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Review
. 2019 Feb 13;11(2):383.
doi: 10.3390/nu11020383.

Folic Acid and Vitamin B12 Administration in CKD, Why Not?

Affiliations
Review

Folic Acid and Vitamin B12 Administration in CKD, Why Not?

Irene Capelli et al. Nutrients. .

Abstract

Patients affected by chronic kidney disease (CKD) or end-stage renal disease (ESRD) experience a huge cardiovascular risk and cardiovascular events represent the leading causes of death. Since traditional risk factors cannot fully explain such increased cardiovascular risk, interest in non-traditional risk factors, such as hyperhomocysteinemia and folic acid and vitamin B12 metabolism impairment, is growing. Although elevated homocysteine blood levels are often seen in patients with CKD and ESRD, whether hyperhomocysteinemia represents a reliable cardiovascular and mortality risk marker or a therapeutic target in this population is still unclear. In addition, folic acid and vitamin B12 could not only be mere cofactors in the homocysteine metabolism; they may have a direct action in determining tissue damage and cardiovascular risk. The purpose of this review was to highlight homocysteine, folic acid and vitamin B12 metabolism impairment in CKD and ESRD and to summarize available evidences on hyperhomocysteinemia, folic acid and vitamin B12 as cardiovascular risk markers, therapeutic target and risk factors for CKD progression.

Keywords: cardiovascular disease; chronic kidney disease; end-stage renal disease; folic acid; hyperhomocysteinemia; vitamin B12.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Homocysteine Metabolism in physiological condition (A) and in renal disease (B). CSE: cystathionine gamma-lyase; CBS: cystathionine beta synthase.
Figure 2
Figure 2
Hyperhomocysteinemia-induced amplification of atherosclerosis and inflammation in chronic kidney disease (CKD) patients. Abbreviations: NO, Nitric Oxide.

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References

    1. Go A.S., Chertow G.M., Fan D., McCulloch C.E., Hsu C.Y. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N. Engl. J. Med. 2004;351:1296–1305. doi: 10.1056/NEJMoa041031. - DOI - PubMed
    1. Foley R.N., Parfrey P.S., Sarnak M.J. Epidemiology of cardiovascular disease in chronic renal disease. J. Am. Soc. Nephrol. 1998;9:S16–S23. doi: 10.1053/ajkd.1998.v32.pm9820470. - DOI - PubMed
    1. Jha V., Garcia-Garcia G., Iseki K., Li Z., Naicker S., Plattner B., Saran R., Wang A.Y., Yang C.W. Chronic kidney disease: Global dimension and perspectives. Lancet. 2013;382:260–272. doi: 10.1016/S0140-6736(13)60687-X. - DOI - PubMed
    1. McCullough P.A., Steigerwalt S., Tolia K., Chen S.C., Li S., Norris K.C., Whaley-Connell A., KEEP Investigators Cardiovascular disease in chronic kidney disease: Data from the Kidney Early Evaluation Program (KEEP) Curr. Diab. Rep. 2011;11:47–55. doi: 10.1007/s11892-010-0162-y. - DOI - PMC - PubMed
    1. Ekdahl K., Soveri I., Hilborn J., Fellström B., Nilsson B. Cardiovascular disease in hemodialysis: Role of the intravascular innate immune system. Nat. Rev. Nephrol. 2017;13:285–296. doi: 10.1038/nrneph.2017.17. - DOI - PubMed

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