The pathophysiology and management of vascular calcification in chronic kidney disease patients

ABSTRACT

Introduction

Vascular calcification (VC) which is the pathological mineral deposition in the vascular system, predominantly at the intimal and medial layer of the vessel wall, is an important comorbidity in patients with chronic kidney disease (CKD) leading to significant morbidity and mortality while necessitating appropriate treatment. Our review aims to provide an in-depth analysis of the current understanding of VC.

Areas covered

In this review, we first discuss the pathophysiology of VC in CKD patients, then we explain the methods to predict and assess VC. Afterwards, we provide the currently available as well as the potential therapeutic approaches of VC. We finally discuss our understanding regarding the current situation surrounding VC in our expert opinion section.

Expert opinion

Predicting, assessing and treating VC is crucial and the future advances in the field of research surrounding VC will potentially occur in one or more of these three areas of clinical management. There is a current lack of evidence and consensus regarding specific therapeutic options for alleviating VC and this situation may not necessitate VC to be determined, detected, and documented before the available options are implemented. Regardless, the prediction and assessment of VC is still important and requires further improvement together with the developments in therapeutic alternatives. The future has the potential to bring better research which would guide and improve the management of this patient group. A more specialized approach consisting of targeted therapies and more tailored management plans for patients with CKD and VC is on the horizon.

KEYWORDS:

• Vascular calcification
• chronic kidney disease
• intimal calcification
• therapeutics

Article highlights

• One of the most common comorbidities in patients with chronic kidney disease (CKD) is vascular calcification (VC), which is the pathological mineral deposition in the vascular system, predominantly in the medial layer of the vessel wall leading to significant morbidity and mortality.

• Increased osteogenic markers, phenotypic change in the cells, multiple-signaling pathways, and alteration of minerals and vitamins contribute to this calcification process.

• The diagnosis and monitoring of VC can be achieved via several imaging modalities, such as plain radiographs, ultrasonography, and computed tomography. Additionally, some biomarkers that play a role in VC, may help with the prediction, diagnosis, and evaluation of VC.

• Some of the proposed alternatives to reach therapeutic goals in VC include decreasing inflammation and bone disorders as well as maintaining a good vitamin and mineral balance.

• There is a current lack of evidence and consensus surrounding the specific therapeutic options for the alleviation of VC and this situation may not necessitate VC to be determined, detected, and documented before the available options are implemented. Regardless, the prediction and assessment of VC is still important and requires further improvement together with the developments in therapeutic alternatives.

• Predicting, assessing, and treating VC is crucial and the future advances in the field of research surrounding VC will potentially occur in one or more of these three areas of clinical management. The future has the potential to bring better research, which would guide and improve the management of this patient group. A more specialized approach consisting of targeted therapies and more tailored management plans for patients with CKD and VC is on the horizon.

Declaration of Interest

Authors declare that they have no conflict of interest. The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer Disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded