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Updated: Feb 22, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Pathophysiology and treatment of cardiovascular disease in pediatric chronic kidney disease
Nadine Khouzam1, Katherine Wesseling-Perry2
1Children's Hospital Los Angeles, Los Angeles, CA, USA.
Insights
Cardiovascular disease significantly impacts patients with chronic kidney disease (CKD), leading to early mortality. Understanding CKD
Area of Science:
- Nephrology and Cardiovascular Medicine
Background:
- Chronic kidney disease (CKD) drastically reduces life expectancy, with cardiovascular disease (CVD) as the primary cause of mortality in pediatric patients.
- Unlike general populations, CKD-associated CVD involves vascular endothelial dysfunction, medial arterial calcification, and cardiac dysfunction, often without traditional risk factors.
- The mechanisms driving these vascular pathologies in CKD, including vascular smooth muscle cell to osteoblast-like transition and altered bone/mineral metabolism, are not fully understood.
Purpose of the Study:
- To elucidate the complex pathogenesis of cardiovascular complications in chronic kidney disease.
- To investigate the role of bone and mineral metabolism in CKD-associated cardiovascular disease progression.
- To identify optimal therapeutic strategies for mitigating cardiovascular dysfunction, vascular calcification, and premature mortality in CKD patients.
Main Methods:
- Review of existing literature on CKD pathophysiology and cardiovascular complications.
- Analysis of the mechanisms linking vascular calcification, bone/mineral metabolism, and cardiovascular events in CKD.
- Evaluation of current therapeutic approaches for renal osteodystrophy and their impact on cardiovascular outcomes.
Main Results:
- Cardiovascular disease in CKD arises from distinct pathways including vascular calcification and dysfunction, differing from general population atherosclerosis.
- Altered bone and mineral metabolism, particularly vascular smooth muscle cell transition, are key contributors to progressive cardiovascular disease in CKD.
- Existing therapies for renal osteodystrophy show some impact but do not fully address the early origins of CVD in CKD.
Conclusions:
- Cardiovascular disease in CKD is multifactorial, involving unique vascular pathologies and metabolic derangements.
- Therapeutic interventions targeting bone and mineral metabolism influence cardiovascular disease progression in CKD patients.
- Optimal treatment strategies are needed to address the early development of cardiovascular complications and reduce mortality in CKD.
Abstract:
Life expectancy in patients with all stages of chronic kidney disease (CKD) falls far short of that in the general population. Cardiovascular disease is the leading cause of mortality in pediatric patients with CKD. In contrast to the intimal atherosclerotic lesions that characterize cardiovascular disease in the general population, vascular endothelial dysfunction, medial arterial calcification, and cardiac dysfunction contribute to cardiovascular pathological conditions in CKD. The pathogenesis of these lesions, the origins of which can be identified in the absence of traditional cardiovascular risk factors, is incompletely understood. CKD-mediated vascular calcification in CKD is characterized by a transition of vascular smooth muscle cells to an osteoblast-like phenotype and altered bone and mineral metabolism are strongly linked to progressive cardiovascular disease in this population. Renal osteodystrophy therapies, including phosphate binders, vitamin D analogs, and calcimimetics, have an impact on the progression of cardiovascular disease. However, cardiovascular disease has its origins before the development of secondary hyperparathyroidism, and optimal therapeutic regimens that minimize cardiac dysfunction, vascular calcification, and early mortality remain to be defined.
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