Jody A.

Charnow, Editor
August 24, 2016
General News

CKD Progression Delay Observed With Folic

Acid Therapy
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Enalapril plus folic acid treatment was associated with a 56% reduction in the odds of CKD
progression compared with enalapril alone.

Folic acid treatment may delay progression of chronic kidney disease (CKD) among patients
with mild to moderate CKD, according to investigators.

Our study is the first to show significant renal protection from folic acid therapy in a population
without folic acid fortification, a team led by Fan Fan Hou, MD, PhD, of Southern Medical
University in Guangzhou, China, reported online ahead of print in JAMA Internal Medicine.

In the Renal Substudy of the China Stroke Primary Prevention Trial, hypertensive patients
treated with a combination of enalapril and folic acid had a 21% decrease in the odds of CKD
progressionthe primary outcomecompared with those who received enalapril alone. They
also had a significantly slower rate of decline in estimated glomerular filtration rate (eGFR):
1.28% vs 1.42% per year. Among individuals with CKD at baseline, folic acid therapy was
associated with a significant 56% reduction in the odds of CKD progression, a significant 33%
reduction in the odds of a rapid decline in renal function (defined as an average decline in eGFR
of 5 mL/min/1.73 m2 or more per year), and a significant 44% slower decline in renal function
(0.96% vs 1.72% per year). Dr Hou and colleagues observed no significant between-group
differences among participants without CKD at baseline.

Given the magnitude of renal protection suggested by this study as well as the safety and the
low cost, the potential role of folic acid therapy in the clinical management of patients with CKD
in regions without folic acid fortification should be vigorously examined, Dr Hou's team
concluded.

The study included 15,104 hypertensive without a history of major cardiovascular disease who
were randomly assigned to daily treatment with either 10 mg enalapril plus 0.8 mg folic acid
(7545 participants) or 10 mg enalapril alone (7559 participants). The study population had a
median follow-up of 4.5 years. Of the 15,104 participants, 1671 had CKD at baseline and 13,433
did not. The researchers defined CKD as an eGFR less than 60 mL/min/1.73 m 2 and/or
proteinuria at baseline.

Dr Hou and colleagues defined CKD progression as a decrease in eGFR of 30% or more and to a
level below 60 mL/min/1.73 m2 if the baseline eGFR was 60 mL/min/1.73 m2, or a decrease in
eGFR of 50% of more if the baseline eGFR was less than 60 mL/min/1.73 m2; or the
development of end-stage renal disease.

In an editorial accompanying the new report, Patrick J. Stover, PhD, of the Division of
Nutritional Sciences at Cornell University in Ithaca, New York, and colleagues noted that the
study showed that enalapril interacts with folate in human physiology. They pointed out that
enalapril treatment alone in the absence of supplemental folic acid increased serum folate by 5.1
ng/mL. While the mechanisms for this interaction are unknown and should be explored, this
drug-nutrient interaction may underlie the secondary prevention of renal function decline
observed in this study, they wrote

http://www.renalandurologynews.com/chronic-kidney-disease-ckd/ckd-progression-delay-observed-
with-folic-acid-therapy/article/517779/