ABSTRACT
BACKGROUND: Cardiovascular disease starts early in the course of chronic kidney disease (CKD) and is the leading cause of death in patients with end-stage renal disease. Since high-sensitivity cardiac troponin T (hs-cTnT) can detect much lower levels of myocardial injury than conventional assays, it may be useful for studying the earliest stages of heart disease in patients with CKD. OBJECTIVE: To evaluate the association of circulating hs-cTnT with LV structural and functional abnormalities detected by echocardiography among dialysis dependent and non-dialysis dependent CKD patients. METHODS: This study was conducted on 107 subjects divided into three groups. Group I consisted of CKD patients on conservative treatment (n = 42), Group II: hemodialysis patients (n = 42), Group III: control group: age and sex matched healthy volunteers (n = 23). All subjects were subjected to clinical examination, biochemical evaluation including estimation of hs-cTnT and Echo-Doppler study of cardiac structure and function. RESULTS: There was a significant increase in LAV (p < 0.01), LVM (p < 0.01) in both patient groups compared to the control group. Mitral annular plane systolic excursion (MAPSE) was significantly decreased in both patient groups compared to the control group (p < 0.01, p < 0.05) and in group I compared to group II (p < 0.05) with a significant decrease in S velocity in group I compared to groups II and III (p < 0.01). There was a significant decrease in Vp (p < 0.01) with a significant increase in AEF (p < 0.01) in both patients' groups compared to the control group and AEF was significantly increased in group II compared to group I (p < 0.01). Ea velocity and Ea/Aa decreased significantly (p < 0.01) with significant increase in Aa velocity (p < 0.05, p < 0.01), E/Ea (p < 0.01) and E/Vp (p < 0.05) in both patient groups compared to the control group. There was a significant increase in hs-cTnT levels in both patient groups compared to the control group (P < 0.01). We found a positive correlation between hs-cTnT levels and LAV (r = 0.291, p < 0.03), IVST (r = 0.374, p < 0.004), PWT (r = 0.309, p < 0.02), LVM (r = 0.282, p < 0.03), A wave velocity (r = 0.271, p < 0.04), E/Ea (r = 0.506, p < 0.0001), PCWP (r = .507, p < 0.0001) and a negative correlation between hs-cTnT and MAPSE (r = - 0.300, p < 0.02), S wave velocity (r = - 0.259, p < 0.05), Ea (r = - 626, p < 0.0001), Ea/Aa (r = - 0.543, p < 0.0001). Troponin at the cut-off value of >5 ng/L, revealed 100% sensitivity and 95% specificity with areas under curve (AUC) of 0.998 and accuracy of 95.65% (P < 0.01) for discrimination of Group I vs control group and 76.2% sensitivity and 95.7% specificity with AUC 0.796 and accuracy 71.84% (P < 0.01) for discrimination of group II vs control group. CONCLUSION: Structural and functional cardiac abnormalities are common in CKD patients. Serum hs-cTnT levels increased in CKD patients and was associated with LVH, LAV and some of the echocardiographic parameters of LV systolic and diastolic dysfunction. Our research suggests that hs-cTnT levels may be important for early screening of cardiac structure and function in CKD patients to provide evidence for early intervention.
ABSTRACT
The SEN virus has been tentatively linked to transfusion-associated non-A to E hepatitis. The aim of the present study was to 1) determine the prevalence of SEN virus among Egyptian patients with hepatitis C virus (HCV)-related chronic liver disease and patients undergoing hemodialysis and 2) demonstrate the clinical effect of SEN virus infection on coexistent hepatitis C in terms of severity and probability of developing hepatocellular carcinoma. Polymerase chain reaction was used to detect SEN virus-D and SEN virus-H DNA in serum samples of 74 patients with HCV-related chronic liver disease, 45 uremic patients undergoing maintenance hemodialysis, and 28 healthy controls. SEN virus-D/H DNA was detected in 13.5% of patients with chronic liver disease, 11.1% of patients undergoing hemodialysis, and 7.1% of healthy controls, with no significant differences between patients and the control group. Clinical and biochemical measures did not significantly differ between SEN virus-infected and noninfected patients in the chronic liver disease group or the hemodialysis group. The rate of SEN virus infection was significantly higher in patients with chronic liver disease and hepatocellular carcinoma (33.3%) than in those with chronic liver disease only (8.5%) (P < .05). In conclusion, SEN virus does not seem to be a common infection in Egyptian patients. It has no apparent influence on the severity of coexistent HCV-related chronic liver disease but could be a risk factor for hepatocellular carcinoma in such patients. Further studies are needed to define the etiopathogenic role of SEN virus infection in the development of hepatocellular carcinoma.
