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Vascular calcification of chronic kidney disease: A brief review
Bang-Gee Hsu1,2, Jen-Pi Tsai1,3
1School of Medicine, Tzu Chi University, Hualien, Taiwan.
Insights
Vascular calcification (VC) is common in chronic kidney disease (CKD) and linked to cardiovascular disease risk. This review covers VC mechanisms, imaging, and treatments in CKD patients.
Area of Science:
- Nephrology
- Cardiology
- Vascular Biology
Background:
- Vascular calcification (VC) is highly prevalent in chronic kidney disease (CKD) patients.
- VC contributes significantly to the increased cardiovascular disease (CVD) risk observed in CKD.
- Abnormal mineral homeostasis (hyperphosphatemia, hypercalcemia) exacerbates VC in CKD.
Purpose of the Study:
- To discuss the underlying mechanisms of vascular calcification in CKD.
- To review current imaging modalities for evaluating VC extent and severity.
- To explore potential therapeutic strategies for managing VC.
Main Methods:
- Review of existing literature on vascular calcification mechanisms.
- Analysis of current clinical imaging techniques for VC assessment.
- Synthesis of evidence regarding medical therapies for VC.
Main Results:
- VC pathogenesis involves complex interactions of pro- and anti-calcifying factors regulating vascular smooth muscle cell differentiation.
- Various imaging modalities exist for VC evaluation, each with distinct strengths and weaknesses.
- Emerging evidence supports the efficacy of medical therapies in mitigating VC.
Conclusions:
- VC is a critical complication of CKD with significant cardiovascular implications.
- Accurate assessment of VC through appropriate imaging is essential for risk stratification.
- Further research into effective treatments for VC is warranted to improve patient outcomes.
Abstract:
Vascular calcification (VC) is highly prevalent among patients with chronic kidney disease (CKD). There is growing evidence that there is more underlying this condition than the histological presentation of atherosclerotic plaque and arteriosclerosis and that the risk of cardiovascular disease in the context of CKD might be explained by the presence of VC. While VC has been observed in the absence of overt abnormal mineral metabolism, this association is coupled to abnormal homeostasis of minerals in patients with CKD, due to hyperphosphatemia and hypercalcemia. Furthermore, recent studies have shown that the differentiation of vascular smooth muscle cells into an osteogenic phenotype is highly regulated by pro-calcifying and anti-calcifying factors. There are several imaging modalities currently used in clinical practice to evaluate the extent and severity of VC; each has different advantages and limitations. Although there is no universally accepted method for the treatment of VC, there is growing evidence of the beneficial effects of medical therapy for the condition. This study discusses the mechanism underlying VC, imaging modalities used for evaluation of the condition, and possible treatments.
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