Abstract
Backgrounds: Cardiovascular diseases are still the prominent cause of death in cases of end-stage renal disease, cardiac troponin I (cTnI) can be used for detecting cardiac involvement in asymptomatic cases of end-stage renal disease on hemodialysis. Aim: Determine the direct cardiac consequence of dialysis treatments in children on hemodialysis by measuring high-sensitive troponin-I as a marker of myocardial injury. Subjects and Methods: This case-control study included thirty children with end-stage renal disease on regular hemodialysis; the study group was selected from the nephrology hemodialysis unit of Al-Zahraa Hospital, Al-Azhar University. Another group of thirty healthy children matches age and sex with the patient’s group as a control. Highly Sensitive cTnI (hsTnI) was measured pre and post hemodialysis with a sensitive assay; moreover, ECG, lipid profile including cholesterol, triglyceride, low and high-density lipoprotein (HDL) in the same line with routine investigations for those patients, we used bioimpedance for dry weight assessment in the hemodialysis (HD) group. Results: Children on (HD) have a significantly higher (hsTnI) pre-dialysis (0.250 ± 0.069 ng/ml) compared to post-dialysis (0.187 ± 0.004 ng/ml) with (p, 0.001). With no significant difference between post HD (0.187 ± 0.004 ng/ml) and the control group (0.189 ± 0.005) with (p, 0.090). cTnI is detected in (73.3%) of children pre-dialysis above the cut-off value compared to (3.31%) had a high-level post-dialysis. cTnI is positively correlated with systolic, diastolic blood pressure and heart rate with (r. 0.333, p, 0.001: r. 0.343, p, 0.001: r. 0.276, p, 0.033) respectively and (hsTnI) is negatively correlated with Hb and HDL (r. -0.333, p, 0.009: r. 0.324, p, 0.011). Meanwhile (hsTnI) is positively correlated with serum urea, creatinine, ph, PTH, serum ferritin and positively correlated with QT interval and QTC. Conclusion: cTnI levels rise significantly before hemodialysis, so those patients are exposed to silent myocardial injury pre HD, and fortunately, it is not persistent after hemodialysis except for a few of them had a high level. We strongly advised not to delay dialysis appointments; the nephrology team should aggressively treat those patients to prevent further myocardial damage.
Highlights
Cardiovascular disease (CVD) is the most common cause of death in pediatric CKD patients [1] [2] [3]
Subjects and Methods: This case-control study included thirty children with end-stage renal disease on regular hemodialysis; the study group was selected from the nephrology hemodialysis unit of Al-Zahraa Hospital, Al-Azhar University
With no significant difference between post HD (0.187 ± 0.004 ng/ml) and the control group (0.189 ± 0.005) with (p, 0.090). cardiac troponin I (cTnI) is detected in (73.3%) of children pre-dialysis above the cut-off value compared to (3.31%) had a high-level post-dialysis. cTnI is positively correlated with systolic, diastolic blood pressure and heart rate with (r. 0.333, p, 0.001: r. 0.343, p, 0.001: r. 0.276, p, 0.033) respectively and is negatively correlated with Hb and high-density lipoprotein (HDL) (r. −0.333, p, 0.009: r. 0.324, p, 0.011)
Summary
Cardiovascular disease (CVD) is the most common cause of death in pediatric CKD patients [1] [2] [3]. For children on regular hemodialysis, the mortality associated with cardiac disease is one thousand times higher than in normal children [4]. CVD was the leading cause of mortality in patients undergoing dialysis, affecting 33% of cases in a cohort of US children, followed from 1995 to 2010 [5]. Children and uremia patients with uremia have a similar constellation of ischemia-predisposing factors to adults, including vascular calcification, increased intima-media thickness and pulse wave velocity, early atherosclerosis, and endothelial dysfunction [6] [7], but without significant atheromatous coronary artery disease. It is known that dialysis is cardiotoxic, resulting in a lack of contractility of certain myocardial segments. This mechanism is primarily due to hypoperfusion of the myocardium during dialysis
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