Vascular calcifications as a marker of increased cardiovascular risk: A meta-analysis

Rennenberg, Roger J M W; Kessels, Alphons G.H.; Schurgers, Leon J.; Engelshoven, Jos M. A. van; Leeuw, Peter W. de; Kroon, Abraham A.

doi:10.2147/vhrm.s4822

Cited by 399 publications

(325 citation statements)

References 51 publications

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“…Arterial calcification increases mortality risk by threefold to fourfold. 66 Calcification causes a hard or stable plaque to form in arterial vessels, which is related to arteriolosclerosis, hypertension, left ventricular hypertrophy and aortic valve disease. In vitro and in vivo experiments showed that a high phosphorus load acutely increases endothelial dysfunction by impairing vasodilation, raising the risk for cardiovascular disease.…”

Section: Phosphate Toxicity Associated With Ectopic Calcificationmentioning

confidence: 99%

Dysregulation of phosphate metabolism and conditions associated with phosphate toxicity

Brown

2015

BoneKEy Reports

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Phosphate homeostasis is coordinated and regulated by complex cross-organ talk through delicate hormonal networks. Parathyroid hormone (PTH), secreted in response to low serum calcium, has an important role in maintaining phosphate homeostasis by influencing renal synthesis of 1,25-dihydroxyvitamin D, thereby increasing intestinal phosphate absorption. Moreover, PTH can increase phosphate efflux from bone and contribute to renal phosphate homeostasis through phosphaturic effects. In addition, PTH can induce skeletal synthesis of another potent phosphaturic hormone, fibroblast growth factor 23 (FGF23), which is able to inhibit renal tubular phosphate reabsorption, thereby increasing urinary phosphate excretion. FGF23 can also fine-tune vitamin D homeostasis by suppressing renal expression of 1-alpha hydroxylase (1a(OH)ase). This review briefly discusses how FGF23, by forming a bone-kidney axis, regulates phosphate homeostasis, and how its dysregulation can lead to phosphate toxicity that induces widespread tissue injury. We also provide evidence to explain how phosphate toxicity related to dietary phosphorus overload may facilitate incidence of noncommunicable diseases including kidney disease, cardiovascular disease, cancers and skeletal disorders.

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Section: Phosphate Toxicity Associated With Ectopic Calcificationmentioning

confidence: 99%

Dysregulation of phosphate metabolism and conditions associated with phosphate toxicity

Brown

2015

BoneKEy Reports

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“…At any time, approximately half of patients on conventional hemodialysis (HD) have serum phosphate above the recommended level (1)(2)(3)(4), and nearly all receive additional therapies (beyond HD) to lower phosphate (5). Elevated phosphate contributes to secondary hyperparathyroidism (6,7), elevated FGF23 levels (8,9), and vascular calcification (10 -12), which in turn predispose to mortality in this population (13)(14)(15). Observational studies have consistently demonstrated a potent and dose-dependent association between higher serum phosphate levels and mortality (1,3,(16)(17)(18), cardiovascular mortality and morbidity (3,4), and increased rates of hospitalization (14).…”

Section: Introductionmentioning

confidence: 99%

Prescribed Dietary Phosphate Restriction and Survival among Hemodialysis Patients

Lynch¹,

Lynch²,

Curhan³

et al. 2011

Clinical Journal of the American Society of Nephrology

131

102

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SummaryBackground and objectives Hyperphosphatemia is common among hemodialysis patients. Although prescribed dietary phosphate restriction is a recommended therapy, little is known about the long-term effects on survival.Design, setting, participants, & measurements We conducted a post hoc analysis of data from the Hemodialysis Study (n ϭ 1751). Prescribed dietary phosphate was recorded at baseline and annually thereafter. Marginal structural proportional hazard models were fit to estimate the adjusted association between dietary phosphate restriction and mortality in the setting of time-dependent confounding.Results At baseline, prescribed daily phosphate was restricted to levels Յ870, 871 to 999, 1000, 1001 to 2000 mg, and not restricted in 300, 314, 307, 297, and 533 participants, respectively. More restrictive prescribed dietary phosphate was associated with poorer indices of nutritional status on baseline analyses and a persistently greater need for nutritional supplementation but not longitudinal changes in caloric or protein intake. On marginal structural analysis, there was a stepwise trend toward greater survival with more liberal phosphate prescription, which reached statistical significance among subjects prescribed 1001 to 2000 mg/d and those with no specified phosphate restriction: hazard ratios (95% CIs) 0.73 (0.54 to 0.97) and 0.71 (0.55 to 0.92), respectively. Subgroup analysis suggested a more pronounced survival benefit of liberal dietary phosphate prescription among nonblacks, participants without hyperphosphatemia, and those not receiving activated vitamin D.Conclusions Prescribed dietary phosphate restriction is not associated with improved survival among prevalent hemodialysis patients, and increased level of restriction may be associated with greater mortality particularly in some subgroups.

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“…Arterial disease was also described for Egyptian mummies from 3,500 years ago (18th Dynasty; n = 24) (34, 35): 67% of large arteries were atherosclerotic; of these, 50% were calcified. In modern populations, arterial calcification is a high risk marker for vascular fatal events, with 4-fold more mortality in the following decade (36,37). Coronary atherosclerosis was also found in mummies from dynastic Egypt (34,38), China (1150 BCE), and Alaskan Inuit (430 CE) (39).…”

mentioning

confidence: 99%

Evolution of the human lifespan and diseases of aging: Roles of infection, inflammation, and nutrition

Finch

2009

Proc. Natl. Acad. Sci. U.S.A.

317

284

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Humans have evolved much longer lifespans than the great apes, which rarely exceed 50 years. Since 1800, lifespans have doubled again, largely due to improvements in environment, food, and medicine that minimized mortality at earlier ages. Infections cause most mortality in wild chimpanzees and in traditional forager-farmers with limited access to modern medicine. Although we know little of the diseases of aging under premodern conditions, in captivity, chimpanzees present a lower incidence of cancer, ischemic heart disease, and neurodegeneration than current human populations. These major differences in pathology of aging are discussed in terms of genes that mediate infection, inflammation, and nutrition. Apolipoprotein E alleles are proposed as a prototype of pleiotropic genes, which influence immune responses, arterial and Alzheimer's disease, and brain development.chimpanzee | pathology H umans have the longest life spans of any primate. Even under the conditions of high mortality experienced by hunterforagers, the human life expectancy at birth (LE 0 ) is twice that of wild chimpanzees. This inquiry considers the demographics and pathology of aging in humans and great apes as an approach to understanding how aging processes evolved with longer lifespans. I argue that immune functions and nutrition have been of major importance in the evolution of aging and longevity.

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Vascular calcifications as a marker of increased cardiovascular risk: A meta-analysis

Cited by 399 publications

References 51 publications

Dysregulation of phosphate metabolism and conditions associated with phosphate toxicity

Dysregulation of phosphate metabolism and conditions associated with phosphate toxicity

Prescribed Dietary Phosphate Restriction and Survival among Hemodialysis Patients

Evolution of the human lifespan and diseases of aging: Roles of infection, inflammation, and nutrition

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