Association between Dietary Intake and Coronary Artery Calcification in Non-Dialysis Chronic Kidney Disease: The PROGREDIR Study

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Abstract

Coronary artery calcification (CAC) is a widespread condition in chronic kidney disease (CKD). Diet may play an important role in CAC, but this role is not clear. This study evaluated the association between macro-and micronutrient intakes and CAC in non-dialysis CKD patients. We analyzed the baseline data from 454 participants of the PROGREDIR study. Dietary intake was evaluated by a food frequency questionnaire. CAC was measured by computed tomography. After exclusion of participants with a coronary stent, 373 people remained for the analyses. The highest tertile of CAC was directly associated with the intake of phosphorus, calcium and magnesium. There was a higher intake of pantothenic acid and potassium in the second tertile. After adjustments for confounding variables, the intake of pantothenic acid, phosphorus, calcium and potassium remained associated with CAC in the generalized linear mixed models. In order to handle the collinearity between these nutrients, we used the LASSO (least absolute shrinkage and selection operator) regression to evaluate the nutrients associated with CAC variability. In this approach, the nutrients that most explained the variance of CAC were phosphorus, calcium and potassium. Prospective studies are needed to confirm these findings and assess the role of interventions regarding these micronutrients on CAC prevention and progression.

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Phosphate regulation of vascular smooth muscle cell calcification.

S Jono, M McKee, C Murry … (2000)

Vascular calcification is a common finding in atherosclerosis and a serious problem in diabetic and uremic patients. Because of the correlation of hyperphosphatemia and vascular calcification, the ability of extracellular inorganic phosphate levels to regulate human aortic smooth muscle cell (HSMC) culture mineralization in vitro was examined. HSMCs cultured in media containing normal physiological levels of inorganic phosphate (1.4 mmol/L) did not mineralize. In contrast, HSMCs cultured in media containing phosphate levels comparable to those seen in hyperphosphatemic individuals (>1.4 mmol/L) showed dose-dependent increases in mineral deposition. Mechanistic studies revealed that elevated phosphate treatment of HSMCs also enhanced the expression of the osteoblastic differentiation markers osteocalcin and Cbfa-1. The effects of elevated phosphate on HSMCs were mediated by a sodium-dependent phosphate cotransporter (NPC), as indicated by the ability of the specific NPC inhibitor phosphonoformic acid, to dose dependently inhibit phosphate-induced calcium deposition as well as osteocalcin and Cbfa-1 gene expression. With the use of polymerase chain reaction and Northern blot analyses, the NPC in HSMCs was identified as Pit-1 (Glvr-1), a member of the novel type III NPCs. These data suggest that elevated phosphate may directly stimulate HSMCs to undergo phenotypic changes that predispose to calcification and offer a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions. The full text of this article is available at http://www.circresaha.org.

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Coronary Artery Calcification and Risk of Cardiovascular Disease and Death Among Patients With Chronic Kidney Disease

Jing Chen, Matthew Budoff, Muredach Reilly … (2017)

Question Does coronary artery calcification (CAC) predict cardiovascular disease risk among patients with chronic kidney disease (CKD)? Findings In this prospective cohort study, 1 SD log higher in CAC score was significantly associated with a 40% higher risk of cardiovascular disease, a 44% higher risk of myocardial infarction, and a 39% higher risk of heart failure after adjusting for important risk factors. Inclusion of CAC score led to a significant increase in the C statistic for predicting cardiovascular disease over use of established and novel risk factors among patients with CKD. Meaning Use of the CAC score improves risk prediction for cardiovascular disease, myocardial infarction, and heart failure over use of established and novel risk factors among patients with CKD. Importance Coronary artery calcification (CAC) is highly prevalent in dialysis-naive patients with chronic kidney disease (CKD). However, there are sparse data on the association of CAC with subsequent risk of cardiovascular disease and all-cause mortality in this population. Objective To study the prospective association of CAC with risk of cardiovascular disease and all-cause mortality among dialysis-naive patients with CKD. Design, Setting, and Participants The prospective Chronic Renal Insufficiency Cohort study recruited adults with an estimated glomerular filtration rate of 20 to 70 mL/min/1.73 m 2 from 7 clinical centers in the United States. There were 1541 participants without cardiovascular disease at baseline who had CAC scores. Exposures Coronary artery calcification was assessed using electron-beam or multidetector computed tomography. Main Outcomes and Measures Incidence of cardiovascular disease (including myocardial infarction, heart failure, and stroke) and all-cause mortality were reported every 6 months and confirmed by medical record adjudication. Results During an average follow-up of 5.9 years in 1541 participants aged 21 to 74 years, there were 188 cardiovascular disease events (60 cases of myocardial infarction, 120 heart failures, and 27 strokes; patients may have had >1 event) and 137 all-cause deaths. In Cox proportional hazards models adjusted for age, sex, race, clinical site, education level, physical activity, total cholesterol level, high-density lipoprotein cholesterol level, systolic blood pressure, use of antihypertensive treatment, current cigarette smoking, diabetes status, body mass index, C-reactive protein level, hemoglobin A 1c level, phosphorus level, troponin T level, log N-terminal pro–B-type natriuretic peptide level, fibroblast growth factor 23 level, estimated glomerular filtration rate, and proteinuria, the hazard ratios associated with per 1 SD log of CAC were 1.40 (95% CI, 1.16-1.69; P < .001) for cardiovascular disease, 1.44 (95% CI, 1.02-2.02; P = .04) for myocardial infarction, 1.39 (95% CI, 1.10-1.76; P = .006) for heart failure, and 1.19 (95% CI, 0.94-1.51; P = .15) for all-cause mortality. In addition, inclusion of CAC score led to an increase in the C statistic of 0.02 (95% CI, 0-0.09; P < .001) for predicting cardiovascular disease over use of all the above-mentioned established and novel cardiovascular disease risk factors. Conclusions and Relevance Coronary artery calcification is independently and significantly related to the risks of cardiovascular disease, myocardial infarction, and heart failure in patients with CKD. In addition, CAC improves risk prediction for cardiovascular disease, myocardial infarction, and heart failure over use of established and novel cardiovascular disease risk factors among patients with CKD; however, the changes in the C statistic are small. This cohort study assesses the prospective association of coronary artery calcification with risk of cardiovascular disease and all-cause mortality among dialysis-naive adult patients with chronic kidney disease from 7 US clinical centers.

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Vitamin K supplementation and progression of coronary artery calcium in older men and women.

Bess Dawson-Hughes, Paula O′Shea, Ian K. Williamson … (2009)

Coronary artery calcification (CAC) is an independent predictor of cardiovascular disease. A preventive role for vitamin K in CAC progression has been proposed on the basis of the properties of matrix Gla protein (MGP) as a vitamin K-dependent calcification inhibitor. The objective was to determine the effect of phylloquinone (vitamin K1) supplementation on CAC progression in older men and women. CAC was measured at baseline and after 3 y of follow-up in 388 healthy men and postmenopausal women; 200 received a multivitamin with 500 microg phylloquinone/d (treatment), and 188 received a multivitamin alone (control). In an intention-to-treat analysis, there was no difference in CAC progression between the phylloquinone group and the control group; the mean (+/-SEM) changes in Agatston scores were 27 +/- 6 and 37 +/- 7, respectively. In a subgroup analysis of participants who were > or =85% adherent to supplementation (n = 367), there was less CAC progression in the phylloquinone group than in the control group (P = 0.03). Of those with preexisting CAC (Agatston score > 10), those who received phylloquinone supplements had 6% less progression than did those who received the multivitamin alone (P = 0.04). Phylloquinone-associated decreases in CAC progression were independent of changes in serum MGP. MGP carboxylation status was not determined. Phylloquinone supplementation slows the progression of CAC in healthy older adults with preexisting CAC, independent of its effect on total MGP concentrations. Because our data are hypothesis-generating, further studies are warranted to clarify this mechanism. This trial was registered at clinicaltrials.gov as NCT00183001.

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Journal

Journal ID (nlm-ta): Nutrients

Journal ID (iso-abbrev): Nutrients

Journal ID (publisher-id): nutrients

Title: Nutrients

Publisher: MDPI

ISSN (Electronic): 2072-6643

Publication date (Electronic): 19 March 2018

Publication date Collection: March 2018

Volume: 10

Issue: 3

Electronic Location Identifier: 372

Affiliations

[1 ]Department of Nephrology, Hospital das Clínicas, Faculty of Medicine, University of São Paulo, São Paulo SP 05403-000, Brazil; fernandanogueiraanjos@ 123456hotmail.com (F.S.N.d.A.); smotitan@ 123456gmail.com (S.M.d.O.T.)

[2 ]Heart Institute, Hospital das Clínicas, Faculty of Medicine, University of São Paulo, São Paulo SP 05403-900, Brazil; lgomez928@ 123456gmail.com

[3 ]Department of Nutrition, School of Public Health, University of São Paulo, São Paulo SP 03178-200, Brazil; marchioni@ 123456usp.br

[4 ]Health Sciences Center, Federal University of Espírito Santo, Vitória ES 29043-900, Brazil; maria.molina@ 123456ufes.br

[5 ]General Medicine Unit, Faculty of Medicine, and Hospital Universitário, University of São Paulo, São Paulo SP 05508-000, Brazil; palotufo@ 123456usp.br (P.A.L.); isabensenor@ 123456gmail.com (I.J.M.B.)

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[* ]Correspondence: alissondiegomachado@ 123456hotmail.com ; Tel.: +55-11-98054-1963

[†]

L.M.G. and D.M.L.M. contributed equally and should both be considered as second author.

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Alisson Diego Machado https://orcid.org/0000-0002-1564-5405

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Publisher ID: nutrients-10-00372

DOI: 10.3390/nu10030372

PMC ID: 5872790

PubMed ID: 29562658

SO-VID: ba74c355-ac2d-4925-8362-e8f246e0ce1a

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Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

Association between Dietary Intake and Coronary Artery Calcification in Non-Dialysis Chronic Kidney Disease: The PROGREDIR Study

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Most cited references 44

Phosphate regulation of vascular smooth muscle cell calcification.

Coronary Artery Calcification and Risk of Cardiovascular Disease and Death Among Patients With Chronic Kidney Disease

Vitamin K supplementation and progression of coronary artery calcium in older men and women.

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