Cardiac and vascular adaptation in pediatric patients with chronic kidney disease: role of calcium-phosphorus metabolism.
In children, cardiac abnormalities such as increased left ventricular mass (LVM) and diastolic dysfunction develop at the time of mild to moderate chronic renal insufficiency (CRI) and progress as renal function deteriorates. It was hypothesized that in this age group, vascular abnormalities develop early in the course of chronic kidney disease (CKD) in parallel with cardiac abnormalities and become more severe as end-stage disease is reached. Echocardiography and ultrasound of the carotid artery were performed on 44 patients with CKD stages 2 to 4 (CRI group), 16 patients who were on maintenance dialysis, and 35 healthy individuals. Carotid artery intima-media thickness (cIMT) was measured and distensibility and stiffness were calculated to assess carotid artery structure and function. Both the CRI and dialysis groups had greater cIMT, higher LVM index, and poorer diastolic function than the control subjects (P < 0.0001). Children who were on dialysis had greater cIMT and higher LVM index than those with CRI (P < 0.001) and greater arterial stiffness than both CRI patients and control subjects (P < 0.001). Arterial compliance was similar in CRI and control subjects. In all patients with CKD (CRI and dialysis), increased calcium-phosphorus product predicted increased cIMT. Increased serum phosphorus and intact parathyroid hormone predicted increased arterial stiffness. Elevated intact parathyroid hormone was a predictor of increased LVM index and poor diastolic function. In dialysis patients, the cumulative dose of phosphate binders and calcitriol predicted abnormal vascular structure and function. It is concluded that vascular abnormalities are already present in children and adolescents during early stages of CKD; they are more severe in children who are on maintenance dialysis and are related to abnormal calcium-phosphorus metabolism.
Mitsnefes
Mark M
MM
Division of Nephrology and Hypertension, Cincinnati Children's Hospital, Cincinnati, OH 45229, USA. mark.mitsnefes@cchmc.org
Kimball
Thomas R
TR
Kartal
Janis
J
Witt
Sandra A
SA
Glascock
Betty J
BJ
Khoury
Philip R
PR
Daniels
Stephen R
SR
D000222:Adaptation, Physiological; D000293:Adolescent; D000328:Adult; D001808:Blood Vessels / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism*; D002339:Carotid Arteries / Q000473:pathology / Q000503:physiopathology; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D005260:Female; D006321:Heart / Q000503:physiopathology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D010758:Phosphorus / Q000378:metabolism*; D006435:Renal Dialysis; D018487:Ventricular Dysfunction, Left / Q000209:etiology
D010758:Phosphorus; D002118:Calcium