive treatment. There was no significant difference in dietary consumption between time points before and 6 months after KTP. Total cholesterol and low-density lipoprotein cholesterol levels were significantly higher at 6 months after KTP as compared with baseline. Erythrocyte membrane contents of polyunsaturated FA, ω-3 FA, ω-6 FA, and the ω-3 index were significantly higher, but erythrocyte membrane contents of total saturated FAs, total monounsaturated FAs, including oleic acid, total trans-FA, palmitoleic acid, and the ω-6-to-ω-3 ratio were significantly lower at 6 months after KTP. Conclusions Erythrocyte membrane FA contents significantly changed toward a more favorable cardiovascular profile after KTP. These changes in erythrocyte membrane FA contents may be related to improved renal function because of the absence of significant dietary changes.

Background: Catheter-related exit site infection is a major risk factor for the development of peritonitis and can contribute to failure of treatment maintenance in peritoneal dialysis (PD) patients. Although povidone-iodine can be used for exit site care, the irritation induced by the local application of povidone-iodine could lead to secondary infection. Therefore, we evaluated the clinical effectiveness of normal saline compared with povidone-iodine as a method of exit site care in chronic PD patients. Methods: In all, 126 patients undergoing PD treatment for>6 months between January 2006 and December 2009 were enrolled. Data were retrospectively analyzed for the incidence of exit site infection and peritonitis for 2 years prior to and after December 2007. In addition, we identified the incidences of catheter-related infections during follow-ups from January 2010 to December 2013. Results: The participants׳ mean age was 58.8±12.9 years. The incidences of exit site infection and peritonitis were one episode per 64.6 patients–months and one episode per 40.4 patients–months in the povidone-iodine group, respectively, whereas these were one episode per 57.5 patients–months and one episode per 45.6 patients–months in the normal saline group, respectively. Whereas Gram-positive bacteria most frequently caused catheter-related infections in both groups, culture-negative infections were dominant in the normal saline group. Conclusion: Exit site care using normal saline did not increase the incidence of exit site infection and peritonitis. Therefore, normal saline may be an alternative treatment for exit site care in patients receiving PD.

The cracking of enamel coating often occurs because of excessive tensile stress under the product usage environment. The cracks loosen the enamel coating, leading to spalling and peeling and subsequent corrosion of the metal substrate. The cracking is also affected by the residual stress, which complicates the prediction of cracking initiation. The objective of this study is to predict the cracking initiation of the enamel coating by the FE-analysis. The brittle fracture properties of the enamel coating in the FE-analysis were determined by an experimental Vickers indentation fracture (VIF) test and a uniaxial tensile test. The effect of the residual stress of the enamel coating generated by the firing and cooling process on the cracking was considered and analyzed with a four-point bending model by the FE-analysis. To verify the predicted displacement up to the cracking initiation of the enamel from the FE-analysis, a four-point bending test was also performed using the same conditions as the simulation and the results were in agreement with those of the simulation.

The protein 1&alpha, hydroxylase (CYP27B1) was expressed in liver and omega-3 fatty acid (FA) elevated 1,25-dihydroxyvitamin D [1,25(OH)2D] levels in dialysis patients. The aim of this study was to determine whether omega-3 FA and cholecalciferol have effects on vitamin D metabolism related to CYP27B1 and 24-hydroxylase (CYP24) activities in the kidney and liver of 5/6 nephrectomy (Nx) rats. Male Sprague&ndash, Dawley rats were divided into the following groups: sham control, 5/6 Nx, 5/6 Nx treated with cholecalciferol, 5/6 Nx treated with omega-3 FA, and 5/6 Nx treated with cholecalciferol/omega-3 FA. CYP27B1 and CYP24 expression were measured in the liver and kidney. Further, 1,25(OH)2D and 25-hydroxyvitamin D [25(OH)D] levels were measured in serum. Among Nx groups, 1,25(OH)2D and 25(OH)D levels were lowest in the 5/6 Nx group. CYP24 expression was increased in the kidney of the 5/6 Nx rat model, which was found to be reversed by omega-3 FA or cholecalciferol/omega-3 FA supplementation. Decreased CYP27B1 expression was observed in the liver of the 5/6 Nx rats and its expression was recovered by supplementation with cholecalciferol/omega-3 FA. In conclusion, omega-3 FA and cholecalciferol may synergistically increase 1,25(OH)2D levels by inhibiting CYP24 expression in the kidney and liver and activating CYP27B1 expression in the liver of 5/6 Nx rats.

Objectives Protein kinase casein kinase II (PKCK2) has multiple, overlapping roles in induction of apoptosis. Apoptosis can be a common pathway of renal injury caused by a nephrotoxic drug or an injury. We evaluated the role of PKCK2 in cyclosporine (CsA)-induced nephropathy in rats by inhibiting PKCK2 with emodin. Methods Male Sprague-Dawley rats fed a low-sodium diet were divided into four treatment groups: control (0.9% saline injection), CsA (15 mg/kg/d subcutaneously), CsA + emodin (CsA plus emodin 20 mg/kg/d subcutaneously), and emodin only. The expression levels of apoptosis-associated factors and of PKCK2 were examined by Western blot analysis. Results Overexpression of PKCK2 noted with CsA treatment was prevented by emodin, a low-molecular-weight PKCK2 inhibitor, which dampend drug-induced up-regulation phosphorylated p53 and activation of caspases 3, 7, and 8. In addition, emodin prevented increased Bax/Bcl-2 ratio induced by CsA. Emodin prevented up-regulation of PKCK2 by CsA treatment, suggesting that its apoptotic-preventing activity was mediated via PKCK2. Conclusions Our findings indicated that PKCK2 may play a role in apoptotic injury associated with CsA-induced nephropathy in rats.

Background: Niacin supplementation improves dyslipidemia and lowers serum phosphorus levels in patients with chronic kidney disease (CKD). We evaluated whether low-dose niacin supplementation can improve dyslipidemia, lower serum phosphorus levels, and be administered with a low frequency of adverse effects in patients with CKD. Methods: We retrospectively analyzed the clinical records of patients with CKD who had taken niacin from January 2009 to June 2011. We excluded patients with CKD stage 1 and 5. We then enrolled 31 patients with CKD who had taken niacin at a fixed dose of 500 mg/day for 6 months. We also randomly selected 30 patients with CKD who had been taking statin for 9 months as a control group. Results: Among the 34 patients with CKD who were prescribed niacin, five (14%) complained of adverse effects, and three (8%) discontinued niacin. The proportion of patients in the niacin group who had been taking a statin or omega-3 fatty acids was 67.7% and 48.8%, respectively. In the niacin group, high-density lipoprotein cholesterol level was significantly increased and triglyceride level was significantly decreased at 12 and 24 weeks compared with baseline levels (P

BackgroundClinical results of long-term peritoneal dialysis (PD) therapy in patients with liver cirrhosis (LC) and end-stage renal disease (ESRD) are controversial. This study evaluated the clinical outcomes of LC patients undergoing PD.MethodsClinical records were retrospectively collected from a single center between January 2007 and December 2014. An analysis of PD patients with LC and without liver disease was performed using propensity score matching. We further restricted matching by age, gender, and the presence of diabetes mellitus. Two cohorts of 33 patients each were selected. Early technical complications were defined as the presence of catheter-related complications, including malposition, leakage, omental wrapping, obstruction, and requiring a transfer to hemodialysis (HD) within 6 months of initiating PD.ResultsMean PD duration was lower in LC patients (57.2 ± 46.1 months) than in controls (85.8 ± 64.2 months). Blood urea nitrogen, creatinine, and albumin levels were significantly lower in LC patients than in the control group. Cystatin C and cystatin C-based glomerular filtration rates were not significantly different in the LC group compared with those in the controls. We found that the risks for early technical complications, peritonitis, and long-term PD and patient survival were not higher in patients with LC than in those without LC. Ascites were easily controlled, and hepatic encephalopathy did not affect PD maintenance in LC patients.ConclusionsThe clinical outcomes, including technical complications, peritonitis, and patients’ survival, suggest that PD can be used as a renal replacement therapy in ESRD patients with LC.

Background/Aim: Cyclosporine (CsA)-induced kidney injury is characterized by renal dysfunction with inflammatory cell infiltrations, apoptosis and fibrosis. Pleiotropic effects of statins may exert anti-inflammatory, antiapoptotic and antifibrotic actions beyond lipid control. The aim of this study is to investigate whether rosuvastatin (RUS) has anti-inflammatory, antiapoptotic and antifibrotic effects on chronic CsA-induced nephropathy in a rat model. Methods: Male Sprague-Dawley rats fed a low-sodium diet were divided into three treatment groups: control (0.9% saline injection), CsA (15 mg/kg/day by subcutaneous injection), CsA + RUS (10 mg/kg/day by gastric gavage). Renal function, CsA level and lipid levels were measured at the end of 4 weeks. The expression of ED-1, transforming growth factor-β1 (TGF-β1) and α-smooth muscle actin (α-SMA) for inflammation and fibrosis were examined by Western blot analysis. The expression levels of apoptosis-associated factors were examined by Western blot analysis. Apoptosis was evaluated using the terminal deoxynucleotidyl transferase-mediated biotin nick end-labeling (TUNEL) method. Results: Kidney function was decreased in CsA-treated rats compared with controls, which was attenuated by RUS. RUS did not affect the lipid level or the blood CsA level. TUNEL staining showed that RUS inhibited CsA-induced tubular apoptosis. RUS decreased CsA-induced increased expression of Bax/Bcl-2 ratio. The expressions of ED-1, α-SMA, TGF-β1, Smad2/3, Smad4 and p-JNK were increased in CsA-treated rats, which were attenuated by RUS. Tubular atrophy and interstitial fibrosis in CsA-treated rats were attenuated by RUS supplementation. Conclusion: RUS supplementation attenuates proinflammatory and apoptosis-related factors and inhibits the fibrotic pathways including the smad-dependent and smad-independent pathways in a rat model of CsA-induced nephropathy.