Valvular Heart Disease and Calcification in CKD

More Common Than Appreciated

Pablo Ureña-Torres; Luis D'Marco; Paolo Raggi; Xavier García–Moll; Vincent Brandenburg; Sandro Mazzaferro; Ari Lieber; Lluis Guirado; Jordi Bover

Disclosures

Nephrol Dial Transplant. 2020;35(12):2046-2053. 

In This Article

Abstract and Introduction

Abstract

Ischaemic heart disease, sudden cardiac death and arrhythmias, heart failure, stroke and peripheral arterial disease make up >50% of the causes of death in advanced chronic kidney disease (CKD). Calcification of the vascular tree and heart valves is partially related to these complications and has received growing attention in the literature. However, the main focus of research has been on the pathophysiology and consequences of vascular calcification, with less attention being paid to valvular calcification (VC) and its impact on the survival of CKD patients. Although VC has long been seen as an age-related degenerative disorder with minimal functional impact, several studies proved that it carries an increased risk of death and clinical consequences different from those of vascular calcification. In dialysis patients, the annual incidence of aortic valve calcification is nearly 3.3% and the reported prevalence of aortic and mitral VC varies between 25% and 59%. Moreover, calcification of both valves occurs 10–20 years earlier in CKD patients compared with the general population. Therefore, the purpose of this review is to summarize the current knowledge on the pathophysiology and relevance of VC in CKD patients, and to highlight specific clinical consequences and potential therapeutic implications.

Introduction

Cardiovascular (CV) mortality is very high in patients with chronic kidney disease (CKD), outnumbering the onset of end-stage renal disease (ESRD) by >10-fold.[1] In the USA, the mortality rate for patients receiving dialysis was 193/1000 patient years in a recent report, with 42% of deaths attributable to CV causes.[2] Acute myocardial infarction accounted for only 5% of mortality, whereas sudden death accounted for 27%.[2] A similar trend has also been observed in clinical trials demonstrating that atherosclerotic events (i.e. ischaemic heart disease, stroke or peripheral arterial disease) are not necessarily the main cause of mortality in the CKD population.[3–5] In fact, 'non-atherosclerotic' CV events (such as heart failure, arrhythmias, sudden death, haemorrhagic stroke or death due to other or unknown CV causes) are more frequent than classical atherosclerotic CV events in dialysis patients.[6]

A progressive decline in kidney function represents a 'perfect storm' for initiation and progression of vascular/valvular calcification (VC).[7] While research progress and medical literature have mainly focused on the pathophysiology and consequences of vascular calcification, and debate still rages on its relevance and implications, less attention has been paid to VC and its impact on the survival of CKD patients.[8,9] VC is less frequent and much less is known about its pathogenesis despite the fact that it shares common risk factors and pathogenic features with vascular calcification. Despite this, current knowledge implies that VC is associated with an increased risk of death and other clinical complications different from those of vascular calcification.[10] Therefore, the purpose of this review is to briefly summarize the current knowledge on the pathophysiology and clinical relevance of VC in CKD patients, with specific comments on potential therapeutic interventions.

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