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Clinical Journal of the American Society of Nephrology : CJASN logoLink to Clinical Journal of the American Society of Nephrology : CJASN
. 2011 Sep;6(9):2121–2131. doi: 10.2215/CJN.11341210

Cardiovascular Disease Among Hispanics and Non-Hispanics in the Chronic Renal Insufficiency Cohort (CRIC) Study

Ana C Ricardo *, James P Lash *,✉, Michael J Fischer *,†, Claudia M Lora *, Matthew Budoff ‡, Martin G Keane §, John W Kusek ‖, Monica Martinez *, Lisa Nessel , Thomas Stamos *, Akinlolu Ojo **, Mahboob Rahman ††, Elsayed Z Soliman ‡‡, Wei Yang , Harold I Feldman §,, Alan S Go, on behalf of the CRIC and HCRIC Investigators§§
PMCID: PMC3359008  PMID: 21896829

Abstract

Summary

Background and objectives

Hispanics are the largest minority group in the United States. The leading cause of death in patients with chronic kidney disease (CKD) is cardiovascular disease (CVD), yet little is known about its prevalence among Hispanics with CKD.

Design, setting, participants, & measurements

We conducted cross-sectional analyses of prevalent self-reported clinical and subclinical measures of CVD among 497 Hispanics, 1638 non-Hispanic Caucasians, and 1650 non-Hispanic African Americans, aged 21 to 74 years, with mild-to-moderate CKD at enrollment in the Chronic Renal Insufficiency Cohort (CRIC) and Hispanic CRIC (HCRIC) studies. Measures of subclinical CVD included left ventricular hypertrophy (LVH), coronary artery calcification (CAC), and ankle-brachial index.

Results

Self-reported coronary heart disease (CHD) was lower in Hispanics compared with non-Hispanic Caucasians (18% versus 23%, P = 0.02). Compared with non-Hispanic Caucasians, Hispanics had a lower prevalence of CAC >100 (41% versus 34%, P = 0.03) and CAC >400 (26% versus 19%, P = 0.02). However, after adjusting for sociodemographic factors, these differences were no longer significant. In adjusted analyses, Hispanics had a higher odds of LVH compared with non-Hispanic Caucasians (odds ratio 1.97, 95% confidence interval, 1.22 to 3.17, P = 0.005), and a higher odds of CAC >400 compared with non-Hispanic African Americans (odds ratio, 2.49, 95% confidence interval, 1.11 to 5.58, P = 0.03). Hispanic ethnicity was not independently associated with any other CVD measures.

Conclusions

Prevalent LVH was more common among Hispanics than non-Hispanic Caucasians, and elevated CAC score was more common among Hispanics than non-Hispanic African Americans. Understanding reasons for these racial/ethnic differences and their association with long-term clinical outcomes is needed.

Introduction

Hispanics are the largest and fastest growing minority group in the United States (1). Both the incidence and prevalence rates of end-stage renal disease (ESRD) in Hispanics are 1.5 times higher than in non-Hispanics (2). Although it is well established that chronic kidney disease (CKD) is an independent risk factor for cardiovascular disease (CVD) and all-cause mortality (3–5), limited data exist regarding the association of CVD and CKD in Hispanics. This is an area of interest because, in the general population, Hispanics appear to have a survival advantage compared with non-Hispanic Caucasians, despite a higher prevalence of cardiovascular risk factors (6). This observation is referred to as the “Hispanic paradox” and has been inconsistently found in CKD patients. In a large group of individuals with stage 3 or 4 CKD enrolled in Kaiser Permanente of Northern California, Hispanic ethnicity was associated with a lower risk of cardiovascular events and death relative to non-Hispanic Caucasians despite experiencing a higher risk of ESRD (7). In contrast, a study of a nationally representative sample of the U.S. population, the third National Health and Nutrition Examination Survey (NHANES III), demonstrated a nonsignificant trend toward higher mortality in Mexican Americans with CKD than non-Hispanic Caucasians (8). These heterogeneous findings may be due to differences in the populations studied and methodology but underscore the need for further investigation.

We characterize the prevalence of self-reported clinical CVD and measures of subclinical CVD among Hispanics compared with non-Hispanic Caucasians and African Americans enrolled in two prospective observational studies of CKD: the Chronic Renal Insufficiency Cohort (CRIC) and Hispanic CRIC (HCRIC) Studies.

Materials and Methods

Study Design and Participants

We conducted cross-sectional analyses among Hispanic and non-Hispanic participants at enrollment in the CRIC and HCRIC studies. The design, methods, and baseline characteristics of the CRIC study participants have been previously published (9,10). Briefly, the CRIC study is a prospective cohort of 3612 individuals (169 Hispanics and 3443 non-Hispanics), aged 21 to 74 years, with mild-to-moderate CKD, recruited between May 2003 and March 2007 from seven clinical centers across the United States. HCRIC is a parallel study to the CRIC study that recruited 327 Hispanics from the Chicago area from October 2005 through June 2008, using the same inclusion criteria. Among all Hispanic participants, 69% were Mexican American, 16% were Puerto Rican, and 15% had other Latin American ancestry. We decided to combine all Hispanic participants in our analyses because no significant differences were found in the outcomes of interest between Hispanic subgroups. Protocols for both studies were approved by the Institutional Review Board of the participating centers and are in accordance with the principles of the Declaration of Helsinki. Informed consent was obtained from all participants.

Variables and Measurements

Sociodemographic characteristics, and medications were self-reported at entry. Hypertension was defined as systolic BP ≥140 mmHg, diastolic BP ≥90 mmHg, or use of antihypertensive medications. Diabetes was defined as fasting glucose ≥126 mg/dl, random glucose ≥200 mg/dl, or use of insulin or antidiabetic medication. Dyslipidemia was defined as fasting total cholesterol ≥240 mg/dl, low-density lipoprotein (LDL) ≥160 mg/dl, high-density lipoprotein (HDL) ≥40 mg/dl, triglycerides ≥200 mg/dl, or use of lipid-lowering medication. Family history of premature coronary heart disease (CHD) was defined as CHD in male first-degree relative <55 years, or CHD in female first-degree relative <65 years. History of CVD, including heart failure, peripheral arterial disease (PAD), stroke or CHD (defined as history of myocardial infarction [MI] or prior revascularization), was self-reported on a medical history questionnaire in the participant's language of preference (English or Spanish). Subclinical CVD measures included left ventricular hypertrophy (LVH), coronary artery calcification score (CAC), and ankle-brachial index (ABI). LVH was defined as left ventricular mass index (g/m2.7) by transthoracic echocardiography (TTE) >50 in males and >47 in females. CAC was measured in a subcohort of the CRIC study using electron-beam computed tomography (EBCT) or multi-detector computer tomography. The CRIC subcohort was selected as a stratified, weighted random sample of approximately one third of all participants, based on the anticipated distribution within the full cohort. Subcohort participants were assigned to undergo additional, more intensive testing (including iothalamate clearance studies to measure GFR and EBCT). We considered two cut off points for CAC (>100 and >400) as consistent with subclinical CVD. TTE and CAC measurements were performed at the 1-year follow-up visit in the CRIC study. In HCRIC, all participants underwent TTE and CAC measurement at entry. GFR was estimated using the four-variable Modification of Diet in Renal Disease (MDRD) equation (11). Previous MI on electrocardiogram (ECG) was defined as the presence of Major 2 or 3 Minnesota code criteria (12).

Statistical Analysis

Descriptive statistics were summarized as mean (SD) for continuous variables and frequency (proportion) for categorical variables. If the data distributions were skewed, natural logarithmic transformations were conducted and/or data were presented as median (interquartile intervals). Crude and adjusted (for age, gender, education, and estimated GFR [eGFR]) means for CVD risk factors were compared between racial/ethnic groups using ANOVA and t tests, as appropriate. Prevalence of self-reported clinical and subclinical measures of CVD was compared using chi-squared tests. To determine factors independently associated with clinical and subclinical measures of CVD, we fitted multivariate hierarchical logistic regression models that included (1) crude (unadjusted) measures, (2) demographic measures, and (3) clinical measures (see Table 4). These variables were chosen based on bivariate analyses and prior studies (5,13–18). The only variables with >3% missing values were proteinuria/24 h (6%), income (15%), and health insurance (12%); the latter two were not included in the regression models. To compare Hispanics with non-Hispanic groups, each model was run twice, once with non-Hispanic Caucasians as reference and once with non-Hispanic African Americans as reference. All hypothesis tests were two-sided with alpha level = 0.05. Among 3939 subjects enrolled in CRIC/HCRIC, 154 self-identified as member of “other” race/ethnicity were excluded from the analyses. We adopted a complete case analysis approach for all analyses (19); therefore, the final analytic cohorts varied among the different analyses presented: (1) 353 participants were excluded from the multivariate analysis of self-reported CVD due to missing data for one of the covariates, (2) 1857 participants were excluded from CAC analyses because they did not undergo CAC measurement as specified by study design (9), (3) 911 participants were excluded from LVH analyses due to missing data for the outcome (689) or covariates (222), and (4) 398 participants were excluded from ABI analyses because of missing data for this outcome (61) or covariates (337). All statistical analyses were conducted using SAS version 9.1 (SAS Institute, Cary, NC).

Table 4.

Crude and adjusted odds ratio (OR) of clinical and subclinical measures of cardiovascular disease (CVD)

Variables Any self-reported CVD
 CAC >100
 CAC >400
 LVH
 ABI <0.9
OR (95% CI) P value OR (95% CI) P value OR (95% CI) P value OR (95% CI) P value OR (95% CI) P value
Unadjusted
    Hispanic versus NH Caucasian 0.86 (0.69, 1.07) 0.18 0.75 (0.58, 0.97) 0.03 0.69 (0.51, 0.94) 0.02 3.64 (2.86, 4.63) <0.01 1.19 (0.89, 1.60) 0.23
    Hispanic versus NH African American 0.63 (0.50, 0.78) <0.01 0.98 (0.74, 1.29) 0.88 1.11 (0.80, 1.55) 0.52 1.44 (1.13, 1.83) <0.01 0.68 (0.52, 0.90) <0.01
Adjusted for demographic characteristicsa
    Hispanic versus NH Caucasian 1.10 (0.75, 1.62) 0.63 0.89 (0.47, 1.69) 0.73 1.12 (0.56, 2.24) 0.74 2.16 (1.42, 3.27) <0.01 1.26 (0.79, 2.03) 0.33
    Hispanic versus NH African American 0.88 (0.61, 1.28) 0.51 1.45 (0.77, 2.74) 0.25 2.34 (1.17, 4.68) 0.02 1.08 (0.71, 1.62) 0.72 0.88 (0.56, 1.39) 0.60
Adjusted for demographic and clinical characteristicsb
    Hispanic versus NH Caucasian 1.03 (0.68, 1.55) 0.90 0.63 (0.30, 1.33) 0.23 0.86 (0.39, 1.93) 0.72 1.97 (1.22, 3.17) <0.01 1.29 (0.78, 2.13) 0.32
    Hispanic versus NH African American 0.82 (0.55, 1.23) 0.34 1.35 (0.64, 2.82) 0.43 2.49 (1.11, 5.58) 0.03 1.44 (0.90, 2.31) 0.13 1.05 (0.65, 1.70) 0.84
    Age 1.06 (1.05, 1.07) <0.01 1.10 (1.08, 1.11) <0.01 1.09 (1.07, 1.11) <0.01 1.03 (1.02, 1.04) <0.01 1.05 (1.04, 1.07) <0.01
    Gender (female versus male) 0.66 (0.54, 0.79) <0.01 0.32 (0.24, 0.42) <0.01 0.36 (0.26, 0.50) <0.01 0.86 (0.70, 1.06) 0.15 1.03 (0.81, 1.29) 0.83
Education
    <7th grade versus college graduate 1.20 (0.75, 1.91) 0.45 0.72 (0.37, 1.40) 0.30 0.83 (0.39, 1.73) 0.61 2.50 (1.37, 4.53) <0.01 1.12 (0.63, 1.99) 0.70
    7th to 12th grade versus college graduate 1.23 (0.94, 1.60) 0.13 1.18 (0.75, 1.84) 0.50 1.47 (0.90, 2.40) 0.13 1.70 (1.24, 2.33) <0.01 1.49 (1.07, 2.08) 0.02
    HS diploma versus college graduate 1.29 (1.01, 1.64) 0.04 1.37 (0.94, 1.98) 0.10 1.58 (1.05, 2.38) 0.03 1.44 (1.10, 1.88) <0.01 1.54 (1.13, 2.09) <0.01
    Some college versus college graduate 1.38 (1.12, 1.71) <0.01 1.18 (0.86, 1.62) 0.30 1.05 (0.73, 1.50) 0.80 1.35 (1.07, 1.70) 0.01 1.34 (1.00, 1.78) 0.05
eGFR (10 ml/min/1.73 m2 increase) 0.90 (0.84, 0.97) <0.01 0.89 (0.79, 1.00) 0.05 0.95 (0.82, 1.09) 0.45 0.86 (0.79, 0.93) 0.02 0.78 (0.71, 0.86) <0.01
Proteinuria (natural log) 1.08 (1.01, 1.15) 0.02 1.03 (0.93, 1.13) 0.58 1.06 (0.95, 1.18) 0.28 1.17 (1.09, 1.26) <0.01 0.95 (0.88, 1.02) 0.17
Diabetes (yes versus no) 1.63 (1.37, 1.95) <0.01 2.67 (2.02, 3.51) <0.01 2.08 (1.52, 2.83) <0.01 1.03 (0.84, 1.25) 0.81 1.76 (1.40, 2.21) <0.01
Hyperlipidemia (yes versus no) 2.26 (1.76, 2.90) <0.01 1.69 (1.21, 2.37) <0.01 1.93 (1.25, 2.97) <0.01 1.09 (0.86, 1.39) 0.48 2.04 (1.46, 2.84) <0.01
BMI 1.01 (1.00, 1.02) 0.29 1.01 (0.99, 1.03) 0.47 1.00 (0.98, 1.02) 0.95 1.15 (1.13, 1.17) <0.01 1.00 (0.99, 1.02) 0.77
Systolic BP (10-mmHg increase) 1.01 (0.97, 1.05) 0.80 1.07 (1.00, 1.14) 0.05 1.05 (0.97, 1.12) 0.23 1.21 (1.15, 1.28) <0.01 1.06 (1.01, 1.12) 0.02
Current smoker (yes versus no) 1.33 (1.06, 1.69) 0.02 1.56 (1.03, 2.35) 0.03 1.43 (0.90, 2.28) 0.13 1.43 (1.09, 1.89) 0.01 2.19 (1.67, 2.88) <0.01
Family history of premature CHD 1.80 (1.46, 2.20) <0.01 1.84 (1.33, 2.56) <0.01 1.91 (1.34, 2.73) <0.01 1.27 (0.99, 1.62) 0.06 1.16 (0.90,1.51) 0.25
Serum hemoglobin 0.96 (0.91, 1.01) 0.14 0.91 (0.83, 0.99) 0.03 0.87 (0.79, 0.95) <0.01 0.87 (0.82, 0.93) <0.01 0.97 (0.91, 1.04) 0.45
hs-CRP (1 SD) 1.03 (0.96, 1.12) 0.40 1.00 (0.85, 1.16) 0.95 0.97 (0.81, 1.16) 0.71 1.00 (0.91, 1.09) 0.92 1.12 (1.03, 1.22) <0.01
Serum phosphate 1.06 (0.93, 1.22) 0.37 1.35 (1.09, 1.66) <0.01 1.41 (1.21, 1.78) <0.01 — — 1.08 (0.91, 1.27) 0.39
Corrected serum calcium 1.03 (0.86, 1.22) 0.79 1.04 (0.79, 1.38) 0.76 0.95 (0.70, 1.31) 0.77 — — 0.93 (0.75, 1.15) 0.51
Total iPTH — — 1.00 (1.00, 1.00) 0.43 1.00 (1.00, 1.00) 0.63 — — — —
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CAC, coronary artery calcium; CVD, cardiovascular disease; LVH, left ventricular hypertrophy; ABI, ankle-brachial index; CI, confidence interval; OR, odds ratio; NH, non-Hispanic; eGFR, estimated glomerular filtration rate; HS, high school; BP, blood pressure; Hs-CRP, high-sensitivity C-reactive protein; SD, standard deviation; iPTH, intact parathyroid hormone; BMI, body mass index.

a

Adjusted for age, gender, education, and clinical site.

b

Additionally adjusted for all variables listed. CVD, CAC, and ABI models were additionally adjusted for serum phosphate and calcium. Intact PTH (iPTH) was only analyzed in the CAC models.

Results

Participant Characteristics and Unadjusted Prevalence of Cardiovascular Risk Factors

Among 3785 CRIC/HCRIC participants in our final analytic cohort (497 Hispanics [H]), 1638 non-Hispanic Caucasians [C], 1650 non-Hispanic African Americans [A]), 93% met criteria for CKD (eGFR <60 ml/min/1.73 m2 or urine albumin-to-creatinine ratio >30 mg/g) (20). Compared with non-Hispanic Caucasians and African Americans, Hispanics were significantly younger (mean age 56 years [H], 59 years [C], 58 years [A]; P < 0.01; Table 1), more likely to have annual income <$20,000 (63% [H], 16% [C], 39% [A]; P < 0.001), <7th grade education (37% [H], 0.4% [C], 1.2% [A]; P < 0.001), and no health insurance (23% [H]), 3% [C]), 6% [A]; P < 0.001). Only 53% of Hispanics reported ever being seen by a nephrologist, compared with 69% of non-Hispanics Caucasians and 67% of non-Hispanic African Americans (P < 0.001). Hispanics were also more likely to have lower mean eGFR in ml/min/1.73 m2 (37.5 [H], 43.7 [C], 43.5 [A]; P < 0.001), and higher median proteinuria in g/24 h (0.7 [H], 0.1 [C], 0.2 [A]; P < 0.001). The following cardiovascular risk factors were significantly more common in Hispanics than non-Hispanic Caucasians and African Americans: diabetes (67% [H], 40% [C], 51% [A]; P < 0.001); mean HDL in mg/dl (43 [H], 47 [C], 49 [A]; P < 0.001); and mean serum phosphate in mg/dl (4.0 [H], 3.6 [C], 3.8 [A]; P < 0.001). Compared with non-Hispanic Caucasians, Hispanics were more likely to have higher systolic BP in mmHG (136 [H] versus 122 [C], P < 0.001); diastolic BP in mmHG (73 [H] versus 69 [C], P < 0.001); hemoglobin A1C (7% [H] versus 6.3% [C], P < 0.001); and lower mean hemoglobin in g/dl (12.1 [H] versus 13.2 [C], P < 0.001). Differences in these cardiovascular risk factors were statistically significant even after adjustment for age, gender, education, and eGFR (data not shown). In contrast, only 6% of Hispanics reported current cigarette smoking, compared with 9% of non-Hispanic Caucasians and 19% of non-Hispanic African Americans (P = 0.01).

Table 1.

Baseline characteristics of participants

Demographic Characteristics Overall (n = 3785) Hispanic (n = 497) Non-Hispanic Caucasian (n = 1638) P1 Non-Hispanic African American (n = 1650) P2
Age, years 58.2 (11) 56.3 (12) 58.9 (11) <0.01 58.1 (11) <0.01
Gender, n (%) <0.01
    Male 2076 (55) 288 (58) 982 (60) 0.43 806 (49)
    Female 1709 (45) 209 (42) 656 (40) 844 (51)
Annual household income, n (%) <0.01 <0.01
    <$20,000 1213 (32) 313 (63) 254 (16) 646 (39)
    $20,001–$50,000 925 (24) 92 (19) 416 (25) 417 (25)
    $50,001–$100,000 694 (18) 24 (5) 455 (28) 215 (13)
    >$100,000 369 (10) 12 (2) 295 (18) 62 (4)
    Missing 584 (15) 56 (11) 218 (13) 310 (9)
Education, n (%) <0.01 <0.01
    <7th grade 210 (6) 183 (37) 7 (0.4) 20 (1.2)
    7th to 12th grade 610 (16) 110 (22) 83 (5) 417 (25)
    High school diploma 728 (19) 71 (14) 291 (18) 366 (22)
    Some college 1112 (29) 78 (16) 467 (29) 567 (34)
    College graduate 1125 (30) 55 (11) 790 (48) 280 (17)
Health insurance, n (%) <0.01 <0.01
    Yes 3085 (82) 322 (65) 1442 (88) 1321 (80)
    No 256 (7) 113 (23) 48 (3) 95 (6)
    Missing 444 (12) 62 (12) 148 (9) 234 (14)
Ever seen a nephrologist 2503 (66) 265 (53) 1131 (69) <0.01 1107 (67) <0.01
Kidney function measures
    Serum creatinine, mg/dl 1.75 (0.6) 1.88 (0.6) 1.59 (0.5) <0.01 1.9 (0.6) 0.77
    eGFR, ml/min/1.73 m2 42.8 (13) 37.5 (13) 43.7 (13) <0.01 43.5 (14) <0.01
eGFR categories, ml/min/1.73 m2, n (%)
    <30 734 (19) 151 (30) 278 (17) <0.01 305 (18) <0.01
    30 to <40 939 (25) 162 (33) 389 (24) 388 (24)
    40 to <50 999 (26) 107 (22) 462 (28) 430 (26)
    50 to <60 722 (19) 51 (10) 349 (21) 322 (20)
    >60 391 (10) 26 (5) 160 (10) 205 (12)
24-hour urine protein, g, median (IQR) 0.18 (0.1–0.9) 0.72 (0.1–3.3) 0.12 (0.1–0.5) <0.01 0.24 (0.1–1.1) <0.01
Traditional cardiovascular risk factors
    Current cigarette smoker, n (%) 504 (13) 29 (6) 155 (9) 0.01 320 (19) <0.01
    Hypertension, n (%) 3269 (86) 443 (89) 1293 (79) <0.01 1533 (93) 0.01
    Systolic BP, mmHg 129 (22) 136 (24) 122 (19) <0.01 133 (23) 0.01a
    Diastolic BP, mmHg 72 (13) 73 (13) 69 (11) <0.01 74 (14) 0.07
    Diabetes mellitus, n (%) 1831 (48) 334 (67) 649 (40) <0.01 848 (51) <0.01
    Hemoglobin A1C 6.7 (2) 7 (2) 6.3 (1) <0.01 6.9 (2) 0.29
    BMI, kg/m2 32 (8) 32 (7) 31 (8) 0.20 33 (8) <0.01
    Total cholesterol, mg/dl 184 (45) 189 (54) 180 (42) <0.01a 186 (46) 0.14
    LDL cholesterol, mg/dl 103 (36) 104 (40) 99 (32) 0.03a 106 (37) 0.24
    HDL cholesterol, mg/dl 48 (15) 43 (13) 47 (15) <0.01 49 (16) <0.01
    Family history of premature CHD, n (%) 603 (16) 50 (10) 322 (20) <0.01 231 (14) 0.02
Nontraditional cardiovascular risk factors
    Hemoglobin, g/dl 12.6 (2) 12.1 (2) 13.2 (2) <0.01 12.2 (2) 0.19
    Serum calcium corrected for albumin,b mg/dl 9.2 (0.5) 9.2 (0.4) 9.2 (0.4) 0.56 9.3 (0.5) 0.01
    Serum phosphorus, mg/dl 3.7 (0.7) 4 (0.7) 3.6 (0.6) <0.01 3.8 (0.7) <0.01
    Total iPTH, pg/ml, median (IQR) 54 (35–90) 62 (41–102) 43 (30–69) <0.01a 67 (41–115) 0.09
    hs-CRP, mg/dl, Median (IQR) 2.6 (1.1–6.6) 2.5 (1.0–5.7) 2.15 (0.9–5.2) 0.26 3.3 (1.3–8.2) <0.01
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Values indicate mean (standard deviation) unless otherwise specified. eGFR, estimated glomerular filtration rate; hs-CRF, high-sensitivity C-reactive protein; IQR, interquartile range; P1, Hispanic versus Non-Hispanic Caucasian; P2, Hispanic versus Non-Hispanic African American.

a

No longer significant after adjustment for age, gender, education, eGFR.

b

Corrected calcium = Measured serum calcium + [0.8*(4–serum albumin)].

Prevalence of Clinical CVD

Compared with non-Hispanic Caucasians, Hispanics had lower prevalence of self-reported CHD (18% [H] versus 23% [C], P = 0.02; Table 2). The prevalence of any self-reported CVD, heart failure, and PAD was similar between Hispanics and non-Hispanic Caucasians. Compared with non-Hispanic African Americans, Hispanics had a significantly lower prevalence of any self-reported CVD (28% [H] versus 38% [A], P < 0.001), heart failure (7% [H] versus 13% [A], P < 0.001), and stroke (7% [H] versus 14% [A], P < 0.001). Self-reported CHD and PAD prevalence were similar between Hispanics and non-Hispanic African Americans (Table 2).

Table 2.

Prevalence of cardiovascular disease (CVD)*

Variables Overall (n = 3785) Hispanic (n = 497) Non-Hispanic Caucasian (n = 1638) P1 Non-Hispanic African American (n = 1650) P2
Self-reported history of CVD
    Any CVD 1272 (34) 138 (28) 507 (31) 0.18 627 (38) <0.01
    CHD (MI or coronary revascularization) 827 (22) 90 (18) 376 (23) 0.02 361 (22) 0.07
    Heart failure 371 (10) 37 (7) 117 (7) 0.82 217 (13) <0.01
    Stroke 382 (10) 37 (7) 118 (7) 0.86 227 (14) <0.01
    Peripheral arterial disease 257 (7) 35 (7) 105 (6) 0.62 117 (7) 0.97
Subclinical Measures of CVD
    CAC score >100 719 (37) 115 (34) 359 (41) 0.03 245 (35) 0.88
    CAC score >400 415 (22) 65 (19) 225 (26) 0.02 125 (18) 0.52
    Left ventricular hypertrophy 1663 (54) 282 (71) 538 (40) <0.01 843 (63) <0.01
    Ankle-brachial index <0.9 611 (16) 72 (15) 206 (13) 0.23 333 (20) <0.01
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*

Values indicate n (%) unless otherwise specified. CAC, coronary artery calcium score; IQR, interquartile range; P1, Hispanic versus non-Hispanic Caucasian; P2, Hispanic versus non-Hispanic African American.

Prevalence of Subclinical Measures of CVD

Compared with non-Hispanic Caucasians, Hispanics had lower prevalence of CAC >100 (34% [H] versus 41% [C], P = 0.03); higher prevalence of LVH (71% [H] versus 40% [C], P < 0.001); and similar prevalence of abnormal ABI (15% [H] versus 13% [C], P = 0.2; Table 2). Compared with non-Hispanic African Americans, Hispanics had a significantly lower prevalence of ABI <0.9 (15% [H] versus 20% [A], P = 0.007), higher prevalence of LVH (71% [H] versus 63% [A], P = 0.003), and similar prevalence of CAC (>100). Using an alternative cutoff for CAC (>400), similar patterns between Hispanics and non-Hispanics were observed (Table 2).

Stratified Analyses of Clinical and Subclinical Outcomes

Among participants with eGFR <30 ml/min/1.73 m2, Hispanics had significantly lower prevalence of self-reported CVD, CAC >100, and CAC >400, as compared with non-Hispanic Caucasians (P < 0.05; Table 3). Differences in high CAC prevalence was less pronounced when compared with non-Hispanic African Americans. Prevalent LVH was significantly higher in Hispanics than non-Hispanic Caucasians within every strata of abnormal eGFR (P < 0.0001; Table 3). Thirty-two percent of Hispanics with eGFR <30 ml/min/1.73 m2 had CAC >100, compared with 53% of non-Hispanic Caucasians (P = 0.003) and 46% of non-Hispanic African Americans (P = 0.05; Table 3; Figure 1a).

Table 3.

Clinical and subclinical measures of cardiovascular disease by estimated glomerular filtration rate (eGFR) in ml/min/1.73 m2*

eGFR, ml/min/1.73m2 Hispanic Non-Hispanic Caucasian P1 Non-Hispanic African American P2
Self-reported Cardiovascular Disease, n (%)
    <30 42 (28) 115 (41) <0.01 135 (44) <0.01
    30 to <40 52 (32) 143 (37) 0.30 174 (45) <0.01
    40 to <50 30 (28) 154 (33) 0.29 165 (38) 0.05
    50 to <60 10 (20) 75 (21) 0.76 106 (33) 0.06
    ≥60 4 (15) 20 (13) 0.68 47 (23) 0.38
Coronary artery calcium score >100, n (%)
    <30 32 (32) 61 (53) <0.01 47 (46) 0.05
    30 to <40 43 (38) 91 (50) 0.05 43 (34) 0.44
    40 to <50 26 (34) 99 (41) 0.25 69 (35) 0.80
    50 to <60 11 (33) 83 (35) 0.81 59 (36) 0.75
    ≥60 3 (18) 25 (23) 0.60 27 (22) 0.67
Coronary artery calcium score >400, n (%)
    <30 18 (18) 37 (32) 0.02 28 (27) 0.12
    30 to <40 24 (21) 61 (34) 0.03 27 (21) 0.95
    40 to <50 14 (18) 61 (25) 0.20 31 (16) 0.65
    50 to <60 7 (21) 52 (22) 0.90 27 (17) 0.52
    ≥60 2 (12) 14 (13) 0.88 12 (10) 0.80
Left ventricular hypertrophy, n (%)
    <30 104 (83) 121 (54) <0.01 182 (76) 0.14
    30 to <40 90 (70) 139 (45) <0.01 223 (69) 0.72
    40 to <50 57 (63) 151 (40) <0.01 219 (63) 0.92
    50 to <60 24 (65) 93 (31) <0.01 141 (54) 0.20
    ≥60 7 (37) 34 (25) 0.26 78 (45) 0.48
Ankle-brachial index <0.9, n (%)
    <30 35 (24) 53 (20) 0.30 86 (28) 0.31
    30 to <40 23 (15) 68 (18) 0.37 84 (22) 0.05
    40 to <50 5 (5) 51 (11) 0.05 88 (21) <0.01
    50 to <60 7 (14) 32 (9) 0.26 62 (19) 0.39
    ≥60 2 (8) 2 (1) 0.04 13 (7) 0.82
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*

Values indicate n (%). P1, Hispanic versus non-Hispanic Caucasian; P2, Hispanic versus non-Hispanic African American.

Figure 1.

Figure 1.

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Prevalence of coronary artery calcium scores (0, 1 to 100, >100 to 400, >400) by race/ethnicity among participants with eGFR <30ml/min/1.73m2 (1a) and diabetes (1b). NH, non-Hispanic.

In stratified analysis by gender, the prevalence of self-reported CHD was significantly lower among Hispanic males (19%) compared with non-Hispanic Caucasian males (30%, P < 0.001). Among participants with diabetes, the prevalence of CHD was also lower in Hispanics (21%) compared with non-Hispanic Caucasians (33%, P < 0.001; data not shown). ECG evidence of previous MI was similar across racial/ethnic groups (8% [H], 7% [C], 9% [A]; P > 0.05). Forty percent of Hispanics with diabetes had CAC >100, compared with 64% of non-Hispanic Caucasians (P < 0.0001; Figure 1b). This difference was not observed in participants without diabetes (data not shown).

Multivariate Analysis of Clinical and Subclinical Outcomes

In fully adjusted logistic regression models, the prevalence odds of LVH were two times higher among Hispanics compared with non-Hispanic Caucasians (95% confidence interval 1.2 to 3.2, P = 0.005) (Table 4). The fully adjusted prevalence odds of CAC >400 were 2.5 times higher among Hispanics compared with non-Hispanic African Americans (95% confidence interval 1.1 to 5.6, P = 0.03). Adjusted prevalence odds of self-reported clinical CVD, CAC >100, and ABI <0.9 were similar across racial/ethnic groups.

Achievement of Therapeutic Goals for CVD Prevention

Several differences across racial/ethnic groups were found with respect to the unadjusted prevalence of achievement of guideline-recommended goals for secondary prevention of CVD (Table 5) (21). Compared with non-Hispanic Caucasians and African Americans, Hispanics with self-reported CVD were less likely to take daily aspirin (48% [H], 68% [C], 58% [A]; P < 0.04) and to have hemoglobin A1C <7% (39% [H], 62% [C], 53% [A]; P < 0.001). Compared with non-Hispanic Caucasians, Hispanics with self-reported CVD were less likely to exercise regularly (39% [H] versus 53% [C], P = 0.005) and less likely to have BP <130/80 mmHg (40% [H] versus 62% [C], P < 0.001). Compared with non-Hispanic African Americans, Hispanics were more likely to have a waist circumference <40 in for men and <35 in for women (35% [H] versus 22% [A], P = 0.003). Use of renin-angiotensin system (RAS) blockers and β-blockers was similar between groups.

Table 5.

Achievement of guideline-recommended goals for secondary prevention of CVD among participants with any self-reported CVD at baseline

Variables Hispanic n = 138
 Non-Hispanic Caucasian n = 507
 Non-Hispanic African American n = 627
n (%) n (%) P n (%) P
Not current smoker 132 (96) 454 (90) 0.03 488 (78) <0.01
BP <130/80 mmHG 55 (40) 316 (62) <0.01 244 (39) 0.84
LDL ≤100 101 (73) 361 (71) 0.65 352 (56) <0.01
Physical activity 30 min/day, at least 5 d/wk 51 (39) 257 (53) <0.01 259 (44) 0.23
BMI <25 kg/m2 13 (9) 74 (15) 0.12 76 (12) 0.37
Waist circumference: men <40 in, women <35 in 47 (35) 154 (31) 0.35 138 (22) <0.01
Hg A1C <7% 54 (39) 313 (62) <0.01 333 (53) <0.01
Aspirin use 66 (48) 343 (68) <0.01 363 (58) 0.03
RAS blocker use 100 (73) 397 (79) 0.13 479 (77) 0.30
β-blocker use 104 (76) 346 (69) 0.11 452 (73) 0.40
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BMI, body mass index; Hg, hemoglobin; RAS, renin-angiotensin system.

Discussion

At the time of enrollment in the CRIC/HCRIC studies, Hispanics with CKD were at significant socioeconomic disadvantage and had a higher prevalence of most traditional and nontraditional CVD risk factors compared with non-Hispanics, even after accounting for differences in kidney function. However, Hispanics generally had a lower prevalence of most self-reported and subclinical measures of CVD, with the exception of LVH, which was exceptionally common among Hispanics. Furthermore, Hispanics with self-reported CVD were less likely to achieve therapeutic goals for secondary prevention of CVD, including regular exercise, BP, and glycemic control. To our knowledge, our study is the first systematic evaluation of the clinical epidemiology of CVD in Hispanics with CKD across a wide range of age and in comparison with other racial/ethnic groups.

Similar to our findings, in a general population sample from NHANES III, the prevalence of self-reported CHD was lower in Mexican Americans despite the higher prevalence of diabetes, hypertension, and physical inactivity compared with non-Hispanic Caucasians (22). Possible explanations for these disparities between Hispanics and non-Hispanics include biologic or genetic differences, and cultural variation in disease self-report. In addition, limited access to medical care might decrease the possibility of being diagnosed with a mild cardiovascular event.

Nearly two thirds of Hispanics with CKD had poorly controlled hypertension (BP >130/80 mmHG), a rate which was almost twofold higher than that observed in non-Hispanic Caucasians in our cohort. Similarly, within NHANES III, Mexican Americans had the highest rate of uncontrolled hypertension (23). In addition to poorly achieved recommended BP goals, Hispanics were less likely to achieve many other recommended goals for secondary prevention of CVD. The generally poor rates of use of these preventive measures may be related to lack of access to medical care, as evidenced by lack of health insurance in 23% of Hispanics and late or no referral for nephrology care, ineffective patient-provider communication, factors associated with acculturation, and low adherence to medication and medical advice (24).

We observed a significantly higher prevalence of LVH among Hispanics compared with non-Hispanic Caucasians, as the adjusted prevalence was nearly twice that in the former compared with the latter group. Given the known relationship between hypertension and LVH, this finding is likely best attributed to the higher rates of poor BP control among Hispanics (25,26). Other factors that may explain this increased risk include higher body mass index and lower hemoglobin observed in Hispanics compared with non-Hispanic Caucasians (16). Our findings are consistent with prior studies of non-CKD populations in which Hispanics have been found to have higher prevalence of LVH compared with non-Hispanics (27–29). In the Multi-Ethnic Study of Atherosclerosis (MESA), Hispanics were similarly almost twice as likely as non-Hispanic Caucasians to have LVH after adjustment for hypertension and other covariates (28). These results have clinical relevance because LVH is known to be an independent predictor of cardiovascular morbidity and mortality, and, therefore, more aggressive BP control among Hispanics could contribute to reducing LVH among this group (25,30).

We considered two cut-off points for CAC (>100 and >400) as consistent with subclinical CVD based on prior studies suggesting that these cut-off points are associated with increased risk of cardiovascular disease events and all-cause mortality (31–38). Consistent with the lower prevalence of self-reported CHD among Hispanics with CKD compared with non-Hispanic Caucasians, we also found a lower prevalence of CAC >100. Similar results were observed in the subgroups of participants with advanced CKD and diabetes. In adjusted analyses of the combined CRIC and HCRIC cohorts, this difference was attenuated and no longer statistically significant, which could be due to the small number of Hispanics who underwent CAC measurement. Similarly, in a non-CKD cohort, the prevalence of coronary calcification (CAC >0) was significantly lower in Hispanics compared with Caucasians, after adjustment for coronary risk factors (31). In contrast, the risk for CAC >400 was two times greater in Hispanics than non-Hispanic African Americans, even after adjustment for sociodemographic and clinical factors. Few studies have compared CAC in Hispanics with CKD with other racial/ethnic groups. A cross-sectional study of 90 nondialyzed patients with diabetes (60 Hispanics and 30 African Americans) reported more prevalent and severe CAC among individuals with diabetic nephropathy but did not provide a direct comparison between Hispanics and African Americans (37).

It has been reported previously that the prevalence of peripheral arterial disease in the general population is higher among African Americans than Hispanics (13,39,40). Our study is the first to report the prevalence of measured peripheral arterial disease in a cohort of Hispanics with CKD not yet on dialysis. Similar to prior studies in patients without CKD, we found that Hispanics had lower prevalence of abnormal ABI than non-Hispanic African Americans, which was not present in adjusted analyses and appeared to be explained by differences in sociodemographic factors.

Our study has limitations. First, the majority of Hispanics were recruited at a single center and, therefore, findings may not be generalizable to all U.S. Hispanics. However, the composition of the HCRIC cohort is reflective of the heterogeneity of the U.S. Hispanic population in terms of country of origin and education (1,8,41). Moreover, the socioeconomic disadvantages observed in HCRIC are similar to those found in Hispanics with CKD in a recent NHANES III analysis (8). Also, findings from our cohorts may not be generalizable to all types to kidney disease, such as glomerulonephritis. However, the CRIC study is representative of the ESRD population in which diabetes and hypertension are the primary diagnosis for over 70% of patients (10). Second, clinical CVD was ascertained by self-report of prior history of MI or coronary revascularization, which might be influenced by recall bias. However, this methodology is commonly used in clinical research, and the excellent or substantial agreement between self-reported CHD and the medical record has been previously demonstrated in patients with ESRD (42). Third, we estimated GFR using the MDRD formula, which has not been validated in Hispanics; however, this formula has been used in other studies of Hispanics with CKD (8,43).

Hispanics in CRIC and HCRIC had worse BP control and a higher prevalence of LVH compared with non-Hispanic Caucasians. Moreover, Hispanics with CKD had the lowest rate of achievement of CVD therapeutic targets. The health disparities found in our study are likely the result of a complex interplay among multiple factors at the individual and community levels, the health care system, and society as a whole. The long-term impact of our findings on renal and cardiovascular outcomes will be evaluated in subsequent longitudinal analyses. Future research should be dedicated to examine etiologic factors that may explain our findings.

Disclosures

James P. Lash received relevant support from the National Institute of Digestive, Diabetes and Kidney Diseases (R01 DK072231, U01 DK060980). Ana C. Ricardo received research support from the University of Illinois at Chicago (UIC) Center for Clinical and Translational Science (CCTS), Award Number UL1RR029879 from the National Center for Research Resources. Claudia Lora received research support from the University of Illinois at Chicago (UIC) Center for Clinical and Translational Science (CCTS) KL2 Scholars Program, Award Number UL1RR029879 from the National Center for Research Resources. Michael Fischer received support from a Department of Veterans Affairs (VA) Health Services Research and Development (HSR&D) Career Development Award. Alan S. Go received relevant support from the National Institute of Digestive, Diabetes and Kidney Diseases (U01 DK060902, R01DK072231, U01DK082223), and the National Heart, Lung and Blood Institute (U19HL091179).

Acknowledgments

This work was funded under a cooperative agreement from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK; 5U01DK060990, 5U01DK060984, 5U01DK06102, 5U01DK061021, 5U01DK061028, 5U01DK60980, 5U01DK060963, 5U01DK060902), and an R01 DK072231 (HCRIC). In addition, this work was supported in part by institutional Clinical Translational Science Awards (CTSA) and other National Institutes of Health (NIH) grants: Johns Hopkins University UL1 RR-025005; University of Maryland GRCR M01 RR-16500; Case Western Reserve University Clinical and Translational Science Collaborative (University Hospitals of Cleveland, Cleveland Clinic Foundation, and MetroHealth) UL1 RR-024989; University of Michigan GCRC M01 RR-000042, CTSA UL1 RR-024986; University of Illinois at Chicago Clinical Research Center, M01 RR-013987–06; Tulane/LSU/Charity Hospital General Clinical Research Center RR-05096; University of Pennsylvania CTSA UL1 RR-024134; Kaiser NIH/NCRR UCSF-CTSI UL1 RR-024131, 5K24DK002651. Additional support was provided by the National Center for Minority Health and Health Disparities, National Institutes of Health, and Department of Veterans Affairs Health Services Research and Development Service (MJF, Career Development Award).

University of Pennsylvania Scientific & Data Coordinating Center: Harold I. Feldman, MD, MSCE (PI), J. Richard Landis, PhD, Dina H. Appleby, MS, Shawn Ballard, MS, Denise Cifelli, MS, Robert M. Curley, MS, Jennifer Dickson, Marie Durborow, Stephen Durborow, Melanie Glenn, MPH, Asaf Hanish, MPH, Christopher Helker, MSPH, Elizabeth S. Helker, RN, Amanda Hyre Anderson, PhD, MPH, Marshall Joffe, MD, PhD, MPH, Scott Kasner, MD, MSCE, FAHA, Stephen E. Kimmel, MD, MSCE, Shiriki Kumanyika, PhD, MPH, Lisa Nessel, MSS, MLSP, Emile R. Mohler, III, MD, Steven R.Messe, MD, Nancy Robinson, PhD, Leigh Rosen, MUEP, J. Sanford Schwartz, MD, Sandra Smith, Joan Stahl, MS, Kelvin Tao, PhD, MS, Valerie L. Teal, MS, Xin Wang, MS, Dawei Xie, PhD, Peter Yang, PhD, Xiaoming Zhang, MS; University of Pennsylvania Medical Center: Raymond R. Townsend, MD (PI), Manjunath Balaram, *Thomas P. appola, MD, ScM, Debbie Cohen, MD, Magdalena Cuevas, Mark J. Duckworth, *Daniel L. Dries, MD, Virginia Ford, MSN, CRNP, Colin M. Gorman, *Juan Grunwald, MD, Holly M. Hannah, Peter A. Kanetsky, PhD, MPH, Krishna Kellem, Lucy Kibe, MS, *Mary B. Leonard, MD, MSCE, *Maureen Maguire, PhD, Stephanie McDowell, John Murphy, MD, *Muredach Reilly, MB, *Sylvia E. Rosas, MD, Wanda M. Seamon, Angie Sheridan, MPH, Karen Teff, MD; The Johns Hopkins University: Lawrence J. Appel, MD, MPH (PI), Cheryl Anderson, PhD, MPH, Jeanne Charleston, RN, Nyya Etheredge, Bernard Jaar, MD, MPH, Kelly Mantegna, Carla Martin, Edgar “Pete” Miller, MD, Patience Ngoh, Julia Scialla, MD, Steve Sozio, MD, MHS, Sharon Turban, MD, MHS, Hemalatha Venkatesh; University of Maryland: Jeffrey Fink, MD, MS (Co-PI), Wanda Fink, RN, BSN, Afshin Parsa, MD, MPH, Beth Scism, Stephen Seliger, MD, MS, Matthew Weir, MD; University Hospitals of Cleveland Case Medical Center: Mahboob Rahman, MD (PI), Valori Corrigan, RN, Renee Dancie, CMA, Genya Kisin, MA, Radhika Kanthety, Louise Strauss, RN, Jackson T. Wright Jr., MD, PhD; MetroHealth Medical Center: Jeffrey Schelling, MD (Co-PI), Patricia Kao, MD (Co-PI), Ed Horowitz, MD (Co-PI), Jacqui Bjaloncik, Theresa Fallon, John R. Sedor, MD, Mary Ann Shella, RN, BSN, Jacqueline Theurer, J. Daryl Thornton, MD, MPH; Cleveland Clinical Foundation: Martin J. Schreiber, MD (Co-PI), Martha Coleman, RN, Richard Fatica, MD, Sandra Halliburton, PhD, Carol Horner, BSN, RN, Teresa Markle, BS, Mohammed A. Rafey, MD, MS, Annette Russo, Stephanie Slattery, RN, Rita Spirko, RN, MSN, Kay Stelmach, RN, Velma Stephens, LPN, Lara Danziger-Isakov, MD, MPH; University of Michigan at Ann Arbor: Akinlolu Ojo, MD, PhD (PI), Baskaran Sundaram, MD, Jeff Briesmiester, Denise Cornish-Zirker, BSN, Crystal Gadegbeku, MD, Nancy Hill, Kenneth Jamerson, MD, *Matthias Kretzler, MD, Bruce Robinson, MD, Rajiv Saran, MD, Bonnie Welliver, BSN, CNN, Jillian Wilson, Eric Young, MD, MS; St. John's Health System: Susan P. Steigerwalt, MD, FACP (Co-PI), Keith Bellovich, DO, Jennifer DeLuca, Sherry Gasko, BSRN, Gail Makos, RN, MSN, Chantal Parmelee, Shahan Smith, Kathleen Walls; Wayne State University: John M. Flack, MD, MPH (Co-PI), James Sondheimer, MD, Mary Maysura, Stephen Migdal, MD, M. Jena Mohanty, MD, Yanni Zhuang, BSN; University of Illinois at Chicago: James P. Lash, MD (PI), Jose Arruda, MD, Carolyn Brecklin, MD, Eunice Carmona, BA, Janet Cohan, MSN, Michael Fischer, MD, MSPH, Anne Frydrych, MS, RD, Amada Lopez, *Claudia Lora, MD, Monica Martinez, Adriana Matos, Alejandro Mercado, Brenda Moreno, Patricia Meslar, MSN, Ana Ricardo, MD, MPH, Thomas Stamos, MD, *Eve Van Cauter, PhD; Tulane University Health Science Center: Jiang He, MD, PhD (PI), Brent Alper, MD, Vecihi Batuman, MD, Lydia A. Bazzano, MD, PhD, Bernadette Borja, Adriana Burridge, MPH, Jing Chen, MD, MSc, Catherine Cooke, Patrice Delafontaine, MD, Karen B. DeSalvo, MD, MPH, MSc, Vivian A. Fonseca, MD, Lee Hamm, MD, Michelle R. Hurly, RN, BSN, Julie Legarde, Eva Lustigova, MPH, *Paul Muntner, PhD, Maria Patrocollo-Emerson, MPH, Lindsey Powers, Shea Shelton, Claire Starcke, Paul Whelton, MD, MSc; Kaiser Permanente of Northern California: Alan S. Go, MD (PI), Lynn M. Ackerson, PhD, Pete Dorin, MPA, Daniel Fernandez, Nancy G. Jensvold, MPH, Joan C. Lo, MD, Juan D. Ordonez, MD, MPH, Rachel Perloff, Thida Tan, MPH, Daphne Thompson, Gina M. Valladares, Annette Wiggins, RN, Diana B. Wong, RN, MPH, Jingrong Yang, MA; University of California, San Francisco: Chi-yuan Hsu, MD, MSc (Co-PI), Glenn M. Chertow, MD, MPH, *Nisha Bansal, MD, *Manju Kurella, MD, MPH, *Michael G. Shlipak, MD, MPH, *Kristine Yaffe, MD, National Institute of Diabetes and Digestive and Kidney Diseases, John W. Kusek, PhD, Andrew S. Narva, MD; Scientific Advisory Committee: Kathy Faber-Langendoen, MD, Bryce A. Kiberd, MD, Elisa T. Lee, PhD, Julia Lewis, MD, William McClellan, MD, MPH, Timothy Meyer, MD, David Nathan, MD, John B. Stokes, MD, Herman Taylor, MD, Peter W. Wilson, MD; University of New Mexico: *Vallabh Shah, PhD; George Washington University: *Dominic Raj, MD, DM; University of Miami: *Myles Wolf, MD, MMSc; Consultants- Harvard School of Medicine: Paul M. Ridker, MD; Central Lab-University of Pennsylvania: Daniel J. Rader, MD, Anna DiFlorio, Ted Mifflin, Linda Morrell, Megan L. Wolfe; GFR Lab-Cleveland Clinic: Phillip Hall, MD, Henry Rolin, Sue Saunders; EBT Reading Center-UCLA: Mathew Budoff, MD, Chris Dailing; ECG Reading Center-Wake Forest: Elsayed Z. Soliman, MD, MSc, MS, Zhu-Ming Zhang, MD; Echo Reading Center-University of Pennsylvania: Martin St. John Sutton, MBBS, Martin G. Keane, MD, FACC, FAHA; University of Pennsylvania, CTRC, CTSA: UL1 RR-024134; The Johns Hopkins University: UL1 RR-025005; University of Maryland GCRC: M01 RR-16500; Case Western Reserve University Clinical and Translational Science Collaborative (University Hospitals of Cleveland, Cleveland Clinic Foundation, and MetroHealth): UL1 RR-024989; University of Michigan: GCRC grant number M01 RR-000042, CTSA grant number UL1 RR-024986; University of Illinois at Chicago CTSA: UL1RR029879; Tulane/LSU/Charity Hospital General Clinical Research Center: RR-05096; Kaiser NIH/NCRR UCSF-CTSI UL1 RR-024131; PI, principal investigator; CTRC, Clinical and Translational Research Center; GCRC, General Clinical Research Center. *Ancillary investigator.

We acknowledge and are thankful for the time and commitment of the CRIC participants to the study.

Footnotes

Published online ahead of print. Publication date available at www.cjasn.org.

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