IntroductionAdipose tissue releases bioactive factors termed adipokines. Visfatin is an adipokine that plays an active role promoting vascular inflammation and atherosclerosis. The purpose of this study was to determine the association between serum visfatin levels and carotid atherosclerosis in diabetic and non-diabetic patients on maintenance hemodialysis (HD) in order to clarify the role of serum visfatinas, a risk factor for cardiovascular complications in HD patients.MethodsForty patients on maintenance hemodialysis were enrolled in this case-control study in 2015. They were subdivided into two groups, i.e., a diabetic group (n = 20) and a non-diabetic group (n = 20). Twenty healthy subjects who were age and gender matched were included as a control group. Carotid Duplex studies were performed on all patients, and serum visfatin was determined by a competitive enzyme immunoassay.ResultsHD patients showed a highly significant increase in serum visfatin, urea, creatinine, Ca×Ph, K, fasting glucose, triglycerides, LDL levels, and a significant decrease in eGFR, Na, HDL, and Hb compared to the control group. Also, serum visfatin levels showed a highly significant increase in the diabetic HD group compared to both the non-diabetic HD and control groups. Serum visfatin showed a highly significant increase in non-diabetic HD patients compared to the control group. Carotid intima-media thickness (IMT) showed a highly significant increase in HD group compared to the control group. Serum visfatin correlated positively with serum urea, creatinine, glucose, and IMT, but it was negatively correlated with eGFR, Na, and HDLConclusionWe concluded that serum visfatin is increased in HD patients with and without diabetes. Moreover, its association with IMT may be involved in the pathogenesis of atherosclerosis in CRF patients.

Background: There are many studies about the epidemiology of hepatitis E virus (HEV) in the general population, but the data about HEV infection among patients with end-stage renal disease (ESRD) give conflicting results. Although the parenteral route may be involved in the transmission of HEV infection, several investigators have suggested that fecal-oral transmission is the primary transmission mode. We aimed to identify the seroprevalence of HEV in hemodialysis (HD) patients compared to the seroprevalence of HBV and HCV infection, and examine the role of parenteral transmission. Methodology: Eighty-four patients from TBRI's HD unit who had been receiving dialysis for more than six months were involved in the study. All the patients were subjected to detailed medical history, full clinical examination, and routine investigations, including virology screening and abdominal ultrasound. HEV seropositivity was investigated by ELISA for HEV-Ab (IgG), while active viremia was assessed by RT-PCR for HEV RNA. Results: Out of the 84 patients, anti-HEV IgG antibodies were detected in five cases (6.0%). A minor (P=0.001) and a moderate (P=0.01) increase in liver echogenicity by ultrasound were significantly correlated with HEV seropositivity. Blood transfusion and HEV seropositivity did not significantly correlate (P=0.6). Neither HBsAg nor HCV-Ab was related to anti-HEV antibody seropositivity. HEV RT-PCR was only positive in one case. Conclusion: Compared to HCV (34.5%), the prevalence of HEV seropositivity was low (6%) in our patients. Parenteral transmission of HEV was less likely. HEV routine screening may help lower the related morbidity and mortality in HD patients.

BACKGROUND: Sirtuins silent information regulator 1 (SIRT) is histone deacetylases that act as antioxidants and involved in the pathogenesis of cardiovascular diseases (CVD) which are the major complications of chronic kidney disease (CKD). Transcription factor 7-like 2 (TCF7L2) genetic polymorphisms could contribute to the risk of CVD as TCF7L2 proteins regulate vascular remodeling. AIM: We tried to demonstrate the role of genetic polymorphisms: rs7069102 and rs10823108 in SIRT1 gene and rs7903146 in TCF7L2 gene in the development of CVD in CKD Egyptian patients. METHODS: This study included 120 CKD patients (60 with CVD and 60 without CVD) and 60 age and sex-matched healthy subjects as a control group. Routine laboratory investigations were performed and genotyping for candidate single nucleotide polymorphisms was done by Taqman-real-time polymerase chain reaction. RESULTS: The frequency of the C allele of rs7069102 was significantly higher in CKD patients with CVD as compared to the normal control group (p < 0.001) and as compared to CKD patients without CVD (p < 0.001). Percentages of AG and GG genotypes of rs10823108 were significantly higher in CKD patients with CVD as compared to the normal control group (p = 0.002, 0.035, respectively). The frequency of the T allele of rs7903146 was significantly higher in CKD patients with CVD as compared to the normal control group (p < 0.001). CONCLUSION: We found that C allele of rs7069102, GG and AG genotypes of rs10823108 in the SIRT1 gene and T allele of rs7903146 in TCF7L2 gene have a potential role in the pathogenesis and the risk of CVD development in CKD Egyptian patients.

BACKGROUND: Hepatorenal syndrome (HRS) is a devastating consequence of liver cirrhosis that is clinically categorized into two subtypes. Acute malfunction of renal role, as measured by an elevation in blood creatinine, significantly underestimates the loss in renal function in cirrhotic individuals; more accurate biomarkers are desperately required in cirrhotic patients. AIM: The present study set out to uncover new biomarkers for the early prediction of AKI in cirrhotic cases. A comprehensive panel of biomarkers was investigated to get a clear insight into the pathogenesis of HRS. PATIENTS AND METHODS: Participants in this study were 70 individuals from the hepatogastroenterology unit of the Theodor Bilharz Research Institute (TBRI). Detailed medical data and a physical examination were recorded. Three groups of patients have been identified; Group 1: 30 cases with compensated liver cirrhosis and normal kidney functions. Group 2: 20 cases with decompensated liver cirrhosis and normal kidney functions. Group 3: 20 cases with decompensated liver cirrhosis proved hepatorenal syndrome Type 2 h. The following biomarkers were detected in serum using the sandwich-ELISA method: Human L-arginine ELISA kit, human neutrophil gelatinase related lipocalin (NGAL), human noradrenaline (NA), human asymmetrical dimethylarginine (ADMA), human symmetric dimethylarginine (SDMA), human nitric oxide (NO), and human renin. RESULTS: There was a highly significant difference between Groups 1 and 2 in NITRIC and ADMA. Significant differences between Groups 2 and 3 in NGAL, noradrenalin, and SDMA were observed. There was a significant difference (Group 2 vs. Group 3) in renin, NITRIC, ADMA, and L-ARGININE. There was highly significant differentiation (Group 2 vs. Group 3) in NGAL, noradrenalin, and SDMA. There was highly significant variation as per odd ratio and confidence interval between (Group 3 vs. Group 2) in NGAL. CONCLUSION: Assessment of renal biomarkers in individuals with decompensated cirrhosis gives critical information on the etiology of AKI. Further, it may aid in the diagnosis and prognosis of AKI. Renin, NITRIC, ADMA, and L-ARGININE could be used as biomarkers to indicate HRS in individuals with advanced cirrhosis.