BackgroundPeritoneal fibrosis is a common complication in patients treated with long-term peritoneal dialysis. The aim of this study was to identify the microRNAs (miRNAs) involved in regulation of peritoneal fibrosis in a rat model of peritoneal dialysis.MethodsTwenty-four Sprague–Dawley (SD) rats were randomly allocated into three groups: (i) Control group (Cg, n = 8); (ii) Saline group (Sg, n = 8): daily intraperitoneal injection with 0.9% normal saline; (iii) Hypertonic dialysate group (HDg, n = 8): daily intraperitoneal injection with 4.25% peritoneal dialysis solution. Rats were sacrificed after four weeks for histological evaluation of peritoneal membrane and the expression of α-SMA and COL-1. A miRNA screen was performed using microarray analysis to identify differentially expressed miRNAs, which were then validated by real-time PCR.ResultsCompared with the control and the saline groups, hypertonic dialysate group showed impaired peritoneal function accompanied by a spectrum of morphological changes including thicker peritoneal membrane, higher collagen deposition, infiltration of mononuclear cells and neovascularization in the peritoneum. Increased mRNA and protein levels of α-SMA and COL-1 were observed in hypertonic dialysate group, indicating the progression of peritoneal fibrosis. The miRNA screen identified 8 significantly down-regulated miRNAs (miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b) and one highly up-regulated miRNA (miR-122) in the hypertonic dialysate group. The results were confirmed by real-time PCR.ConclusionsAltered miRNA expression in peritoneum was found in the rat model of peritoneal fibrosis, indicating that these miRNAs may be associated with pathogenesis of peritoneal fibrosis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12882-015-0039-z) contains supplementary material, which is available to authorized users.

: Objectives Data on angiotensin receptor-neprilysin inhibitor (ARNI) sacubitril-valsartan (SV) in patients undergoing maintenance dialysis is scarce. Our study aimed to investigate the effect of SV on patients undergoing dialysis. Methods We retrospectively reviewed the data of end-stage kidney disease (ESRD) patients undergoing either peritoneal dialysis (PD) or hemodialysis (HD) in our center. A total of 51 patients receiving SV treatment were enrolled in the SV group. Another 51 age and sex-matched patients on dialysis without SV treatment were selected as the control group. All the patients were regularly followed up in the dialysis clinic. Their clinical, biochemical, and echocardiographic parameters were all recorded at baseline and during follow-up. The effect and safety of SV were further analyzed. Results A total of 102 ESRD patients on dialysis (51 patients in the SV group and 51 patients in the control group) were finally enrolled. The median follow-up time was 349 days (interquartile range [IQR]: 217–535 days). The level of B-type natriuretic peptide (BNP) (median [IQR] before and after SV treatment: 596.35 pg/ml [190.6–1714.85] vs. 188.7 pg/ml [83.34–600.35], p < 0.001) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) (median [IQR]: 6316.00 pg/ml [4552.00–28598.00] vs. 5074.00 pg/ml [2229.00–9851.00], p = 0.022) were significantly decreased after treatment with SV. The variant rate of left ventricular ejection fraction (LVEF) was significantly higher in the SV group compared to the control group, especially in the PD subgroup. No significant difference was found in other echocardiographic parameters between SV and control group. Subgroup analysis of the PD group showed an increase in daily PD ultrafiltration (median [IQR]: 400 ml/d [200-500] vs. 500 ml/d [200–850], p = 0.114) after SV treatment. Variant rate of overhydration (OH) measured by the body composition monitor (BCM) of the SV group were significantly different from the control group (median [IQR]: −13.13% [−42.85%–27.84%] vs. 0% [−17.95%–53.85%], p = 0.049). The rate of hyperkalemia was slightly higher but without significant difference before and after the introduction of SV (19.6% vs. 27.5%, p = 0.350). No event of hypotension and angioedema were observed. Conclusions SV might have a cardio-protective role in ESRD patients undergoing dialysis, especially in PD patients. Serum potassium should be monitored during the treatment.

Objective Chronic pre-dialysis hyponatremia is not rare in maintenance hemodialysis (MHD) patients. However, the association between chronic pre-dialysis hyponatremia and mortality is uncertain due to multiple potential confounders such as hyperglycemia, fluid overload, and malnutrition. This study aimed to more comprehensively evaluate the association between chronic pre-dialysis hyponatremia and clinical outcomes in MHD patients. Methods We analyzed the data of 194 MHD patients with regular real-time measurements of pre-dialysis serum sodium from July 2015 to March 2021. Hyponatremia was defined as SNa ≤ 135 mmol/L and normonatremia as SNa > 135 mmol/L and < 145 mmol/L. We evaluated the association of baseline pre-dialysis serum sodium (SNa) and time-averaged SNa (TASNa) levels with all-cause mortality or new major adverse cardiovascular events (MACE) in MHD patients. Furthermore, the SNa levels were glucose, serum albumin, and fluid overload adjusted. The associations between SNa levels and all-cause mortality or new MACE were analyzed using time-varying Cox regression models. Results Among the total of 194 patients, 24 patients died and 45 new MACE occurred during a mean 35.2-month follow-up period. The baseline pre-dialysis SNa level was 137.1 ± 2.8 mmol/L (127–144 mmol/L). Kaplan–Meier survival analysis showed that there were no significant differences in all-cause mortality or new MACE between hyponatremia and normonatremia groups according to baseline pre-dialysis SNa or glucose-corrected SNa (gcSNa). The mean values of both TASNa and time-averaged glucose-corrected SNa (TAgcSNa) were 136.9 ± 2.4 mmol/L and 138.3 ± 2.0 mmol/L, respectively. Kaplan–Meier survival analysis showed that patients with pre-dialysis hyponatremia had higher all-cause mortality or new MACE compared with normonatremia patients whether grouped on TASNa or TAgcSNa. Cox models showed an increased risk of all‐cause mortality and new MACE in MHD patients with pre-dialysis hyponatremia based on TASNa or TAgcSNa. Even after full adjustment including time-dependent age and dialysis vintage, gender, diabetes, time-averaged weight gain (TAWG), and serum albumin, patients with pre-dialysis hyponatremia based on TASNa (HR 2.89; 95% CI 1.18–7.04; model 3) or TAgcSNa (HR 5.03; 95% CI 1.87–13.57; model 3) had approximately twofold or fourfold greater risk of all-cause mortality, respectively, compared with those with normonatremia. The risk of new MACE was also significantly elevated in patients with pre-dialysis hyponatremia based on TASNa (HR 3.86; 95% CI 2.13–7.01; model 1) or TAgcSNa (HR 2.43; 95% CI 1.14–5.15; model 1). After adjustment for time-dependent age and dialysis vintage, gender, diabetes, TAWG, and serum albumin, patients with pre-dialysis hyponatremia based on TASNa (HR 2.33; 95% CI 1.16–4.68; model 3) had a higher risk of new MACE compared with those with normonatremia. Conclusions Pre-dialysis time-averaged hyponatremia is independently associated with increased risks of all-cause mortality or new MACE in MHD patients. The baseline SNa level is not a predictor of clinical outcomes due to its variation over time. Hyperglycemia, fluid overload, and malnutrition do not have a significant impact on the risk association between chronic hyponatremia and all-cause mortality or new MACE in MHD patients.

Hemodialysis tunneled-cuffed catheterrelated atrial thrombus complicated with asymptomatic pulmonary emboli Dear Editor, Catheter-related right atrial thrombus (CRAT), especially complicated with pulmonary embolism (PE), is rarely reported and heedlessly overlooked in hemodialysis patients (1). It may lead to serious, even fatal, complications (2). A 35-yearold female with end-stage renal disease due to IgA nephritis was referred to our hospital on April 2016 for establishment of hemodialysis vascular access. A tunneled cuffed catheter (TCC) (Palindrome, Tyco Healthcare Group LP, Mansfield, MA, USA) was established through the right internal jugular vein, with the tip located in right atrium. Hemodialysis was started through the TCC three times weekly in a local hospital. The patient was given epoetin (EPO) but without regular dose adjustments. A routine transthoracic echocardiography (TTE) on May 9 th , 2016, revealed a large CRAT 2.7 cm × 2.4 cm in size, close to the tricuspid annulus, connected to the right atrial wall, and fixed around the catheter tip (Fig. 1). The CRAT moved back and forth due to heart movement, colliding with the right atrial wall. The patient was immediately admitted to our hospital, although having no discomfort. A physical examination was normal but laboratory results were significant for elevated D-dimer (314 ng/mL), hemoglobin (136 g/L) and creatinine (1247 µmol/L). Hemodialysis with the TCC was continued. EPO was stopped according to 2012 Kidney Disease Improving Global Outcomes (KDIGO) guidelines (3), and was later restarted with a decreased dose when reviewed hemoglobin value was 106 g/L. Catheter removal was delayed because of a high risk of clots breaking off and entering the pulmonary artery (4). Low-molecular-weight heparin, fraxiparine, 4100 IU/day was subcutaneously initiated and especially administered after each dialysis session. Transcatheter urokinase 250,000 IU/day was simultaneously administered over 4 hours. Seven days after the therapy, a repeated TTE showed that the CRAT had become enlarged, so a larger dosage of 500,000 IU/day urokinase was continued in the same way as above. Unfortunately, the patient had to transfer to a local hospital because of her medical insurance. Anticoagulant and thrombolytic therapy had been withheld for 15 days. On May 31, 2016, the patient was readmitted to our hospital without discomfort, and TTE showed stable CRAT 3.0 cm × 1.5 cm. Fraxiparine was re-administered as above. Her D-dimer value was increased to 2552 ng/mL. Computed tomography pulmonary angiogram (CTPA) subsequently demonstrated bilateral minor pulmonary emboli. An intensified thrombolysis was performed with transcatheter urokinase 750,000 IU/day over 8 hours. Six days later (5), the CRAT shrank to 2.0 cm × 1.5 cm, and had detached from the right atrial free wall. Subsequent removal of the TCC was performed uneventfully. Afterwards, thrombolysis with the urokinase was stopped but the anticoagulation with fraxiparine continued as above. Review CTPA showed complete dissolution...

Target: To compare the ultrasound characteristics between functional, mature arteriovenous fistulas and functional, non-mature arteriovenous fistulas and to identify the predictors of arteriovenous fistula maturation in the forearm. Methods: Patients with newly set-up functional arteriovenous fistulas were enrolled in this prospective cohort study. Ultrasound examinations were conducted pre-operatively and post-operatively. The inner vessel diameter, blood flow volume, and resistance index were measured and compared between the maturation group (Group M) and non-maturation group (Group N). Baseline parameters were calculated to determine the predictors of non-maturation of arteriovenous fistulas. Results: All 52 patients with functional arteriovenous fistulas, who were categorized into Group M (25 patients, 48.08%) and Group N (27 patients, 51.92%), finished 24 weeks of follow-up after arteriovenous fistula surgery. The arteriovenous fistulas displayed a significant and rapid increase in the vessel diameter (mean increase of 1.34 times in the arteries and 1.92 times in the veins) and blood flow volume (mean increase of 9.29 times of the arteries and 43.66 times of the veins) and a decrease in the resistance index (mean decrease in 48.00% in the arteries) 8 weeks after surgery. Group N had a lesser increase in the vessel diameters (1.78 times vs 2.06 times, t = −3.136, p = 0.003) and blood flow volume (33.98 times vs 54.11 times, t = −2.383, p = 0.021) of the cephalic vein draining segments (a6) than Group M. The baseline diameter of a6 was the only independent predictor (regression coefficient = 26.229, p = 0.008) of maturation of the functional arteriovenous fistulas after correcting for sex, age, diabetes kidney disease, weight, and height. Conclusion: The baseline diameter of the cephalic vein was the only predictor of arteriovenous fistula maturation based on the pre-operative ultrasound measurements in Chinese hemodialysis patients.