Professional Documents
Culture Documents
Author Manuscript
J Ren Nutr. Author manuscript; available in PMC 2015 May 01.
Published in final edited form as:
NIH-PA Author Manuscript
Abstract
Objective—This study examined rates and determinants of vitamin D supplementation among
Chronic Renal Insufficiency Cohort (CRIC) participants and determined the association between
dose and 25-hydroxyvitamin D (25(OH)D) level. The 2010 Institute of Medicine Report noted a
significant increase in vitamin D supplementation in the general population, but use in chronic
kidney disease (CKD) is unknown.
minute per 1.73 m2. Of the cohort, 54.9% was male, 42.1% were Black, and 48.4% were diabetic.
Multivariable logistic generalized estimating equations were used to examine determinants of
supplementation use assessed annually between 2003 and 2011. Cross-sectional linear regression
NIH-PA Author Manuscript
models, based on a subset of 1,155 participants, assessed associations between supplement dose
and 25(OH)D level, measured by high-performance liquid chromatography coupled with tandem
mass spectrometry.
Results—The proportion of participants reporting supplement use increased (P < .0001), from
10% at baseline to 44% at 7-year follow-up visits. This was largely due to initiation of products
containing only ergocalciferol or cholecalciferol. The odds of supplementation were greater in
older, female, non-Black, married participants with greater education and lower body mass index.
Among participants taking supplementation, dose was positively associated with 25(OH)D level,
adjusted for race, season, diabetes, dietary intake, eGFR, and proteinuria. Only 3.8% of non-Black
and 16.5% of Black participants taking a supplement were deficient (<20 ng/mL), whereas 22.7%
of non-Black and 62.4% of Black participants not reporting supplement use were deficient.
Introduction
In recent years, the potential role of 25-hydroxyvitamin D (25(OH)D) deficiency in a wide
range of diseases has been increasingly recognized and widely publicized. These include
cardiovascular disease, malignancy, insulin resistance, diabetes, autoimmune disease,
infection, impaired physical function, fractures, and mortality.1 As a result of the increased
awareness of the potential importance of vitamin D status, the number of clinical assays of
25(OH)D levels and the use of calciferol supplementation has increased dramatically in the
general population, as reported in the 2010 Institute of Medicine (IOM) Report on Dietary
Reference Intakes for Calcium and Vitamin D.2 A recent population-based Canadian study
also reported secular increases in vitamin D supplementation use and 25(OH)D levels over
10 years.3 Trends of supplementation use among patients with chronic kidney disease
(CKD) are unknown.
NIH-PA Author Manuscript
25(OH)D deficiency is common in CKD, especially non-Caucasian patients4 and those with
advanced disease.5 Recent studies in CKD linked 25(OH)D deficiency with
hyperparathyroidism, insulin resistance, anemia, inflammation, CKD progression, and
mortality.5-13 CKD is associated with a heavy burden of cardiovascular, metabolic, and
infectious complications, and 25(OH)D deficiency may be an important modifiable risk
factor. The 2003 Kidney Disease Outcomes Quality Initiative guidelines recommended
supplementation for CKD Stages 3 to 4 with hyperparathyroidism and a 25(OH)D level less
than 30 ng/mL.14 The 2009 Kidney Disease Improving Global Outcomes guidelines
recommended more expanded testing for all patients with CKD Stages 3 to 5 and treatment
strategies as in the general population without establishing a target level.15 Studies in the
general population suggest that large doses (>2,000 IU/day) are required to correct and
maintain adequate 25(OH)D levels.16,17 Compared with the general population, CKD
patients have additional risk factors for 25(OH)D deficiency, including urinary losses of
vitamin D-binding protein and albumin, decreased 25(OH)D production by uremic skin in
response to ultraviolet B ray exposure,18 and decreased dairy intake due to phosphate
NIH-PA Author Manuscript
restriction.
The objectives of this study were 2-fold. First, we examined vitamin D supplementation use
at annual visits among all Chronic Renal Insufficiency Cohort (CRIC) study participants to
identify determinants and trends of supplementation use. Second, we examined the cross-
sectional relationship between calciferol dose and serum 25(OH)D levels in a subset of
CRIC participants who completed a detailed assessment of vitamin D dose at a single visit.
Methods
Study Population
The CRIC study is a multicenter prospective observational study established by the National
Institute of Diabetes and Digestive and Kidney Diseases to examine risk factors for CKD
progression and cardiovascular disease.19 A total of 3,939 ethnically and racially diverse
participants, aged 21 to 74 years, with mild to moderate CKD were recruited from 2003 to
NIH-PA Author Manuscript
2008 on the basis of age-specific estimated glomerular filtration rate (eGFR; 20-70 mL/
minute per 1.73 m2) at 7 clinical sites.20 The protocol was approved by the institutional
review board at each site. Participants provided informed consent.19-21
Data Collection
Detailed information regarding demographics, medical history, quality of life, health
behaviors, and physical activity were collected by research coordinator interview and
questionnaire at the baseline visit, as previously described.19
Blood and urine specimens were collected annually, and eGFR (mL/minute per 1.73 m2)
was calculated using the Modification of Diet in Renal Disease formula on the basis of
serum creatinine.22 Proteinuria was assessed by 24-hour urine collection.
Dietary information was collected at baseline and every other year using the National
Cancer Institute's Dietary History Questionnaire (DHQ). This validated instrument assesses
food frequency and amount in the past year to compute average daily nutrient intake,
NIH-PA Author Manuscript
including vitamin D.23 The DHQ assesses usual dietary intake of 124 food items on the
basis of national dietary intake data from the 1994 to 1996 U.S. Department of Agriculture's
Continuing Survey of Food Intake in Individuals. After being manually reviewed for
completeness, DHQs were analyzed using the National Cancer Institute's DietCalc software.
Approximately 10% of DHQs were excluded because unlikely values were reported for total
energy intake (i.e., <600 or >4,000 kcal for women and <800 or >5,000 kcal for men).
Medication use was assessed at each annual visit by research coordinator interview and
completion of the Concomitant Medication (CMED) form. Participants were asked to bring
a list of their medications and supplements taken in the prior 30 days. Name, dose, units, and
frequency were recorded and matched to drug codes from the Medication Reference Tool in
the data management system. A total of 72 drug codes identified a medication or supplement
A subset of the full CRIC cohort at 4 selected clinical centers completed a single visit
between 2008 and 2010 at the time of physical function testing in which augmented
procedures were used to obtain detailed vitamin D intake. Research coordinators at these
sites were trained to elicit a detailed vitamin D supplementation history using the Vitamin D
Concomitant Medication (DCMED) form, in addition to the CMED form, at this visit.
Participants were asked to bring medication and supplement bottles to record formulation,
frequency, route, and calciferol content of all calciferol-containing medications used in the
prior 3 months.
In the subset that completed this DCMED form, stored serum specimens from the same visit
were used to measure 25(OH)D levels by high-performance liquid chromatography coupled
with tandem mass spectrometry. This assay gave a linear response from 1.3 to 135 ng/mL
for 25(OH)D2 and 25(OH)D3 and the limit of quantitation (signal-to-noise ratio ≥ 10) was
NIH-PA Author Manuscript
1.3 ng/mL. The interassay coefficients of variation were 7.3% to 10.0% and 4.2% to 4.9%
for 25(OH)D2 and 25(OH)D3, respectively. The specimens were collected and run at the end
of the study; thus, they were not available to the participants or research team at each site.
Statistical Analysis
Descriptive statistics, including mean and standard deviation for normally distributed
variables, median and inter-quartile range (IQR) for skewed variables, and proportions for
categorical variables, were used to characterize baseline participant characteristics and
supplementation use at each visit.
Two primary analyses were conducted. First, in the full cohort of participants, a
multivariable logistic generalized estimating equation model was fit to identify determinants
of supplementation use. Study visits after transplantation or initiation of dialysis were
excluded. Because of concern for greater ascertainment of calciferol supplementation among
participants at clinical centers using the DCMED form, we compared supplementation use
before and after research coordinators from these sites were trained to use the DCMED form
NIH-PA Author Manuscript
and to clinical centers using the CMED form. Using a piecewise logistic regression analysis,
we found that neither the log odds of supplementation (P = .829) nor the rate of change in
supplementation (P = .727) at DCMED centers increased more immediately after DCMED
training than at CMED centers. Therefore, study visits after training were included, and
sensitivity analyses excluding these visits did not alter results.
The second primary analysis was performed in the subset of the cohort that had both dose
information and levels available. Spearman's rank correlation coefficient (ρ) was used to
separately assess the relationship between supplementation dose and 25(OH)D level for
NIH-PA Author Manuscript
Black and non-Black participants. Linear regression was used to examine the association
between 25(OH)D level and calciferol supplementation dose, adjusted for determinants of
25(OH)D level, including age, sex, race, ethnicity, physical activity (a surrogate for sun
exposure), BMI, diabetes, proteinuria, socioeconomic status, dietary vitamin D, and eGFR.
Because 25(OH)D level was logarithmically transformed for anal ysis, results were
presented as the percentage difference in predicted level compared with the reference
category. The exponentiated regression coefficient for a particular covariate represents the
ratio of 25(OH)D level for that category relative to the reference category. Analyses were
performed using Stata, version 11.2 (College Station, TX), with 2-sided tests of hypotheses
and a P value less than .05 as the criterion for statistical significance.
Results
Trends in Vitamin D Supplementation Use Among All CRIC Participants
The baseline characteristics of the 3,939 CRIC participants are summarized in Table 1. The
NIH-PA Author Manuscript
median duration of follow-up was 5 (IQR 3-6) years with a total of 20,983 visits. Among all
participants, rates of reported use of any product containing a calciferol increased
dramatically according to calendar and study year (Fig. 1). Use increased with longer
participation in CRIC, from 10% at the baseline visits to 44% at the 7-year visits. Similar
trends were observed in analyses limited to the 708 participants with 7 years of follow-up.
Supplementation increased with later calendar year, from 10% at visits in 2003 to 43% at
visits in 2011. The increase was primarily driven by use of products containing
ergocalciferol or cholecalciferol alone, whereas use of products containing calcium and
calciferol increased less markedly (Fig. 2). Use of active vitamin D sterols remained stable
at 2% to 3% over this same time period. The predominant formulation of calciferol switched
from ergocalciferol (69.3% of supplements in 2003) to cholecalciferol (77.2% of
supplements in 2010).
ergocalciferol or cholecalciferol in the preceding 3 months. Many were taking more than 1
vitamin D product. Among participants who reported supplementation, the median dose was
500 (IQR 400-1000) IU/day.
NIH-PA Author Manuscript
There was a significant dose response relationship between supplementation use and
25(OH)D level adjusted for race, season, diabetes, dietary vitamin D, proteinuria, and eGFR.
The results of the linear regression model are presented in Table 4. The effect of
supplementation (>400 IU/day) was greater than any other predictors in the model. There
was a significant interaction between Black race and supplementation use as indicated by the
relatively greater increase in level for each vitamin D dose among the Black participants. In
contrast, there was no interaction between CKD stage or supplement type (calcium-
containing vs. vitamin D alone) and supplementation dose in its association with 25(OH)D
level. Physical activity, BMI, cause of CKD, sex, age, and smoking status were not
independent predictors of 25(OH)D level.
When total daily dose of calciferol was separated by formulation in this model, 1,000 IU of
cholecalciferol was associated with a 29.0% higher 25(OH)D level as compared with no
supplementation (P < .001); 1,000 IU of ergocalciferol was associated with a 14.7% higher
25(OH)D level as compared with no supplementation (P = .008), consistent with a lower
potency.
NIH-PA Author Manuscript
When models were fit for 25(OH)D2 and 25(OH)D3 levels separately, greater daily
cholecalciferol (D3) dose was associated with greater 25(OH)D3 levels (P < .001) whereas
greater daily ergocalciferol (D2) dose was associated with greater 25(OH)D2 levels (P < .
001).
Discussion
Reported use of calciferol supplements increased markedly in the CRIC cohort over time,
primarily because of increased use of single-nutrient products containing ergo-calciferol or
cholecalciferol. Supplementation was associated with markedly greater vitamin D levels,
especially among Black participants. To our knowledge, this is the first study to examine
There was a wide range of daily vitamin D dosage. The 2010 IOM report recommended 600
IU/day for people younger than 70 years of age and 800 IU/day for people older than 70
years of age with a maximum tolerated dose of 4,000 IU/day.2 Among CRIC participants
taking a supplement, the median dose was 500 IU per day, and 1% of participants were
taking 4,000 IU/day or more. Median dietary vitamin D intake was 112 IU/day and did not
differ among those participants who were or were not taking a supplement. This is much
NIH-PA Author Manuscript
lower than the median intake reported in the IOM report for the general population, which
ranges from 272 to 396 IU/day depending on life stage and may be related to phosphorus
restriction with consequent reductions in dairy intake.
One could hypothesize that there would be minimal association between supplement dose
and level in a cross-sectional analysis because patients would be a combination of those
prescribed vitamin D because of severe deficiency with those who were taking a supplement
regardless of level. However, our analysis reveals that supplement use was associated with
significantly higher vitamin D levels, with a dose-response relationship, and had a stronger
association than any other factor in the model. A recent study reported that supplementation
use was an important predictor of vitamin D levels in a healthy, northern European
population26; however, this had not been previously assessed in patients with CKD.
Furthermore, this is the first study to examine racial differences in the relationship between
vitamin D supplementation and levels. Longitudinal measures of vitamin D levels were not
available to assess the response to supplementation or baseline levels. However, it was
surprising to note that even modest doses of supplementation were associated with higher
NIH-PA Author Manuscript
levels.
Two large previous reports have demonstrated mixed results regarding the relationship
between 25(OH)D levels and eGFR. Chonchol and colleagues analyzed data from the Third
National Health and Nutrition Examination Survey and showed that 25(OH)D levels were
low only among those with advanced CKD (eGFR 15-29 mL/min ute per 1.73 m2) after
adjustment for age, sex, ethnicity, BMI, physical activity, intake of milk and vitamin D
supplements, and season.5 However, in the Study to Evaluate Early Kidney Disease, Levin
and colleagues reported no relationship between 25(OH)D level and eGFR after adjustment
for age, gender, ethnicity, diabetes, urinary albumin, calcium, and phosphorus.27 Our study
obtained detailed information regarding supplement use and dose, which we also
demonstrated to be highly prevalent and an important predictor of level. Although
unadjusted analysis suggested an association of lower 25(OH)D levels with lower eGFR,
this association did not persist after adjusting for supplement use dosage, dietary intake,
season, diabetes, and proteinuria. In fact, lower eGFR was associated with a slightly higher
NIH-PA Author Manuscript
level in our full model. In this cross-sectional analysis, we were not able to assess changes in
eGFR or changes in 25(OH)D level.
Levels and dose information were only available for a subset of CRIC participants at
selected clinical centers that used augmented techniques to collect information on
NIH-PA Author Manuscript
supplementation use. All participants at these clinical centers were eligible to collect these
supplemental data, and 86% did so. These high participation rates make selection bias
unlikely. These study participants were somewhat healthier compared with the remainder of
the CRIC cohort. This likely reflects survival to this later visit (87% of visits were
performed 3-5 years after enrollment) and varying baseline participant characteristics of the
participating clinical sites. Given that the primary goal was to relate supplement dose and
vitamin D level, it is unlikely that these differences introduced a significant bias.
Because detailed vitamin D dose information and 25(OH)D levels were available only at a
single visit, our current data could not assess the longitudinal effect of vitamin D
supplementation and changes in parathyroid hormone or other bone mineral metabolism
laboratory values such as calcium and phosphorus. Future studies will be needed to assess
this relationship as well as the association with clinical outcomes such as fracture.
Practical Application
This study revealed an increasing use of calciferol supplementation among participants in
NIH-PA Author Manuscript
the CRIC study and that supplementation use was associated with greater 25(OH)D levels.
Predictors of supplementation use included socioeconomic factors in addition to expected
demographic factors. Given the recent call for interventional trials using nutritional vitamin
D,2 these results demonstrate the challenges of completing these studies, especially because
these participants are likely representative of other individuals who would be recruited for
future clinical trials; specifically, a large and increasing proportion of CKD patients are
taking vitamin D and that this supplementation use is associated with high levels.
Acknowledgments
Support: This CRIC ancillary study was supported by National Institutes of Health grants R01DK077128 and
K24DK076808 (M.B.L.); cooperative agreement project grants 5U01DK060990, 5U01DK060984, 5U01DK06102,
5U01DK061021, 5U01DK061028, 5U01DK60980, 5U01DK060963, and 5U01DK060902 from the National
Institute of Diabetes and Digestive and Kidney Diseases; and grants UL1RR024134, UL1RR025005,
M01RR16500, UL1RR024989, M01RR000042, UL1RR024986, UL1RR029879, RR05096, and UL1RR024131
from the National Institutes of Health.
NIH-PA Author Manuscript
References
1. Holick MF. Vitamin D deficiency. N Engl J Med. 2007; 357:266–281. [PubMed: 17634462]
2. Ross, AC.; Taylor, CL.; Yaktine, AL.; Del Valle, HB. Dietary Reference Intakes for Calcium and
Vitamin D. Institute of Medicine; Washington, DC: 2010.
3. Berger C, Greene-Finestone LS, Langsetmo L, et al. Temporal trends and determinants of
longitudinal change in 25-hydroxyvitamin D and parathyroid hormone levels. J Bone Miner Res.
2012; 27:1381–1389. [PubMed: 22407786]
4. Melamed ML, Astor B, Michos ED, Hostetter TH, Powe NR, Muntner P. 25-hydroxyvitamin D
levels, race, and the progression of kidney disease. J Am Soc Nephrol. 2009; 20:2631–2639.
[PubMed: 19875805]
5. Chonchol M, Scragg R. 25-Hydroxyvitamin D, insulin resistance, and kidney function in the Third
National Health and Nutrition Examination Survey. Kidney Int. 2007; 71:134–139. [PubMed:
17082756]
6. Stefikova K, Spustova V, Krivosikova Z, et al. Insulin resistance and vitamin D deficiency in
patients with chronic kidney disease stage 2-3. Physiol Res. 2011; 60:149–155. [PubMed:
20945958]
7. Lac PT, Choi K, Liu IA, Meguerditchian S, Rasgon SA, Sim JJ. The effects of changing vitamin D
NIH-PA Author Manuscript
levels on anemia in chronic kidney disease patients: a retrospective cohort review. Clin Nephrol.
2010; 74:25–32. [PubMed: 20557863]
8. Patel NM, Gutierrez OM, Andress DL, Coyne DW, Levin A, Wolf M. Vitamin D deficiency and
anemia in early chronic kidney disease. Kidney Int. 2010; 77:715–720. [PubMed: 20130525]
9. Isakova T, Gutierrez OM, Patel NM, Andress DL, Wolf M, Levin A. Vitamin D deficiency,
inflammation, and albuminuria in chronic kidney disease: complex interactions. J Ren Nutr. 2011;
21:295–302. [PubMed: 20817560]
10. Stubbs JR, Idiculla A, Slusser J, Menard R, Quarles LD. Cholecalciferol supplementation alters
calcitriol-responsive monocyte proteins and decreases inflammatory cytokines in ESRD. J Am Soc
Nephrol. 2010; 21:353–361. [PubMed: 20007751]
11. Barreto DV, Barreto FC, Liabeuf S, et al. Vitamin D affects survival independently of vascular
calcification in chronic kidney disease. Clin J Am Soc Nephrol. 2009; 4:1128–1135. [PubMed:
19443628]
12. Ravani P, Malberti F, Tripepi G, et al. Vitamin D levels and patient outcome in chronic kidney
disease. Kidney Int. 2009; 75:88–95. [PubMed: 18843258]
13. Jean G, Lataillade D, Genet L, et al. Impact of hypovitaminosis D and alfacalcidol therapy on
survival of hemodialysis patients: results from the French ARNOS study. Nephron Clin Pract.
2011; 118:c204–c210. [PubMed: 21178377]
NIH-PA Author Manuscript
14. K/DOQI Clinical Practice Guidelines for bone metabolism and disease in chronic kidney disease.
Am J Kidney Dis. 2003; 42(4 Suppl 3):S1–S201. [PubMed: 14520607]
15. KDIGO Clinical Practice Guideline for the diagnosis, evaluation, prevention, and treatment of
Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Kidney Int Suppl. 2009:S1–
S130.
16. Barger-Lux MJ, Heaney RP, Dowell S, Chen TC, Holick MF. Vitamin D and its major
metabolites: serum levels after graded oral dosing in healthy men. Osteoporos Int. 1998; 8:222–
230. [PubMed: 9797906]
17. Heaney RP. Vitamin D in health and disease. Clin J Am Soc Nephrol. 2008; 3:1535–1541.
[PubMed: 18525006]
18. Jacob AI, Sallman A, Santiz Z, Hollis BW. Defective photoproduction of cholecalciferol in normal
and uremic humans. J Nutr. 1984; 114:1313–1319. [PubMed: 6330321]
19. Feldman HI, Appel LJ, Chertow GM, et al. The Chronic Renal Insufficiency Cohort (CRIC) study:
design and methods. J Am Soc Nephrol. 2003; 14(7 Suppl 2):S148–S153. [PubMed: 12819321]
20. Lash JP, Go AS, Appel LJ, et al. Chronic Renal Insufficiency Cohort (CRIC) study: baseline
characteristics and associations with kidney function. Clin J Am Soc Nephrol. 2009; 4:1302–1311.
[PubMed: 19541818]
NIH-PA Author Manuscript
21. Fischer MJ, Go AS, Lora CM, et al. CKD in Hispanics: baseline characteristics from the CRIC
(Chronic Renal Insufficiency Cohort) and Hispanic-CRIC studies. Am J Kidney Dis. 2011;
58:214–227. [PubMed: 21705121]
22. Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D. A more accurate method to estimate
glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in
Renal Disease Study Group. Ann Intern Med. 1999; 130:461–470. [PubMed: 10075613]
23. Subar AF, Thompson FE, Kipnis V, et al. Comparative validation of the Block, Willett, and
National Cancer Institute food frequency questionnaires: the Eating at America’s Table Study. Am
J Epidemiol. 2001; 154:1089–1099. [PubMed: 11744511]
24. Heaney RP. Vitamin D—baseline status and effective dose. N Engl J Med. 2012; 367:77–78.
[PubMed: 22762324]
25. Bischoff-Ferrari HA, Willett WC, Orav EJ, et al. A pooled analysis of vitamin D dose
requirements for fracture prevention. N Engl J Med. 2012; 367:40–49. [PubMed: 22762317]
26. Zgaga L, Theodoratou E, Farrington SM, et al. Diet, environmental factors, and lifestyle underlie
the high prevalence of vitamin D deficiency in healthy adults in Scotland, and supplementation
reduces the proportion that are severely deficient. J Nutr. 2011; 141:1535–1542. [PubMed:
21697298]
27. Levin A, Bakris GL, Molitch M, et al. Prevalence of abnormal serum vitamin D, PTH, calcium,
NIH-PA Author Manuscript
and phosphorus in patients with chronic kidney disease: results of the study to evaluate early
kidney disease. Kidney Int. 2007; 71:31–38. [PubMed: 17091124]
NIH-PA Author Manuscript
Figure 1.
Trends in calciferol supplementation use in the CRIC study over time. Patients reporting a
calciferol-containing supplement on the CMED at 19,503 annual visits of the full cohort of
CRIC participants from 2003 to 2011. CMED, Concomitant Medication form; CRIC,
Chronic Renal Insufficiency Cohort.
NIH-PA Author Manuscript
Figure 2.
Trends in type of calciferol supplementation use. Patients reporting a calciferol-containing
NIH-PA Author Manuscript
supplement on the CMED at 19,503 annual visits of the full cohort of CRIC participants
from 2003 to 2011. CMED, Concomitant Medication form; CRIC, Chronic Renal
Insufficiency Cohort.
NIH-PA Author Manuscript
Figure 3.
Vitamin D level by reported daily supplement dosage for Black and non-Black participants.
NIH-PA Author Manuscript
Data from 1,155 participants who completed a single study visit to obtain detailed vitamin D
intake history at the time of physical function testing, collected using the DCMED. Dashed
reference line at 20 ng/mL, below which is considered deficient. Spearman test for trend
with P < .001 for Black and non-Black participants. DCMED, Vitamin D Concomitant
Medication form.
NIH-PA Author Manuscript
Table 1
Table 2
Results of Multivariable Logistic Generalized Estimating Equation Model of Calciferol Supplementation Use
NIH-PA Author Manuscript
BMI, body mass index; CI, confidence interval; OR, odds ratio.
Data from full cohort (N = 3,531) with a total of 19,019 annual visits and adjusted for clinical site.
NIH-PA Author Manuscript
Table 3
BMI, body mass index; DCMED, Vitamin D Concomitant Medication form; eGFR, estimated glomerular filtration rate; 25(OH)D, 25-
hydroxyvitamin D.
All characteristics were recorded at the participants’ vitamin D study visit (2008-2010) when augmented procedures and DCMED form were used
to assess supplementation use. Continuous variables are presented as median (interquartile range). Categorical variables are presented as
percentages.
NIH-PA Author Manuscript
NIH-PA Author Manuscript
Table 4
Determinant Relative Percent Change Compared With Reference Group (95% CI)
Vitamin D supplement (IU/d) Non-Black Black
0 Reference Reference
>0-400 26.5% (16.9, 36.9)* 60.8% (43.8, 79.9)*
>400-800 46.4% (32.3, 62.0)* 125.8% (92.2, 165.2)*
>800 61.0% (47.6, 75.7)* 127.1% (96.9, 161.9)*
Season
Summer Reference
Winter –11.1% (–15.8, –6.1)
Marital status
Not married Reference
Married 7.9% (2.1, 14.0)†
Dietary vitamin D (IU/d)
<200 Reference
NIH-PA Author Manuscript
CI, confidence interval; eGFR, estimated glomerular filtration rate; 25(OH)D, 25-hydroxyvitamin D.
Data from subset cohort that completed a single vitamin D study visit, and augmented procedures were used to assess vitamin D supplement use (n
= 1,155).
*
P ≤ .001.
†
P < .05.