Cardiovascular Disease in Children with Chronic Kidney Disease

Division of Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229-3039, USA.
Journal of the American Society of Nephrology (Impact Factor: 9.34). 03/2012; 23(4):578-85. DOI: 10.1681/ASN.2011111115
Source: PubMed


More than a decade ago, cardiovascular disease (CVD) was recognized as a major cause of death in children with advanced CKD. This observation has sparked the publication of multiple studies assessing cardiovascular risk, mechanisms of disease, and early markers of CVD in this population. Similar to adults, children with CKD have an extremely high prevalence of traditional and uremia-related CVD risk factors. Early markers of cardiomyopathy, such as left ventricular hypertrophy and dysfunction, and early markers of atherosclerosis, such as increased carotid artery intima-media thickness, carotid arterial wall stiffness, and coronary artery calcification, are frequently present in these children, especially those on maintenance dialysis. As a population without preexisting symptomatic cardiac disease, children with CKD potentially receive significant benefit from aggressive attempts to prevent and treat CVD. Early CKD, before needing dialysis, is the optimal time to both identify modifiable risk factors and intervene in an effort to avert future CVD. Slowing the progression of CKD, avoiding long-term dialysis and, if possible, conducting preemptive transplantation may represent the best strategies to decrease the risk of premature cardiac disease and death in children with CKD.

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    • "In the very recent and large Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial, Rahman et al.68 reported no difference in cardiovascular mortality, coronary heart disease, cardiovascular disease, stroke, or ESRD in participants with an estimated GFR <60, between using chlorthalidone and amlodipine, or chlorthalidone and lisinopril. Because there are several valuable review articles in the literature on the subject, we refer interested readers to them.69 "
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    ABSTRACT: The cardiovascular burden of end stage renal disease (ESRD) in children has recently received more attention, and some authors have recommended that the origins of the increase in cardiovascular morbidity and mortality be found in childhood. In this comprehensive review of the literature, we aim to review the main and most recent studies evaluating cardiovascular risk factors in pediatric kidney disease patients. The literature suggests that ESRD, even in the pediatric population, is associated with a high rate of cardiovascular morbidity and mortality, and needs serious attention. Unfortunately, there is extreme scarcity of data on the efficacy of preventive strategies on cardiovascular morbidity and mortality in pediatric patients with renal disease. Therefore, authors of the current article recommend future studies to be directed to find beneficial and/or potential harmful effects of different interventions conventionally used in this population, including lifestyle modifications and pharmaceutical therapy on cardiovascular indices. Moreover, the effects of these drugs on the renal function of children with minimal kidney disease should be evaluated.
    ARYA Atherosclerosis 03/2014; 10(2):118-128.
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    • "In adult-onset ESRD, therapeutic interventions, such as an increase of the dialysis frequency and a stricter control of hypertension, hyperphosphatemia and anemia have been investigated to reduce cardiac mortality in patients with LVH [7]. Recently, Mitsnefes et al. emphasized the importance of frequent dialysis in children [8]. Small single-center studies have shown clinical improvements in LVH and function when children receive dialysis more frequently than the traditional, thrice-weekly schedule [9,10]. "
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    ABSTRACT: Monitoring of the appearance of left ventricular hypertrophy (LVH) by echocardiography is currently recommended for in the management of children with End-stage renal disease (ESRD). In order to investigate the validity of this method in ESRD children, we assessed the intra- and inter-observer reproducibility of the diagnosis LVH. Echocardiographic measurements in 92 children (0--18 years) with ESRD, made by original analysists, were reassessed offline, twice, by 3 independent observers. Smallest detectable changes (SDC) were calculated for continuous measurements of diastolic interventricular septum (IVSd), Left ventricle posterior wall thickness (LVPWd), Left ventricle end-diastolic diameter (LVEDd), and Left ventricle mass index (LVMI). Cohen's kappa was calculated to assess the reproducibility of LVH defined in two different ways. LVHWT was defined as Z-value of IVSd and/or LVPWd>2 and LVHMI was defined as LVMI> 103 g/m2 for boys and >84 g/m2 for girls. The intra-observer SDCs ranged from 1.6 to 1.7 mm, 2.0 to 2.6 mm and 17.7 to 30.5 g/m2 for IVSd, LVPWd and LVMI, respectively. The inter-observer SDCs were 2.6 mm, 2.9 mm and 24.6 g/m2 for IVSd, LVPWd and LVMI, respectively. Depending on the observer, the prevalence of LVHWT and LVHMI ranged from 2 to 30% and from 8 to 25%, respectively. Kappas ranged from 0.4 to 1.0 and from 0.1 to 0.5, for intra-and inter- observer reproducibility, respectively. Changes in diastolic wall thickness of less than 1.6 mm or LVMI less than 17.7 g/m2 cannot be distinguished from measurement error in individual children, even when measured by the same observer. This limits the use of echocardiography to detect changes in wall thickness in children with ESRD in routine practice.
    BMC Nephrology 08/2013; 14(1):170. DOI:10.1186/1471-2369-14-170 · 1.69 Impact Factor
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    • "Despite the availability of a number of treatment options for hypertension, cardiovascular, and renal disease, the prevalence, morbidity, and mortality of these diseases in children and adults remain very high [1]. Therefore, elucidation of the causality and pathogenesis of these diseases is critical. "
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    ABSTRACT: A growing body of evidence supports the concept that changes in the intrauterine milieu during "sensitive" periods of embryonic development or in infant diet after birth affect the developing individual, resulting in general health alterations later in life. This phenomenon is referred to as "developmental programming" or "developmental origins of health and disease." The risk of developing late-onset diseases such as hypertension, chronic kidney disease (CKD), obesity or type 2 diabetes is increased in infants born prematurely at <37 weeks of gestation or in low birth weight (LBW) infants weighing <2,500 g at birth. Both genetic and environmental events contribute to the programming of subsequent risks of CKD and hypertension in premature or LBW individuals. A number of observations suggest that susceptibility to subsequent CKD and hypertension in premature or LBW infants is mediated, at least in part, by reduced nephron endowment. The major factors influencing in utero environment that are associated with a low final nephron number include uteroplacental insufficiency, maternal low-protein diet, hyperglycemia, vitamin A deficiency, exposure to or interruption of endogenous glucocorticoids, and ethanol exposure. This paper discusses the effect of premature birth, LBW, intrauterine milieu, and infant feeding on the development of hypertension and renal disease in later life as well as examines the role of the kidney in developmental programming of hypertension and CKD.
    International Journal of Nephrology 11/2012; 2012(4):760580. DOI:10.1155/2012/760580
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