Vitamin K status, all-cause mortality, and cardiovascular disease in adults with chronic kidney disease: the Chronic Renal Insufficiency Cohort.
cardiovascular disease
chronic kidney disease
mortality
nutrition
vitamin K
Journal
The American journal of clinical nutrition
ISSN: 1938-3207
Titre abrégé: Am J Clin Nutr
Pays: United States
ID NLM: 0376027
Informations de publication
Date de publication:
04 03 2022
04 03 2022
Historique:
received:
09
09
2021
accepted:
10
11
2021
pubmed:
18
11
2021
medline:
20
4
2022
entrez:
17
11
2021
Statut:
ppublish
Résumé
Vascular calcification contributes to cardiovascular disease (CVD) and mortality in individuals with chronic kidney disease (CKD). Vitamin K-dependent proteins function as calcification inhibitors in vascular tissue. We sought to determine the association of vitamin K status with mortality and CVD events in adults with CKD. Plasma dephospho-uncarboxylated matrix gla protein ((dp)ucMGP), which increases when vitamin K status is low, and plasma phylloquinone (vitamin K1), which decreases when vitamin K status is low, were measured in 3066 Chronic Renal Insufficiency Cohort participants (median age = 61 y, 45% female, 41% non-Hispanic black, median estimated glomerular filtration rate [eGFR] = 41 mL/min/1.73m2). The association of vitamin K status biomarkers with all-cause mortality and atherosclerotic-related CVD was determined using multivariable Cox proportional hazards regression. There were 1122 deaths and 599 atherosclerotic CVD events over the median 12.8 follow-up years. All-cause mortality risk was 21-29% lower among participants with plasma (dp)ucMGP <450 pmol/L (n = 2361) compared with those with plasma (dp)ucMGP ≥450 pmol/L (adjusted HRs [95% CIs]: <300 pmol/L = 0.71 [0.61, 0.83], 300-449 pmol/L = 0.77 [0.66, 0.90]) and 16-19% lower among participants with plasma phylloquinone ≥0.50 nmol/L (n = 2421) compared to those with plasma phylloquinone <0.50 nmol/L (adjusted HRs: 0.50, 0.99 nmol/L = 0.84 [0.72, 0.99], ≥1.00 nmol/L = 0.81 [0.70, 0.95]). The risk of atherosclerotic CVD events did not significantly differ across plasma (dp)ucMGP or phylloquinone categories. Two biomarkers of vitamin K status were associated with a lower all-cause mortality risk but not atherosclerotic CVD events. Additional studies are needed to clarify the mechanism underlying this association and evaluate the impact of improving vitamin K status in people with CKD.
Sections du résumé
BACKGROUND
Vascular calcification contributes to cardiovascular disease (CVD) and mortality in individuals with chronic kidney disease (CKD). Vitamin K-dependent proteins function as calcification inhibitors in vascular tissue.
OBJECTIVES
We sought to determine the association of vitamin K status with mortality and CVD events in adults with CKD.
METHODS
Plasma dephospho-uncarboxylated matrix gla protein ((dp)ucMGP), which increases when vitamin K status is low, and plasma phylloquinone (vitamin K1), which decreases when vitamin K status is low, were measured in 3066 Chronic Renal Insufficiency Cohort participants (median age = 61 y, 45% female, 41% non-Hispanic black, median estimated glomerular filtration rate [eGFR] = 41 mL/min/1.73m2). The association of vitamin K status biomarkers with all-cause mortality and atherosclerotic-related CVD was determined using multivariable Cox proportional hazards regression.
RESULTS
There were 1122 deaths and 599 atherosclerotic CVD events over the median 12.8 follow-up years. All-cause mortality risk was 21-29% lower among participants with plasma (dp)ucMGP <450 pmol/L (n = 2361) compared with those with plasma (dp)ucMGP ≥450 pmol/L (adjusted HRs [95% CIs]: <300 pmol/L = 0.71 [0.61, 0.83], 300-449 pmol/L = 0.77 [0.66, 0.90]) and 16-19% lower among participants with plasma phylloquinone ≥0.50 nmol/L (n = 2421) compared to those with plasma phylloquinone <0.50 nmol/L (adjusted HRs: 0.50, 0.99 nmol/L = 0.84 [0.72, 0.99], ≥1.00 nmol/L = 0.81 [0.70, 0.95]). The risk of atherosclerotic CVD events did not significantly differ across plasma (dp)ucMGP or phylloquinone categories.
CONCLUSIONS
Two biomarkers of vitamin K status were associated with a lower all-cause mortality risk but not atherosclerotic CVD events. Additional studies are needed to clarify the mechanism underlying this association and evaluate the impact of improving vitamin K status in people with CKD.
Identifiants
pubmed: 34788785
pii: S0002-9165(22)00209-X
doi: 10.1093/ajcn/nqab375
pmc: PMC8895220
doi:
Substances chimiques
Biomarkers
0
Vitamin K
12001-79-5
Vitamin K 1
84-80-0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
941-948Subventions
Organisme : NCATS NIH HHS
ID : UL1 TR002548
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK060984
Pays : United States
Organisme : NIDDK NIH HHS
ID : U24 DK060990
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK060963
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK060990
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK111392
Pays : United States
Investigateurs
J Lawrence Appel
(JL)
S Alan Go
(SA)
P James Lash
(PJ)
G Robert Nelson
(GR)
Mahboob Rahman
(M)
Panduranga S Rao
(PS)
Vallabh O Shah
(VO)
Mark L Unruh
(ML)
Commentaires et corrections
Type : CommentIn
Informations de copyright
© The Author(s) 2021. Published by Oxford University Press.
Références
Am J Physiol Renal Physiol. 2014 Oct 15;307(8):F891-900
pubmed: 25143458
J Am Coll Cardiol. 2019 Oct 8;74(14):1823-1838
pubmed: 31582143
Am J Clin Nutr. 2020 Jun 1;111(6):1170-1177
pubmed: 32359159
Kidney Int. 2013 May;83(5):835-44
pubmed: 23344475
Nutrients. 2015 Aug 18;7(8):6991-7011
pubmed: 26295257
Methods Enzymol. 1997;282:408-21
pubmed: 9330305
Nutrients. 2016 Jan 02;8(1):
pubmed: 26729160
Biomed Chromatogr. 2009 Dec;23(12):1276-82
pubmed: 19488978
Am J Clin Nutr. 2013 Jul;98(1):197-208
pubmed: 23719555
Physiol Genomics. 2006 Oct 3;27(1):86-94
pubmed: 16835353
PLoS One. 2012;7(10):e47991
pubmed: 23118917
Ren Fail. 2019 Nov;41(1):244-256
pubmed: 31014155
Sci Rep. 2019 Dec 5;9(1):18452
pubmed: 31804541
J Clin Endocrinol Metab. 1998 Sep;83(9):3258-66
pubmed: 9745439
Genomics. 2000 May 15;66(1):1-14
pubmed: 10843799
Clin J Am Soc Nephrol. 2009 Aug;4(8):1302-11
pubmed: 19541818
Nephrol Dial Transplant. 2014 Jul;29(7):1385-90
pubmed: 24285428
J Am Heart Assoc. 2015 Nov 23;4(11):
pubmed: 26597152
J Am Soc Nephrol. 2020 Oct;31(10):2434-2445
pubmed: 32817311
Clin J Am Soc Nephrol. 2010 Apr;5(4):590-7
pubmed: 20167683
Int Urol Nephrol. 2019 Mar;51(3):527-534
pubmed: 30689181
Adv Nutr. 2013 Jul 01;4(4):463-73
pubmed: 23858094
J Thromb Haemost. 2007 Dec;5(12):2503-11
pubmed: 17848178
J Am Coll Cardiol. 2021 Sep 14;78(11):1145-1165
pubmed: 34503684
J Gerontol A Biol Sci Med Sci. 2020 Mar 9;75(4):792-797
pubmed: 31056634
J Nutr. 2003 Mar;133(3):873S-874S
pubmed: 12612172
J Nutr. 2003 Aug;133(8):2565-9
pubmed: 12888638
Clin J Am Soc Nephrol. 2015 Nov 6;10(11):2073-83
pubmed: 26265715
Clin Nutr. 2015 Apr;34(2):235-40
pubmed: 24745600
Hypertension. 2016 Sep;68(3):590-6
pubmed: 27456517
Semin Nephrol. 2013 Mar;33(2):93-105
pubmed: 23465497
Kidney Int. 2014 Aug;86(2):286-93
pubmed: 24429407
Clin J Am Soc Nephrol. 2017 Jul 7;12(7):1181-1189
pubmed: 28242844
Adv Chronic Kidney Dis. 2008 Oct;15(4):396-412
pubmed: 18805386
Int Urol Nephrol. 2019 Nov;51(11):2037-2044
pubmed: 31529295
Am J Kidney Dis. 2021 Feb;77(2):235-244
pubmed: 32768632
Am J Kidney Dis. 2019 Jun;73(6):827-836
pubmed: 30686529
Am J Kidney Dis. 2012 Feb;59(2):186-95
pubmed: 22169620
PLoS One. 2021 Feb 24;16(2):e0247623
pubmed: 33626087
Int J Mol Sci. 2020 Aug 21;21(17):
pubmed: 32839405
Clin Kidney J. 2021 Jan 28;14(9):2114-2123
pubmed: 34476095
Am J Kidney Dis. 2012 Aug;60(2):250-61
pubmed: 22658574
Clin J Am Soc Nephrol. 2010 Apr;5(4):568-75
pubmed: 20133489
Kidney Int Rep. 2020 Aug 06;5(10):1729-1737
pubmed: 33102965
J Am Soc Nephrol. 2020 Jan;31(1):186-196
pubmed: 31704740