Skip to main content

Main menu

  • Home
  • Content
    • Published Ahead of Print
    • Current Issue
    • Subject Collections
    • JASN Podcasts
    • Archives
    • Saved Searches
    • ASN Meeting Abstracts
  • Authors
    • Submit a Manuscript
    • Author Resources
  • Editorial Team
  • Subscriptions
  • More
    • About JASN
    • Alerts
    • Advertising
    • Editorial Fellowship Program
    • Feedback
    • Reprints
    • Impact Factor
  • ASN Kidney News
  • Other
    • CJASN
    • Kidney360
    • Kidney News Online
    • American Society of Nephrology

User menu

  • Subscribe
  • My alerts
  • Log in
  • Log out
  • My Cart

Search

  • Advanced search
American Society of Nephrology
  • Other
    • CJASN
    • Kidney360
    • Kidney News Online
    • American Society of Nephrology
  • Subscribe
  • My alerts
  • Log in
  • Log out
  • My Cart
Advertisement
American Society of Nephrology

Advanced Search

  • Home
  • Content
    • Published Ahead of Print
    • Current Issue
    • Subject Collections
    • JASN Podcasts
    • Archives
    • Saved Searches
    • ASN Meeting Abstracts
  • Authors
    • Submit a Manuscript
    • Author Resources
  • Editorial Team
  • Subscriptions
  • More
    • About JASN
    • Alerts
    • Advertising
    • Editorial Fellowship Program
    • Feedback
    • Reprints
    • Impact Factor
  • ASN Kidney News
  • Follow JASN on Twitter
  • Visit ASN on Facebook
  • Follow JASN on RSS
  • Community Forum
Epidemiology and Outcomes
You have accessRestricted Access

Racial Differences in Early-Onset Renal Disease among Young Adults: The Coronary Artery Risk Development in Young Adults (CARDIA) Study

Catherine O. Stehman-Breen, Daniel Gillen, Michael Steffes, David R. Jacobs, Cora E. Lewis, Catarina I. Kiefe and David Siscovick
JASN September 2003, 14 (9) 2352-2357; DOI: https://doi.org/10.1097/01.ASN.0000083392.11042.14
Catherine O. Stehman-Breen
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Daniel Gillen
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Michael Steffes
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
David R. Jacobs Jr.
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Cora E. Lewis
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Catarina I. Kiefe
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
David Siscovick
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data Supps
  • Info & Metrics
  • View PDF
Loading

Abstract

ABSTRACT. Although 11 million people in the United States have chronic renal insufficiency, little is known about ethnic/racial disparities for early-onset renal impairment. This study sought to determine whether there is an independent association between race/ethnicity and early-onset renal impairment and to identify other risk factors that might account for observed disparities. All Coronary Artery Risk Development in Young Adults subjects in which serum creatinine was measured at the year 15 examination were identified (n = 3554), excluding those who were pregnant at year 15. Potential risk factors at study entry (ages 18 to 30 yr, 1985 to 1986) included age, weight, gender, race/ethnicity, glucose, uric acid, and systolic BP. Renal impairment was defined as creatinine ≥1.5 mg/dl for men and ≥1.2 mg/dl for women at year 15 (ages 33 to 45 yr). Fifty-two (2.7%) women and 39 (2.4%) men had renal impairment at the year 15 examination. In bivariate analyses, the odds of renal impairment among black women was estimated to be 2.4-fold that of white women, and among black men, the odds of renal impairment were 9.0-fold that of white men. In multivariate analysis, the odds of an elevated creatinine among black women compared with white women reduced to a nonsignificant 1.5-fold, whereas among men, the odds of an elevated creatinine among blacks was 11.4-fold that of whites. Although adjustment for baseline glucose levels accounted for much of the association between ethnicity and elevated creatinine among women, adjustment for weight, systolic BP, uric acid, glucose, and socioeconomic status did not account for the association between ethnicity and renal impairment among men. The data suggest that there are ethnic differences in the development of early-onset renal dysfunction. Among women, these differences are modest and largely accounted for by differences in glucose levels early in adult life. Differences in race/ethnicity related risk of early-onset renal impairment are particularly large among men and are not accounted for by the metabolic or socioeconomic factors evaluated. E-mail: cos@u.washington.edu

Renal disease is an important public health problem, disproportionately affecting certain ethnic groups. In particular, black race/ethnicity is associated with more rapid progression of renal disease (1,2⇓) than is white race/ethnicity. Although blacks account for 10% of the general population, they account for >30% of the ESRD population (2–8⇓⇓⇓⇓⇓⇓). The reasons for these disparities are not well understood but may be due to a greater risk of diabetes and hypertension, lower socioeconomic status, and poorer access to health care among blacks. Little is known about the contribution of race/ethnicity to the development of early-onset renal impairment (9) or about the factors that might be responsible for observed associations.

The Coronary Artery Risk Development in Young Adults (CARDIA) Study is a longitudinal study of coronary artery disease risk development in a biethnic population of young adults. CARDIA provides a unique opportunity to identify prospectively risk factors present in early life that predict later development of renal disease. The primary objective of this study was to determine whether there is an independent association between race/ethnicity and early-onset renal impairment among both men and women and to identify other risk factors that might account for observed disparities.

Materials and Methods

Setting and Subjects

Details of the CARDIA study design are described elsewhere (10,11⇓). Briefly, subjects ages 18 to 30 yr were recruited by clinical centers from the populations of four geographic locations (Birmingham, AL; Chicago, IL; Minneapolis, MN; and Oakland, CA) by a stratified random sampling scheme to ensure balance across gender and ethnicity (blacks and whites only). Baseline examinations were performed on 5115 (51%) of eligible subjects contacted in 1985 to 1986. To date, the CARDIA clinical centers have completed five subsequent examinations, after 2, 5, 7, 10 (79% retention), and 15 (73% retention) years of follow-up. For the purposes of this study, we identified all CARDIA subjects in whom serum creatinine was measured at the year 15 examination (n = 3554).

Subject Characteristics

Sociodemographic history was obtained by questionnaire. Age, gender, race/ethnicity, cigarette smoking status (current, past, never), and illicit drug use (yes, no) were determined from the baseline examination. Years of education (<12, 12 to 16, and >16 yr) and employment status (full time, less than full time) were determined from the year 10 examination because baseline information from subjects whose ages ranged between 18 and 30 yr would have inconsistently reflected the impact of these variables at follow-up.

Anthropometric assessments from the baseline and year 10 examinations were used in analyses. Body weight was measured with participants wearing light clothing using a calibrated balance beam scale. Skinfold measurements were obtained as a surrogate measure of body fat and obtained at standard sites using duplicate measurements and the Harpenden calipers (Quinton, Seattle, WA). Averages were used to obtain the sum of skinfolds (11). Waist circumference was measured laterally midway between the iliac crest and the lowest lateral portion of the rib cage and anteriorly midway between the xiphoid process of the sternum and the umbilicus.

BP measurements obtained from the baseline and year 10 examinations were used for this analysis. Three BP were obtained with a random zero sphygmomanometer three times after a 5-min rest, with 1-min intervals between measures; the average of the last two measurements was used in analyses.

Dietary history, physical activity, and fitness were assessed at the baseline examination. Centrally trained and certified interviewers obtained a detailed, quantitative diet history (12). Dietary data were processed with the University of Minnesota Nutrition Coordinating Center Tape 10 nutrient database (13). Physical activity was assessed by questionnaire, and a score was calculated by summing the intensity weighted frequencies of 13 activities reported in the previous year (14). Physical fitness was assessed by calculating the total duration of exercise in seconds obtained from a symptom-limited, graded treadmill exercise test with a modified Balke protocol (15).

When available, we used laboratory data from the baseline examination including plasma cholesterol, fasting insulin, uric acid, glucose, serum calcium, phosphate, and total protein. Glucose from the year 10 examination was used to calculate change in glucose. Comparable measures of baseline and year 15 serum creatinine were not available; therefore, the current analysis investigates predictors of year 15 creatinine only. Fibrinogen (16) and Lp(a) (16) from the year 5 examination and C-reactive protein from the year 15 examination were used in the analysis. Albumin/creatinine excretion was assessed at the years 10 and 15 examinations using a single untimed urine sample with creatinine adjusted for race and gender as described previously (17). Microalbuminuria was defined as a ratio of albumin to creatinine ≥25 mg/g after adjustment for gender and race (A/kC, where k = 0.68*0.88 in black men, 0.88 in black women, 0.68 in white men, and 1 in white women (17)). Diabetes was defined as an 8-h fasting glucose level of >126 mg/dl and/or use of antidiabetic medication. At each examination, blood samples were drawn the morning after an overnight fast (at least 8 h) using EDTA-containing tubes. Plasma and serum were stored at −70° before assay.

Follow-up and Classification of Events

The primary outcome assessed was serum creatinine at the year 15 examination. Although GFR is the gold standard measure of renal function, there are no direct measures of GFR in CARDIA. We chose not to use formulas to estimate GFR, such as the Modification of Diet in Renal Disease or Cockcroft-Gault formulas (18,19⇓), for several reasons. First, because age, gender, race, and weight were predictors of interest and also used in the formulas (20), the use of these formulas would potentially induce a relationship between renal function and the covariates of interest. Second, the use of the formulas assumes an interaction between the components of the formula that may or may not exist in this population. Modeling the interaction with the available data is a more accurate way to determine the functional form of the relationship. Finally, these formulas have not been validated in young adults. We used cut points for creatinine to provide less biased estimates of renal function because several very high creatinine values among black individuals with diabetes weighted the results when creatinine was modeled as a continuous variable. Because there are not standard creatinine values that define renal disease, clinically meaningful cut points that minimized false positives were chosen. Sensitivity analyses using different cut points were also performed. Different cut points were used for men and women because serum creatinine level is dependent on muscle mass and muscle mass is lower among women than men.

Statistical Analyses

Logistic regression was used to estimate the association between race/ethnicity and year 15 creatinine after adjustment for possible confounders. Because of the different cut points used to define renal dysfunction across gender and the intent to assess interactions by race, separate logistic regression models were fit for men and women. Covariates included in each multiple regression model were chosen on the basis of their potential for confounding the association between race/ethnicity and creatinine or on the basis of their potential to predict change independently in renal function. Multiplicative interactions between the primary predictors listed above and race/ethnicity were evaluated to identify possible effect modification by race. Residual diagnostics were analyzed to investigate potential outlying data points and to determine the appropriate functional form of adjustment covariates. Although outlying data points were present in the analysis, the measurements were not found to be highly influential and could not be attributed to obvious data entry error and hence were not excluded.

Results

Characteristics of the study sample, stratified by gender and creatinine level measured at the year 15 examination, are presented in Table 1. Fifty-two (2.7%) women had a serum creatinine of 1.2 mg/dl or higher, and 39 men (2.4%) had a serum creatinine of 1.5 mg/dl or higher at the year 15 examination. Both men and women with high creatinine levels were more likely to be black. The prevalence of elevated creatinine among white women was 1.6% (16 of 987) and 3.7% (36 of 963) among black women, whereas the prevalence of elevated creatinine among white men was 0.6% (5 of 899) and 4.8% (34 of 705) among black men. Both men and women with high creatinine were more likely to be diabetic and have microalbuminuria at year 10. Among women, high creatinine was also associated with greater baseline weight, systolic BP (SBP), and C-reactive protein levels at the year 15 examination. Among men, high creatinine was also associated with greater change in SBP between baseline and year 10, level of education at the year 10 examination, and higher baseline uric acid levels. In most cases in which a variable was statistically significant in only one gender, the estimated direction of association was the same in the other gender.

View this table:
  • View inline
  • View popup

Table 1. Patient characteristics by gender and serum creatinine level at year 15: The CARDIA study, 1985–2001

The association between race and creatinine was found to differ significantly by gender (P = 0.005). Therefore, we undertook separate analyses for men and women. Table 2 presents univariate logistic regression estimates modeling the association between selected risk factors and the odds of elevated year 15 serum creatinine among women and men. The unadjusted odds of renal impairment among black women was estimated to be 2.4-fold that of white women. Important risk factors for renal impairment for women included baseline glucose, weight, and SBP and change in SBP between baseline and the year 10 examination. The unadjusted odds of renal impairment among black men were 9.0-fold that of white men. In addition to ethnicity, important risk factors from bivariate analyses included baseline glucose and uric acid and change in SBP and glucose between baseline and year 10 examinations.

View this table:
  • View inline
  • View popup

Table 2. Gender-stratified univariate logistic regression estimates modeling the probability of elevated creatinine at year 15: the CARDIA study, 1985–2001a

The multivariate logistic regression estimates modeling the association between selected risk factors and the odds of elevated year 15 serum creatinine are presented in Table 3. After adjustment for age, weight and change in weight, SBP and change in SBP, glucose and change in glucose, and uric acid, the risk of elevated creatinine among black women compared with white women reduced to 1.5-fold and was no longer significant. Baseline glucose and change in SBP were the only significant predictors of elevated creatinine among women after adjustment for other risk factors. After adjustment, the risk of increased serum creatinine remained higher among black men when compared with white men (odds ratio, 11.4). Adjustment for age, weight, SBP, uric acid, and glucose did not account for the association between ethnicity and renal impairment among men. In addition to ethnicity, baseline glucose, uric acid, and change in SBP and glucose between baseline and year 10 examinations were independently associated with elevated serum creatinine among men.

View this table:
  • View inline
  • View popup

Table 3. Gender-stratified adjusted logistic regression estimates modeling the probability of elevated creatinine at year 15: the CARDIA study, 1985–2001a

Further analyses sought to identify additional explanatory variables that might account for the association between black ethnicity and high creatinine among men by adding additional variables to models presented in Table 3. Adjustment for year 10 education and employment status did not alter the relationship between race/ethnicity and high creatinine. Adjustment for baseline serum calcium, phosphorous, and total protein; year 5 fibrinogen and Lp(a); or year 15 C-reactive protein levels also failed to account for the association between race/ethnicity and elevated creatinine. The addition of baseline triceps skinfold thickness, waist circumference, total exercise intensity score, and dietary protein intake only minimally reduced the association between black ethnicity and high creatinine.

Discussion

We found an elevated risk for renal impairment in blacks compared with whites, especially among men. The association between ethnicity and renal impairment in men was independent of other risk factors, such as weight, SBP, and glucose assessed 15 yr before creatinine measurement and the change in these risk factors over the initial 10 yr of follow-up. However, the association between ethnicity and renal impairment in women, which was found in bivariate analyses, was no longer significant after adjustment for baseline glucose.

A reduction in the relative risk of renal impairment after adjusting for baseline glucose among women suggests that a higher prevalence of diabetes or glucose intolerance may account at least partially for the differences in renal impairment among black women. The risk of diabetes is greater among blacks than whites, and, in the general population, the risk of renal dysfunction is 2 to 4 times higher among black individuals with diabetes than among white individuals with diabetes (21,22⇓). However, given the relative rarity of renal insufficiency in our generally healthy study sample, this study may have had limited power to detect the moderate associations of race/ethnicity with renal dysfunction noted among women.

The reason that black men may be at greater risk for the development of renal disease is not known. We were unable to demonstrate that disparities in a variety of factors, including education level, employment status, glycemia, or BP, accounted for this association. However, it is possible that unmeasured socioeconomic disparities or environmental factors may account for the association. Further studies are necessary to explore this possibility. Given the recent identification of candidate genes that mediate hypertension, formation of extracellular matrix proteins, and lipid metabolism (23–29⇓⇓⇓⇓⇓⇓), it is also possible that there may be some contribution of genetic factors to the observed ethnic differences in the development of renal impairment.

This study had certain limitations. In an ideal setting, baseline measurements of serum creatinine would have been available to identify subjects with preexisting renal disease at baseline. With this said, participants were only 18 to 30 yr old at baseline, and previous reports suggest that only 0.4 to 0.9% of people in this age range have estimated GFR consistent with significant renal disease (<60 ml/min) (30). In addition, recalibration of baseline creatinine values indicated that there were few subjects with renal dysfunction at baseline. Second, because different cut points were chosen for men and women to account for gender differences in serum creatinine, comparisons of risk of renal impairment between genders should be done with caution. Third, although cut points for creatinine to define renal impairment were chosen to reflect clinically significant renal disease, the ethnic differences identified were also present using lower or higher cut points for creatinine in a sensitivity analysis (data not shown). For example, for levels of serum creatinine >1.1 mg/dl in men and at 0.9 mg/dl in women, the prevalence of renal impairment remained lower for whites than for blacks. It is also possible that factors that were not assessed in this study, such as disparities in access to health care, control of hypertension, and treatment of comorbid conditions, may account for disparities in early-onset renal impairment observed in this study. Ethnic disparities in renal dysfunction may also, in part, be accounted for by the inability to completely account for differences in creatinine production between ethnic groups by adjustment for body fat and weight. Finally, there are a limited number of subjects with renal insufficiency even after 15 yr of follow-up. However, the large population of young adults followed for 15 yr provided a unique opportunity to identify early markers of early-onset renal dysfunction among a biracial cohort of young adults. In addition, clinical and biochemical evaluation was extensive and allowed us to assess a variety of variables that may be relevant to renal disease.

We conclude that there are ethnic differences in the development of early-onset renal dysfunction. Among women, these differences are modest and largely accounted for by differences in glucose levels at the baseline examination. Differences in race/ethnicity-related risk of early-onset renal impairment are particularly large among men and are not accounted for by the metabolic or socioeconomic factors evaluated in this analysis. Future studies should confirm and also identify the basis for the particularly large risk of early-onset renal dysfunction among black men.

Acknowledgments

This study was supported by a Veterans Administration Career Development Award. The data in this manuscript were presented at the American Heart Association Epidemiology Council Meeting 2002.

  • © 2003 American Society of Nephrology

References

  1. ↵
    Cowie CC, Port FK, Wolfe RA, Savage PJ, Moll PP, Hawthorne VM: Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med 321: 1074–1079, 1989
    OpenUrlCrossRefPubMed
  2. ↵
    Klag MJ, Whelton PK, Randall BL, Neaton JD, Brancati FL, Stamler J: End-stage renal disease in African-American and white men. 16-year MRFIT findings. JAMA 277: 1293–1298, 1997
    OpenUrlCrossRefPubMed
  3. ↵
    U.S. Renal Data System: USRDS 1999 Annual Data Report. Bethesda MD, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, 2001
  4. ↵
    Stephens GW, Gillaspy JA, Clyne D, Mejia A, Pollak VE: Racial differences in the incidence of end-stage renal disease in types I and II diabetes mellitus. Am J Kidney Dis 15: 562–567, 1990
    OpenUrlPubMed
  5. ↵
    Burton C, Harris K: The role of proteinuria in the progression of chronic renal failure. Am J Kidney Dis 27: 765–775, 1996
    OpenUrlPubMed
  6. ↵
    Brown TE, Carter BL: Hypertension and endstage renal disease. Ann Pharmacother 28: 359–366, 1994
    OpenUrlPubMed
  7. ↵
    Kopple JD, Greene T, Chumlea WC, Hollinger D, Maroni BJ, Merrill D, Scherch LK, Schulman G, Wang SR, Zimmer GS: Relationship between nutritional status and the glomerular filtration rate: results from the MDRD study. Kidney Int 57: 1688–1703, 2000
    OpenUrlCrossRefPubMed
  8. ↵
    Reddan D, Szczech LA, Klassen PS, Owen WF Jr: Racial inequity in America’s ESRD program. Semin Dial 13: 399–403, 2000
    OpenUrlCrossRefPubMed
  9. ↵
    Jones CA, McQuillan GM, Kusek JW, Eberhardt MS, Herman WH, Coresh J, Salive M, Jones CP, Agodoa LY: Serum creatinine levels in the US population: Third National Health and Nutrition Examination Survey. Am J Kidney Dis 32: 992–999, 1998[published erratum appears in Am J Kidney Dis 35: 178, 2000]
    OpenUrlCrossRefPubMed
  10. ↵
    Hughes GH, Cutter G, Donahue R, Friedman GD, Hulley S, Hunkeler E, Jacobs DR Jr, Liu K, Orden S, Pirie P, et al: Recruitment in the Coronary Artery Disease Risk Development in Young Adults (Cardia) Study. Control Clin Trials 8: 68S–73S, 1987
    OpenUrlCrossRefPubMed
  11. ↵
    Friedman GD, Cutter GR, Donahue RP, Hughes GH, Hulley SB, Jacobs DR Jr, Liu K, Savage PJ: CARDIA: Study design, recruitment, and some characteristics of the examined subjects. J Clin Epidemiol 41: 1105–1116, 1988
    OpenUrlCrossRefPubMed
  12. ↵
    Hilner JE, McDonald A, Van Horn L, Bragg C, Caan B, Slattery ML, Birch R, Smoak CG, Wittes J: Quality control of dietary data collection in the CARDIA study. Control Clin Trials 13: 156–169, 1992
    OpenUrlCrossRefPubMed
  13. ↵
    Tillotson JL, Gorder DD, DuChene AG, Grambsch PV, Wenz J: Quality control in the Multiple Risk Factor Intervention Trial Nutrition Modality. Control Clin Trials 7: 66S–90S, 1986
    OpenUrlCrossRefPubMed
  14. ↵
    Sidney S, Jacobs DR Jr, Haskell WL, Armstrong MA, Dimicco A, Oberman A, Savage PJ, Slattery ML, Sternfeld B, Van Horn L: Comparison of two methods of assessing physical activity in the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Am J Epidemiol 133: 1231–1245, 1991
    OpenUrlPubMed
  15. ↵
    Sidney S, Haskell WL, Crow R, Sternfeld B, Oberman A, Armstrong MA, Cutter GR, Jacobs DR, Savage PJ, Van Horn L: Symptom-limited graded treadmill exercise testing in young adults in the CARDIA study. Med Sci Sports Exerc 24: 177–183, 1992
    OpenUrlPubMed
  16. ↵
    Folsom AR, Qamhieh HT, Flack JM, Hilner JE, Liu K, Howard BV, Tracy RP: Plasma fibrinogen: Levels and correlates in young adults. The Coronary Artery Risk Development in Young Adults (CARDIA) Study. Am J Epidemiol 138: 1023–1036, 1993
    OpenUrlPubMed
  17. ↵
    Jacobs DR Jr, Murtaugh MA, Steffes M, Yu X, Roseman J, Goetz FC.: Gender- and race-specific determination of albumin excretion rate using albumin-to-creatinine ratio in single, untimed urine specimens: The Coronary Artery Risk Development in Young Adults Study. Am J Epidemiol 155: 1114–1119, 2002
    OpenUrlCrossRefPubMed
  18. ↵
    Cockcroft D, Gault M: Prediction of creatinine clearance from serum creatinine. Nephron 16: 13–41, 1976
  19. ↵
    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 130: 461–470, 1999
    OpenUrlCrossRefPubMed
  20. ↵
    Gutman R: Creatinine excretion. Lancet 1: 38, 1970
  21. ↵
    Cowie CC, Port FK, Wolfe RA, Savage PJ, Moll PP, Hawthorne VM: Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med 321: 1074–1079, 1989
  22. ↵
    Brancati FL, Whelton PK, Randall BL, Neaton JD, Stamler J, Klag MJ: Risk of end-stage renal disease in diabetes mellitus: A prospective cohort study of men screened for MRFIT. Multiple Risk Factor Intervention Trial. JAMA 278: 2069–2074, 1997
    OpenUrlCrossRefPubMed
  23. ↵
    Austin MA, Newman B, Selby JV, Edwards K, Mayer EJ, Krauss RM: Genetics of LDL subclass phenotypes in women twins. Concordance, heritability, and commingling analysis. Arterioscler Thromb 13: 687–695, 1993
    OpenUrlAbstract/FREE Full Text
  24. ↵
    Hokanson JE, Brunzell JD, Jarvik GP, Wijsman EM, Austin MA: Linkage of low-density lipoprotein size to the lipoprotein lipase gene in heterozygous lipoprotein lipase deficiency. Am J Hum Genet 64: 608–618, 1999
    OpenUrlCrossRefPubMed
  25. ↵
    Breslow JL: Genetics of lipoprotein abnormalities associated with coronary artery disease susceptibility. Annu Rev Genet 34: 233–254, 2000
    OpenUrlCrossRefPubMed
  26. ↵
    Heller DA, de Faire U, Pedersen NL, Dahlen G, McClearn GE: Genetic and environmental influences on serum lipid levels in twins. N Engl J Med 328: 1150–1156, 1993
    OpenUrlCrossRefPubMed
  27. ↵
    Cullen P, Farren B, Scott J, Farrall M: Complex segregation analysis provides evidence for a major gene acting on serum triglyceride levels in 55 British families with familial combined hyperlipidemia. Arterioscler Thromb 14: 1233–1249, 1994
    OpenUrlAbstract/FREE Full Text
  28. ↵
    Mahaney MC, Blangero J, Rainwater DL, Comuzzie AG, VandeBerg JL, Stern MP, MacCluer JW, Hixson JE.: A major locus influencing plasma high-density lipoprotein cholesterol levels in the San Antonio Family Heart Study. Segregation and linkage analyses. Arterioscler Thromb Vasc Biol 15: 1730–1739, 1995
    OpenUrlAbstract/FREE Full Text
  29. ↵
    Mahaney M, Blangero J, Comuzzie A, VandeBerg JL, Stern MP, MacCluer JW.: Plasma HDL cholesterol, triglycerides, and adiposity. A quantitative genetic test of the conjoint trait hypothesis in the San Antonio Family Heart Study. Circulation 92: 3240–3248, 1995
    OpenUrlAbstract/FREE Full Text
  30. ↵
    Clase CM, Garg AX, Kiberd BA: Prevalence of low glomerular filtration rate in nondiabetic Americans: Third National Health and Nutrition Examination Survey (NHANES III). J Am Soc Nephrol 13: 1338–1349, 2002
    OpenUrlAbstract/FREE Full Text
View Abstract
PreviousNext
Back to top

In this issue

Journal of the American Society of Nephrology: 14 (9)
Journal of the American Society of Nephrology
Vol. 14, Issue 9
1 Sep 2003
  • Table of Contents
  • Index by author
View Selected Citations (0)
Print
Download PDF
Sign up for Alerts
Email Article
Thank you for your help in sharing the high-quality science in JASN.
Enter multiple addresses on separate lines or separate them with commas.
Racial Differences in Early-Onset Renal Disease among Young Adults: The Coronary Artery Risk Development in Young Adults (CARDIA) Study
(Your Name) has sent you a message from American Society of Nephrology
(Your Name) thought you would like to see the American Society of Nephrology web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Racial Differences in Early-Onset Renal Disease among Young Adults: The Coronary Artery Risk Development in Young Adults (CARDIA) Study
Catherine O. Stehman-Breen, Daniel Gillen, Michael Steffes, David R. Jacobs, Cora E. Lewis, Catarina I. Kiefe, David Siscovick
JASN Sep 2003, 14 (9) 2352-2357; DOI: 10.1097/01.ASN.0000083392.11042.14

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Request Permissions
Share
Racial Differences in Early-Onset Renal Disease among Young Adults: The Coronary Artery Risk Development in Young Adults (CARDIA) Study
Catherine O. Stehman-Breen, Daniel Gillen, Michael Steffes, David R. Jacobs, Cora E. Lewis, Catarina I. Kiefe, David Siscovick
JASN Sep 2003, 14 (9) 2352-2357; DOI: 10.1097/01.ASN.0000083392.11042.14
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like

Jump to section

  • Article
    • Abstract
    • Materials and Methods
    • Results
    • Discussion
    • Acknowledgments
    • References
  • Figures & Data Supps
  • Info & Metrics
  • View PDF

More in this TOC Section

  • Survival among Patients with Kidney Failure in Jalisco, Mexico
  • A Population-Based, Prospective Study of Blood Pressure and Risk for End-Stage Renal Disease in China
  • Hepatitis C Virus and Death Risk in Hemodialysis Patients
Show more Epidemiology and Outcomes

Cited By...

  • Effect of Genetic African Ancestry on eGFR and Kidney Disease
  • Arterial Stiffness, Central Pressures, and Incident Hospitalized Heart Failure in the Chronic Renal Insufficiency Cohort Study
  • Vulnerable Populations and the Association between Periodontal and Chronic Kidney Disease
  • Chronic Renal Insufficiency Cohort (CRIC) Study: Baseline Characteristics and Associations with Kidney Function
  • Observational Research Databases in Renal Disease
  • Google Scholar

Similar Articles

Related Articles

  • No related articles found.
  • PubMed
  • Google Scholar

Articles

  • Current Issue
  • Early Access
  • Subject Collections
  • Article Archive
  • ASN Annual Meeting Abstracts

Information for Authors

  • Submit a Manuscript
  • Author Resources
  • Editorial Fellowship Program
  • ASN Journal Policies
  • Reuse/Reprint Policy

About

  • JASN
  • ASN
  • ASN Journals
  • ASN Kidney News

Journal Information

  • About JASN
  • JASN Email Alerts
  • JASN Key Impact Information
  • JASN Podcasts
  • JASN RSS Feeds
  • Editorial Board

More Information

  • Advertise
  • ASN Podcasts
  • ASN Publications
  • Become an ASN Member
  • Feedback
  • Follow on Twitter
  • Password/Email Address Changes
  • Subscribe

© 2021 American Society of Nephrology

Print ISSN - 1046-6673 Online ISSN - 1533-3450

Powered by HighWire