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Arterial calcification is an integral component of active atherosclerosis and is an independent risk factor for cardiovascular disease. Atherosclerosis is a systemic, life-threating disease that may occur at different sites and in various clinical presentations. Intracranial and valvular calcifications are common among dialysis patients and have been associated with poor cardiovascular outcomes. The aim of this study was to assess the clinical impact of valvular and intracranial arterial calcifications on mortality among chronic hemodialysis patients.A blinded neuroradiologist graded intracranial calcifications (ICC) of all hemodialysis patients who underwent brain computerized tomography (CT) from 2015 to 2017 in our institution. Valvular calcifications were assessed by echocardiography. Only hemodialysis patients with available echocardiography and brain CT were included.This study included 119 patients (mean age 70.6 ± 12.6 years, 57.1% men, and mean dialysis vintage 25.8 ± 42.6 months). Among the cohort, 19 (16%) had no cardiac or brain calcifications and 65 (54.6%) had both valvular and intracranial calcifications. Considering the patients with no calcification as the reference group yielded adjusted odds ratios for all-cause mortality of 3.68 (95%CI 1.55-8.75) among patients with any brain calcifications, p = 0.002. While valvular calcifications alone did not increase the 1-year mortality rate, ICC was the most important predictor of all-cause 1-year mortality in the study cohort.We found an independent association between ICC and the risk of death among hemodialysis patients. Assessing ICC may contribute to the risk stratification of hemodialysis patients. These calcifications are no less important than valvular calcifications.

Peritoneal dialysis (PD) causes structural and functional changes in the peritoneal membrane, which are attributed to local inflammatory process. This study assessed the presence of galectin-3 (Gal-3), a known inflammatory modulator, in dialysate effluent and correlated its levels with markers of inflammatory process. Gal-3 levels in serum and dialysate effluent were measured in prevalent PD patients on morning visits (n = 27) or during peritoneal equilibration tests (PET, n = 16), it association with clinical and laboratory parameters, including dialysate/plasma creatinine (D/P creatinine) and interleukin-6 (IL-6) levels was analysed. Gal-3 levels in dialysate effluent correlated with D/P creatinine (0.663, p = 0.005) and dialysate effluent IL-6 levels (0.674, p = 0.002), but not with serum Gal-3 levels or dialysis vintage. Patients who were high transporters had higher Gal-3 levels in dialysate effluent, as compared to lower transporters. In multivariate regression analysis, dialysate IL-6 level was the strongest predictor of dialysate Gal-3 levels. This study found Gal-3 in dialysate effluent correlated with D/P creatinine and dialysate IL-6 levels. These findings may imply that Gal-3 has a role in the intraperitoneal inflammatory process. However, this needs to be investigated further.

Brain atrophy (BA) is often found in neuroimaging of hemodialysis patients, representing parenchymal cerebral damage. Likely contributing factors to BA are age, chronic hypertension, diabetes mellitus and other cardiovascular risk factors of atherosclerosis that are also common among hemodialysis patients. BA may also occur due to focal ischemia and hypoperfusion during hemodialysis. However, data on optimal blood pressure (BP) in these patients are limited. The goal of this study was to determine whether the prevalence and severity of BA would be higher among hemodialysis patients with lower BP. A blinded neuroradiologist graded BA of all hemodialysis patients who underwent brain non-contrast computerized tomography (CT) from 2015 to 2017 in our institution. Age- and sex-matched patients with normal kidney function who underwent brain CT during the same period and technique served as the control group. A total of 280 patients were included in this retrospective study, with average BP of 140/70 mmHg among hemodialysis patients and 142/75 mmHg in the control group. BA was more common in dialysis patients and its severity increased with age and traditional cardiovascular risk factors. We observed a significant negative correlation between diastolic BP (DBP) at dialysis initiation and BA. Average DBP decreased with increasing severity of BA. These findings were observed in both hemodialysis and non-CKD patients. BA was associated with lower DBP, which may induce cerebral hypoperfusion and ischemia. This finding should discourage over-treatment of hypertension among hemodialysis patients.

Background: Predicting the mortality risk of patients un­dergoing hemodialysis (HD) is challenging. Cell-free DNA (cfDNA) is released into circulation from dying cells, and its elevation is predictive of unfavorable outcome. In a pilot study, we found post-HD cfDNA level to be a predictor of all-cause mortality. Thus, the aim of this study was to confirm the prognostic power of cfDNA in a larger prospective cohort study conducted at 2 medical centers. Methods: CfDNA levels were measured by a rapid fluorometric assay on sera obtained before and after 1 HD session. One hundred fifty-three patients were followed up to 46 months for mortality during which time 47 patients died. We compared the predictive value of cfDNA to age, comorbidities, and standard blood tests. Results: Examining standard blood tests, only post-HD cfDNA levels were elevated in the non-survivor group compared to survivors (959 vs. 803 ng/mL, p = 0.04). Pre- and post-HD cfDNA levels correlated with age and diabetes. Patients with elevated cfDNA (>850 ng/mL) showed lower survival than those with normal levels. A Cox proportional hazard regression model demonstrated a significant hazard ratio of 1.92 for post-HD cfDNA levels. Logistic regression models showed that post-HD cfDNA was a significant predictor of mortality at 1–3 years with odd ratios of 4.61, 4.36, and 6.22, respectively. Conclusions: Post-HD cfDNA level was superior to standard blood tests and could serve as a biomarker to assist in decision-making for HD-treated patients.

Background and Aims Peritoneal dialysis (PD) is a common used method for renal replacement therapy. Prolonged PD treatment causes structural and functional changes in the peritoneal membrane which are attributed to local inflammatory process in the peritoneal cavity. Galectin-3 (Gal-3) is a galactoside-binding lectin with pro-inflammatory and pro-fibrotic effects. The aim of this study was to assess correlation between Gal-3 serum and dialysate effluent levels with peritoneal membrane transport characteristics. Method Gal-3 levels in serum and dialysate effluent were measured simultaneously in prevalent PD patients in morning visit or during peritoneal equilibration test (PET). Gal-3 levels were correlated with clinical and laboratory parameters. Interlukin (IL) -6 levels were measured in dialysate effluent. Gal-3 mRNA and protein expression were evaluated after exposure of primary endothelial cell culture to several dialysate solutions. Results 37 PD patients were included in the study; mean age was 65.7±13.1 years, mean dialysis vintage was 17.5±13 months. Gal-3 levels in dialysate effluent correlated with peritoneal equilibration test (PET) results (0.663, p=0.005) and effluent IL-6 levels (0.674, p=0.002) but not with serum Gal-3 levels or dialysis vintage. Patients with high PET results had higher effluent Gal-3 levels as compared average low PET results. In multivariate regression analysis effluent IL-6 level was the most dominant predictor of effluent Gal-3 levels. Gal-3 mRNA and protein expression in primary endothelial cell culture were not affected by stimulation with dialysate solutions. Conclusion Our study demonstrated presence of Gal-3 within the dialysate effluent in PD patients. Gal-3 levels correlated with peritoneal membrane transport characteristics and effluent IL-6 levels suggesting a role in the inflammatory process within the peritoneal cavity.

Background and Aims Intra-cranial arterial calcification (ICAC) in hemodialysis (HD) patients has a prevalence of about 90%, and its severity is correlated with age, hemodialysis vintage and mineral bone disease. Elevated concentrations of calcium and phosphorus are not sufficient to induce medial calcification because of inhibition by pyrophosphate. Alkaline Phosphatase (ALP) promotes vascular calcification by hydrolyzing pyrophosphate. Epigenetic mechanisms regulation by Apabetalone downregulates pathways involved in vascular calcification. This study assessed the combined impact of ICAC and elevated serum ALP on mortality among chronic HD patients. Method vascular calcifications represented by ICAC were measured simultaneous with mineral bone disease parameters including serum ALP of chronic HD patients who underwent non-contrast brain computerized tomography (CT) from 2015 to 2018 in our institution. Results This retrospective study included 153 hemodialysis patients (mean age 71.3±12.1 years, 60.1% male). Of the total cohort, 12(7.8%) had no brain calcifications and 69 (45.1%) had multiple intracranial calcifications. Considering the patients with normal ALP and no calcification as the reference group yielded adjusted odds ratios for all-cause mortality of 4.6 (95%CI 1.7-12.7) among patients with brain calcifications and normal ALP, p=0.003, and odds ratios for all-cause mortality of 6.1 (95%CI 2.1-17.7) among patients with brain calcifications and increased ALP. Conclusion We founded an independent association between ICAC and the risk of death among hemodialysis patients. The combined effect of ICAC and increased ALP was significantly associated with higher odds-ratio for all-cause mortality in chronic HD patients and may contribute to the risk stratification of these patients.

The incidence of stroke in patients undergoing hemodialysis (HD) is eight-to-ten times greater than that of the general population. However, data on the outcome of stroke in these patients are limited. In this retrospective observational cohort study, electronic medical records of all patients undergoing HD from 1.1.2014 to 31.12.2017 at Meir Medical Center, Israel, were reviewed. Stroke was defined as a focal neurological deficit of cerebrovascular origin, and confirmed as ischemic or hemorrhagic by computed tomography. Age- and sex-matched HD patients who did not experience a stroke (HD-NS) and hospitalized stroke patients with normal kidney function (NRF-S) served as the two control groups. Baseline demographic, clinical, and laboratory data were collected. Thrombolytic therapy, duration of hospital stay, and mortality were recorded. Functional status at discharge was assessed by the Modified Rankin Scale. In the cohort study group (HD-S), 52 strokes occurred during 248.3 patient years, an incidence rate of 8.13%, and a stroke rate of 0.19% patients/month. Most strokes in HD patients were ischemic, and only four patients were administered tissue plasminogen activator. HD-S had longer hospitalization than did NRF-S (10.6 ± 9.9 vs. 5.96 ± 5.3 days, p = 0.004) and lower functional status at discharge (Rankin score 3.75 ± 1.57 vs. 2.29 ± 1.89, p

Evaluate the efficacy of retraining and catheter exit site care in reducing peritonitis rates. This interventional study included all prevalent PD patients from 1/2009 to 12/2017 from a single center. Peritonitis rates and causative organisms were assessed and compared in three periods: (1) Before intervention (01/2009–12/2014), (2) after educational intervention: assessment of training process by infection control nurse and repeat training every 3 months, after each peritonitis episode and after hospitalizations > 2 weeks (01/2015–02/2016), and (3) in addition to the measures in period 2, an exit site care protocol including postoperative care, topical antibacterial therapy and nasal Staph aureus screening and eradication was implemented (03/2016–12/2017). The study included 201 patients (149 men, 52 women), mean age was 65.1 ± 12.6 years. After both interventions, including educational and exit site care strategies, peritonitis decreased significantly from 1.05 episodes per patient-year (n = 113) to 0.67 (n = 54); P = 0.017 between periods 1 and 3. The percentage of peritonitis-free patients increased from 27.4 to 52.4 and 55.6%, respectively (P = 0.001 between period 1 vs. 2 and period 1 vs. 3.). Coagulase-negative staph was the most common pathogen, causing 7.56 peritonitis episodes per year, followed by pseudomonas at 4.33 episodes annually and staph aureus at 3.44 episodes per year. Enforcement of an educational program and strict adherence to an exit site care protocol was associated with a significant decrease in peritonitis rates.

Background and Aims Brain atrophy (BA) is a common finding in neuroimaging of hemodialysis (HD) patients, representing a parenchymal cerebral damage. Likely contributing factors to BA are age, chronic hypertension, diabetes mellitus and other cardiovascular risk factors of atherosclerosis that are also common among HD patients. BA may also occur due to focal ischemia and hypoperfusion during HD. However, data on optimal blood pressure (BP) in these patients are limited. The goal of this study was to determine whether the prevalence and severity of BA would be higher among HD patients with lower BP. Method A blinded neuroradiologist graded BA of all HD patients who underwent brain non-contrast computerized tomography (CT) from 2015 to 2017 in our institution. Age-and sex-matched patients with normal kidney function who underwent brain CT during the same period and technique served as the control group Results A total of 280 patients were included in this retrospective study, with average BP of 140/70 mmHg among HD patients and 142/75 mmHg in the control group. BA was more common in dialysis patients and its severity increased with age and traditional cardiovascular risk factors. We observed a significant negative correlation between diastolic BP (DBP) at dialysis initiation and BA. Average DBP decreased with increasing severity of BA. These findings were observed in both HD and non-CKD patients. Conclusion Brain atrophy was associated with lower DBP, which may induce cerebral hypoperfusion and ischemia. This finding should discourage over-treatment of hypertension in hemodialysis patients.

Infection is one of the leading causes of mortality in dialysis patients, second only to cardiovascular disease. This retrospective study assessed the efficacy and clinical outcomes of influenza vaccination among hemodialysis (HD) patients. In the 2014-2015 season, 104 of 164 (63.6%) HD patients were vaccinated for influenza by the outpatient community health system facilities. Significantly more patients, 159 of 170 (93.8%), were vaccinated in 2015-2016 by the hospital dialysis unit staff during an inpatient HD session (P

BACKGROUND. High blood and tissue concentrations of glucose and advanced glycation end-products (AGEs) are thought to play an important role in the development of vascular diabetic complications. Therefore, the impact of extracellular AGEs and different glucose concentrations was evaluated by studying the gene expressions and the underlying cellular pathways involved in the development of inflammatory pro-atherosclerotic processes observed in cultured endothelial cells. METHODS. Fresh human umbilical vein cord endothelial cells (HUVEC) were treated in the presence of elevated extracellular glucose concentrations (5.5-28 mmol/l) with and without AGE-human serum albumin (HSA). Affymetrix GeneChip(R) Human Gene 1.0 ST arrays were used for gene expression analysis (total 20 chips). Genes of interest were further validated using real-time PCR and western blot techniques. RESULTS. Microarray analysis revealed significant changes in some gene expressions in the presence of the different stimuli, suggesting that different pathways are involved. Six genes were selected for validation as follows: thioredoxin-interacting protein (TXNIP), thioredoxin (TXN), nuclear factor of kappa B (NF-kappaB), interleukin 6 (IL6), interleukin 8 (IL8) and receptor of advanced glycation end-products (RAGE). Interestingly, it was found that the association of AGEs together with the highest pathophysiological concentration of glucose (28 mmol/l) diminished the expression of these specific genes, excluding TXN. CONCLUSIONS. In the present model that mimics a diabetic environment, the relatively short-term experimental conditions used showed an unexpected blunting action of AGEs in the presence of the highest glucose concentration (28 mmol/l). The interactive cellular pathways involved in these processes should be further investigated.