Vascular calcification in chronic kidney disease

Abstract

VC (vascular calcification) is highly prevalent in patients with CKD (chronic kidney disease), but its mechanism is multifactorial and incompletely understood. In addition to increased traditional risk factors, CKD patients also have a number of non-traditional cardiovascular risk factors, which may play a prominent role in the pathogenesis of arterial calcification, such as duration of dialysis and disorders of mineral metabolism. The transformation of vascular smooth muscle cells into chondrocytes or osteoblast-like cells seems to be a key element in VC pathogenesis, in the context of passive calcium and phosphate deposition due to abnormal bone metabolism and impaired renal excretion. The process may be favoured by the low levels of circulating and locally produced VC inhibitors. VC determines increased arterial stiffness, left ventricular hypertrophy, a decrease in coronary artery perfusion, myocardial ischaemia and increased cardiovascular morbidity and mortality. Although current therapeutic strategies focus on the correction of phosphate, calcium, parathyroid hormone or vitamin D, a better understanding of the mechanisms of abnormal tissue calcification may lead to development of new therapeutic agents, which could reduce VC and improve cardiovascular outcome in CKD patients. The present review summarizes the following aspects: (i) the pathophysiological mechanism responsible for VC and its promoters and inhibitors, (ii) the methods for detection of VC in patients with CKD, including evaluation of arterial stiffness, and (iii) the management of VC in CKD patients.

Malignant Mönckeberg medial calcific sclerosis

“…

Mönckeberg medial calcific sclerosis (MCS) refers to a calcification of the medial arterial layer that is most found in the muscular arteries of the extremities and occasionally in visceral arteries [1].We describe the case of a 50-year-old woman hospitalized because of acute ischemic lesions, involving her left lower limb, that developed over a few days. She had no conventional risk factors for atherosclerosis, and laboratory tests revealed severe renal insufficiency (serum creatinine 12.8 mg/dl), hyperparathyroidism (serum parathyroid hormone, PTH, 1559 ng/l, normal 10-60), and an elevated calcium-phosphate product (Ca 9.2 mg/dl, P 12.4 mg/dl).

…”

“…ESRD (end-stage renal disease) patients with VCm have less conventional risk factors for atherosclerosis, greater prevalence of Ca-P disorders, and a longer time on hemodialysis [3]. MCS is commonly observed in muscle-type conduit arteries, and is usually revealed in the arteries of the extremities, whereas a systemic distribution with involvement of visceral arteries appears uncommon [1].Four stages of lesion progression are recognized in MCS. In stage 1, calcifications appear as irregular deposits within the media, they are both intracellular and extracellular: the first located in VSMCs, the second associated with damaged and fractured elastic fibers in the extracellular matrix.…”

“…Mönckeberg medial calcific sclerosis (MCS) refers to a calcification of the medial arterial layer that is most found in the muscular arteries of the extremities and occasionally in visceral arteries [1].…”

“…Vascular calcifications are not simply due to Ca-P precipitation, but result from an active, highly regulated process in which vascular smooth muscle cells (VSMCs) undergo apoptosis and are transformed into osteoblastlike cells involved in the mineralization process [1,2]. The prevalence of vascular calcification of the media (VCm) of MCS type is estimated to be ~ 0.5% in adults, with the highest prevalence in type 2 diabetes patients.…”

“…ESRD (end-stage renal disease) patients with VCm have less conventional risk factors for atherosclerosis, greater prevalence of Ca-P disorders, and a longer time on hemodialysis [3]. MCS is commonly observed in muscle-type conduit arteries, and is usually revealed in the arteries of the extremities, whereas a systemic distribution with involvement of visceral arteries appears uncommon [1].…”