Serum magnesium level and arterial calcification in end-stage renal disease

Meema, H. E.; Oreopoulos, Dimitrios G.; Rapoport, A.

doi:10.1038/ki.1987.222

Cited by 181 publications

(124 citation statements)

References 45 publications

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“…Vascular calcification (VC), especially in the arterial media, is probably a major contributor to arteriosclerosis in CKD (127)(128)(129)(130). Numerous autopsy and radiologic studies in the past several decades have demonstrated high rates of calcification of peripheral and central arteries (131)(132)(133)(134)(135)(136)(137)(138)(139)(140), and coronary artery calcification is even common and progressive in young adult hemodialysis patients (141). VC is probably primarily due to abnormal mineral metabolism that is seen in renal failure (141)(142)(143)(144)(145), perhaps through a complex process involving osseous metaplasia of the vascular wall components (118,119,146).…”

Section: Pathophysiology Of Cvd In Ckdmentioning

confidence: 99%

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

Nogueira

Weir

2007

Clinical Journal of the American Society of Nephrology

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D uring the past several decades, the advent and refinement of maintenance dialysis and kidney transplantation have essentially eliminated kidney failure per se as a cause of death in developed countries. However, as patients survive many years after the development of renal failure, comorbidities develop, progress, and ultimately cause death in these individuals. Cardiovascular disease (CVD) has ranked prominent among these comorbidities, accounting for nearly half of the deaths (1). All along the continuum of chronic kidney disease (CKD)-from microalbuminuria to ESRD-a higher risk for CVD has been observed (see Epidemiology of CVD in CKD). In fact, individuals with early CKD are more likely to die of CVD than to develop ESRD (2,3). Then, among those who survive to ESRD, the all-cause CVD mortality in patients with ESRD is many-fold higher than in the general population (4). Unfortunately, the reasons for the association of CKD with CVD are not clearly understood, and the role of various clinical interventions in stemming the CVD epidemic are not well defined. Complicating the issue is the potential variation in the pathophysiology and clinical behavior of CVD through the stages of CKD.3-Hydroxyl-3-methylglutaryl CoA reductase inhibitors (statins) and other lipid-lowering drugs (LLD) have been clearly demonstrated to lessen the morbidity and mortality of CVD in the general population; therefore, there is hope that the use of these drugs may likewise help patients with CKD (In addition, it has been theorized that dyslipidemia may contribute to the progression of CKD, such that LLD may prove to slow CKD progression.) Nevertheless, given differences in epidemiology and pathophysiology of CVD in CKD, there are reasons to question whether the cardiovascular benefits of LLD that are observed in the general population will also be realized in the CKD population. It is widely acknowledged that the current medical literature provides insufficient data to guide the use of LLD in the CKD population, in large part because renal insufficiency has been an exclusion criterion for most of the randomized, controlled studies that have addressed this issue. Although consensus-based guidelines on the treatment of dyslipidemias in individuals with CKD and with kidney transplants have been published by the National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (K/DOQI) Work Groups, the nephrology and cardiology communities recognize the urgent need for high-quality clinical studies on this issue, and this has fueled the publication of subgroup analyses of previous large studies in the general population and the launching of large-scale clinical trials in the CKD population, as summarized in Table 1. To provide the reader with a better appreciation of the important issues that are germane to management of dyslipidemia in CKD, this article (1) briefly summarizes the literature on the benefits of LLD in the general population, (2) demonstrates the limited involvement of individuals with CKD in the studies in the ge...

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Section: Pathophysiology Of Cvd In Ckdmentioning

confidence: 99%

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

Nogueira

Weir

2007

Clinical Journal of the American Society of Nephrology

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“…Decreased magnesium is associated with impaired endothelial function, vasospasm and atherogenesis [49] . In hemodialysis and peritoneal dialysis patients, lower serum magnesium but still within the normal range was associated with an increased severity of vascular calcification [50,51] . In vitro studies have demonstrated the protective effect of increasing magnesium concentration on vascular smooth muscle cell calcification through an upregulation of anti-calcification proteins including matrix gla protein and osteopontin [52][53][54] .…”

Section: Magnesium and Combined Magnesium-calcium Phosphate Bindermentioning

confidence: 99%

Lowering vascular calcification burden in chronic kidney disease: Is it possible?

Disthabanchong

2013

WJN

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High prevalence of atherosclerosis and arterial calcification in chronic kidney disease is far beyond the explanation by common cardiovascular risk factors such as aging diabetes, hypertension and dyslipidemia. The magnitude of coronary artery calcification is independently and inversely associated with renal function. In addition to cardiovascular risk factors, other chronic kidney diseaserelated risks such as phosphate retention, excess of calcium and prolonged dialysis vintage also contribute to the development of vascular calcification. Strategies to lower vascular calcification burden in chronic kidney disease population should include minimizing chronic kidney disease and atherosclerotic risk factors. Current therapies available are non-calcium containing phosphate binders, low dose active vitamin D and calcimimetic agent. The role of bisphosphonates in vascular calcification in chronic kidney disease population remains unclear. Preliminary data on sodium thiosulfate are promising, however, larger studies on efficacy and patient outcomes are necessary. Several large randomized controlled trials have confirmed the lack of benefit of statin in attenuating the progression of vascular calcification.

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“…It has been suggested that two types of MCS may exist, with clinical and histological differences: the first is a benign, slowly progressive, and essentially asymptomatic form with thin medial calcifications and little or no narrowing of the arterial lumen; the second is a malignant, rapidly progressive form in which massive and extensive medial calcifications may displace the internal elastic lamina toward the lumen causing luminal narrowing [5].…”

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confidence: 99%

Malignant Mönckeberg medial calcific sclerosis

et al. 2018

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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). All common causes of renal failure were ruled out as well as paraneoplastic syndromes and autoimmune diseases. Ca-P metabolism was normalized using calcimimetics and calcium-free phosphate binders. Imaging studies, with X-ray, computed tomography (CT) and angiography, showed widespread vascular calcifications involving vertebral, renal, ovarian, hepatic, splenic, visceral, and peripheral arteries of the upper and lower limbs without overt organ or soft tissue calcifications (Fig. 1a-c). Because of the rapid progression of ischemic lesions, multiple amputations involving both lower limbs and hands became necessary. The histological examination of surgical specimens showed smallto-medium-sized muscular arteries displaying dystrophic medial calcifications that were focal or circumferential in the affected tunica media, causing luminal narrowing or sub-occlusion ( Fig. 1d-f). There were no signs of atherosclerosis, and a diagnosis of MCS was made. Parathyroid ultrasound and scintigraphy revealed diffuse enlargement and hypermetabolism of the four glands. Total parathyroidectomy was performed, and histological examination of the excised glands showed diffuse hyperplasia. After parathyroidectomy, no new lesions appeared. There was a progressive healing at the sites of amputation.Chronic kidney disease (CKD) is known to be associated with bone and mineral disorders that present with laboratory alterations in Ca-P metabolism and with vascular calcifications. 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].Four stages of lesion progression are recognized in MCS. In stage 1, calcifications appear as irregular d...

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Serum magnesium level and arterial calcification in end-stage renal disease

Cited by 181 publications

References 45 publications

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs

Lowering vascular calcification burden in chronic kidney disease: Is it possible?

Malignant Mönckeberg medial calcific sclerosis

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