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Understanding carotid artery intima‐media thickness in childhood: Lessons from studies in children with renal transplants

Last year Pediatric Transplantation published a study by researchers from Karolinska Institute (1) who analyzed the utility of ambulatory blood pressure monitoring (ABPM) in children with renal transplants. In their article, the authors showed that a significant proportion of children treated for hypertension and having normal casual blood pressure still had unrecognized, ‘‘masked’’ hypertension by ABPM criteria. Because elevated blood pressure is a well-know risk factor for future cardiovascular disease (CVD), these data raised logical questions: (i) is abnormal ABPM associated with cardiovascular damage? and, if so (ii) can cardiovascular outcome be improved in children who achieved normal blood pressure by ABPM criteria? In this issue of Pediatric Transplantation, Krmar et al. (2) present a follow-up study trying to answer the above questions. To assess cardiovascular damage, authors measured carotid artery intima-media thickness (cIMT). The choice of this marker seems to be logical. Increased cIMT is considered to be an early marker of atherosclerosis: it correlates well with angiographically determined coronary artery disease (CAD) (3), and predicts CVD morbidity and mortality in the general adult population (4, 5) and in adults with chronic kidney disease (CKD) (6). In addition, elevated BP during childhood predicts increased cIMT in young adulthood (7–9), and increased cIMT has been found in pediatric patients with hypertension (10, 11) and renal transplants (12–14). As in other studies, Krmar et al. confirmed increased cIMT in pediatric transplant recipients when compared with healthy children. However, their study features a few major differences from other pediatric studies: (i) this is the first longitudinal study (four-yr follow-up) to assess changes in cIMT in children with renal transplants, (ii) increased cIMT was found in children who had good blood pressure control by both casual and ABPM criteria, and (iii) cIMT did not improve despite continuous normal casual and ambulatory blood pressure during a four-yr follow-up period. The authors argue that ‘‘increased carotid IMT in pediatric renal transplants is not related to BP but more likely to other factor(s) not investigated in this study.’’ As a result, like many other studies, this study produced more questions than answers. First, why do children with renal transplants have increased cIMT? To answer this question, we need to understand when these vascular changes occur and how they progress in the course of CKD prior to renal transplantation. Litwin et al. (13) measured carotid and femoral IMT in 55 children with stage 2–4 CKD, 37 children on dialysis, and 34 children after renal transplantation. Both carotid and femoral IMT were significantly increased in all patient groups and most markedly abnormal in dialysis patients. Carotid IMT correlated with mean past serum calcium-phosphorus (Ca · P) product, the cumulative dose of calcium-based phosphate binders, and the time-averaged mean calcitriol dose. Our own group (15) also showed that both children with mild to moderate CKD and on dialysis had greater cIMT than healthy controls. In our study, children on dialysis had greater cIMT and arterial stiffness than both CKD stage 2–4 patients and controls. Again, elevated Ca · P product predicted increased cIMT, and increased serum phosphorus and iPTH predicted increased arterial stiffness. Taken together, these studies have revealed several important clues to the evolution of vascular changes in children with CKD: (i) as in adults, vascular Pediatr Transplantation 2008: 12: 377–380 Copyright 2008 Blackwell Munksgaard