PMID- 29118764
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220311
IS  - 1664-3828 (Print)
IS  - 1664-5502 (Electronic)
IS  - 1664-5502 (Linking)
VI  - 7
IP  - 4
DP  - 2017 Oct
TI  - Folic Acid and Homocysteine in Chronic Kidney Disease and Cardiovascular Disease 
      Progression: Which Comes First?
PG  - 255-266
LID - 10.1159/000471813 [doi]
AB  - BACKGROUND: Hyperhomocysteinemia (Hhcy) occurs in about 85% of chronic kidney 
      disease (CKD) patients because of impaired renal metabolism and reduced renal 
      excretion. Folic acid (FA), the synthetic form of vitamin B(9), is critical in 
      the conversion of homocysteine (Hcy) to methionine. If there is not enough intake 
      of FA, there is not enough conversion, and Hcy levels are raised. SUMMARY: Hhcy 
      is regarded as an independent predictor of cardiovascular morbidity and mortality 
      in end-stage renal disease. Hhcy exerts its pathogenic action on the main 
      processes involved in the progression of vascular damage. Research has shown Hhcy 
      suggests enhanced risks for inflammation and endothelial injury which lead to 
      cardiovascular disease (CVD), stroke, and CKD. FA has also been shown to improve 
      endothelial function without lowering Hcy, suggesting an alternative explanation 
      for the effect of FA on endothelial function. Recently, the role of FA and Hhcy 
      in CVD and in CKD progression was renewed in some randomized trials. KEY 
      MESSAGES: In the general population and in CKD patients, it remains a topic of 
      discussion whether any beneficial effects of FA therapy are to be referred to its 
      direct effect or to a reduction of Hhcy. While waiting for the results of 
      confirmatory trials, it is reasonable to consider FA with or without 
      methylcobalamin supplementation as appropriate adjunctive therapy in patients 
      with CKD.
FAU - Cianciolo, Giuseppe
AU  - Cianciolo G
AD  - Nephrology, Dialysis, and Transplantation Unit, Department of Experimental, 
      Diagnostic, and Specialty Medicine (DIMES), St. Orsola Hospital, University of 
      Bologna, Bologna, Italy.
FAU - De Pascalis, Antonio
AU  - De Pascalis A
AD  - Nephrology and Dialysis Unit, V. Fazzi Hospital, Lecce, Italy.
FAU - Di Lullo, Luca
AU  - Di Lullo L
AD  - Nephrology and Dialysis Unit, Parodi-Delfino Hospital, Colleferro, Italy.
FAU - Ronco, Claudio
AU  - Ronco C
AD  - International Renal Research Institute (IRRIV), S. Bortolo Hospital, Vicenza, 
      Italy.
FAU - Zannini, Chiara
AU  - Zannini C
AD  - Nephrology, Dialysis, and Transplantation Unit, Department of Experimental, 
      Diagnostic, and Specialty Medicine (DIMES), St. Orsola Hospital, University of 
      Bologna, Bologna, Italy.
FAU - La Manna, Gaetano
AU  - La Manna G
AD  - Nephrology, Dialysis, and Transplantation Unit, Department of Experimental, 
      Diagnostic, and Specialty Medicine (DIMES), St. Orsola Hospital, University of 
      Bologna, Bologna, Italy.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170621
PL  - Switzerland
TA  - Cardiorenal Med
JT  - Cardiorenal medicine
JID - 101554863
PMC - PMC5662962
OTO - NOTNLM
OT  - Cardiovascular disease
OT  - Chronic kidney disease
OT  - Folate pathway
OT  - Homocysteine
OT  - Hyperhomocysteinemia
EDAT- 2017/11/10 06:00
MHDA- 2017/11/10 06:01
PMCR- 2018/10/01
CRDT- 2017/11/10 06:00
PHST- 2017/11/10 06:00 [entrez]
PHST- 2017/11/10 06:00 [pubmed]
PHST- 2017/11/10 06:01 [medline]
PHST- 2018/10/01 00:00 [pmc-release]
AID - crm-0007-0255 [pii]
AID - 10.1159/000471813 [doi]
PST - ppublish
SO  - Cardiorenal Med. 2017 Oct;7(4):255-266. doi: 10.1159/000471813. Epub 2017 Jun 21.