APOL1 Genotype and Race Differences in Incident Albuminuria and Renal Function Decline

Peralta, Carmen A.; Bibbins‐Domingo, Kirsten; Vittinghoff, Eric; Lin, Feng; Fornage, Myriam; Kopp, Jeffrey B.; Winkler, Cheryl A.

doi:10.1681/asn.2015020124

Cited by 124 publications

(109 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Peralta et al previously demonstrated in CARDIA that black persons with the APOL1 high-risk genotype had onset of albuminuria at earlier ages and faster rates of eGFR-cys decline compared to white persons or black persons with the low-risk genotype. 34 Other studies have also demonstrated increased serum cystatin C and albuminuria as independent predictors of incident hypertension. 22,35–37 Our results suggest that in a population of healthy young adults without significant kidney disease, differences in kidney function do not significantly explain race differences in blood pressure changes over time.…”

Section: Discussionmentioning

confidence: 97%

“…25 Subsequent examinations occurred at years 2, 5, 7, 10, 15, 20, and 25. 25,34,38 Retention rates for these follow-up examinations were high at 90%, 86%, 81%, 77%, 74%, 72%, and 72%, respectively. 6 The CARDIA study was approved by the institutional review boards of each participating institution.…”

Section: Methodsmentioning

confidence: 93%

“…34,38 Among them, 1700 were white and 1330 were self-reported black Americans who had previously been genotyped for the APOL1 risk variants. 34,38 Briefly, CARDIA is a prospective cohort study designed to study risk factors for cardiovascular disease among young adults. Beginning in 1985–1986, 5115 white and black individuals, aged 18–30 years, were recruited from one of four sites (Birmingham, Alabama; Chicago, Illinois; Minneapolis, Minnesota; and Oakland, California).…”

Section: Methodsmentioning

confidence: 99%

“…Beginning in 1985–1986, 5115 white and black individuals, aged 18–30 years, were recruited from one of four sites (Birmingham, Alabama; Chicago, Illinois; Minneapolis, Minnesota; and Oakland, California). 25,34,38 The initial examination included the standardized collection of multiple risk factors relevant to the development of coronary artery disease. 25 Subsequent examinations occurred at years 2, 5, 7, 10, 15, 20, and 25.…”

Section: Methodsmentioning

confidence: 99%

See 3 more Smart Citations

APOL1 genetic variants are not associated with longitudinal blood pressure in young black adults

Chen

Estrella

Vittinghoff

et al. 2017

Kidney International

Self Cite

View full text Add to dashboard Cite

Whether APOL1 polymorphisms contribute to the excess risk of hypertension among blacks is unknown. To assess this we evaluated whether self-reported race and, in blacks, APOL1 risk variants (high-risk [2 risk alleles] versus low-risk [0–1 risk allele]) were associated with longitudinal blood pressure. Blood pressure trajectories were determined using linear mixed-effects (slope) and latent class models (5 distinct groups) during 25 years of follow-up in the Coronary Artery Risk Development in Young Adults Study. Associations of race and APOL1 genotypes with blood pressure change, separately, using linear mixed-effects and multinomial logistic regression models, adjusting for demographic, socioeconomic, and traditional hypertension risk factors, anti-hypertensive medication use, and kidney function were evaluated. Among 1700 whites and 1330 blacks (13% APOL1 high-risk, mean age 25 years; 46% male) mean mid-, ([systolic + diastolic blood pressure]/2), systolic and diastolic blood pressures were 89, 110, 69 mmHg, respectively. One percent of participants used anti-hypertensive medications at baseline. Compared to whites, blacks, regardless of APOL1 genotype, had significantly greater increases in mid-blood pressure and were more likely to experience significantly increasing mid-blood pressure trajectories with adjusted relative risk ratios of 5.21 and 7.27 for moderate-increasing and elevated-increasing versus low-stable blood pressure, respectively. Among blacks, longitudinal mid-blood pressure changes and mid-blood pressure trajectory classification were similar by APOL1 risk status. Modeling systolic and diastolic blood pressure as outcomes yielded similar findings. From young adulthood to mid-life, blacks have greater blood pressure increases versus whites that are not fully explained by traditional risk factors. Thus APOL1 variants are not associated with longitudinal blood pressure in blacks.

show abstract

Section: Discussionmentioning

confidence: 97%

Section: Methodsmentioning

confidence: 93%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

APOL1 genetic variants are not associated with longitudinal blood pressure in young black adults

Chen

Estrella

Vittinghoff

et al. 2017

Kidney International

Self Cite

View full text Add to dashboard Cite

show abstract

“…15 In a sample of 3030 adults with mean baseline age of 35 years and 9 years of follow-up, both APOL1 Figure 1. Median, 10th, and 90th percentile eGFR decline from mean baseline eGFR over 25 years varied by race/APOL1 status.…”

Section: Discussionmentioning

confidence: 99%

Race, APOL1 Risk, and eGFR Decline in the General Population

Grams

Rebholz²,

Chen³

et al. 2016

JASN

127

125

View full text Add to dashboard Cite

The APOL1 high-risk genotype, present in approximately 13% of blacks in the United States, is a risk factor for kidney function decline in populations with CKD. It is unknown whether genetic screening is indicated in the general population. We evaluated the prognosis of APOL1 high-risk status in participants in the population-based Atherosclerosis Risk in Communities (ARIC) study, including associations with eGFR decline, variability in eGFR decline, and related adverse health events (AKI, ESRD, hypertension, diabetes, cardiovascular disease, pre-ESRD and total hospitalization rate, and mortality). Among 15,140 ARIC participants followed from 1987-1989 (baseline) to 2011-2013, 75.3% were white, 21.5% were black/APOL1 low-risk, and 3.2% were black/APOL1 high-risk. In a demographic-adjusted analysis, blacks had a higher risk for all assessed adverse health events; however, in analyses adjusted for comorbid conditions and socioeconomic status, blacks had a higher risk for hypertension, diabetes, and ESRD only. Among blacks, the APOL1 high-risk genotype associated only with higher risk of ESRD in a fully adjusted analysis. Black race and APOL1 high-risk status were associated with faster eGFR decline (P,0.001 for each). However, we detected substantial overlap among the groups: median (10th-90th percentile) unadjusted eGFR decline was 1.5 (1.0-2.2) ml/min per 1.73 m 2 per year for whites, 2.1 (1.4-3.1) ml/min per 1.73 m 2 per year for blacks with APOL1 low-risk status, and 2.3 (1.5-3.5) ml/min per 1.73 m 2 per year for blacks with APOL1 high-risk status. The high variability in eGFR decline among blacks with and without the APOL1 high-risk genotype suggests that population-based screening is not yet justified.

show abstract

Genomics, Health Disparities, and Missed Opportunities for the Nation’s Research Agenda

West

Blacksher

Burke

2017

JAMA

View full text Add to dashboard Cite

The completion of the Human Genome Project occurred at a time of increasing public attention to health disparities. In 2004, Sankar and colleagues 1 suggested that this coincidental timing resulted in an inappropriate emphasis on the contribution of genomics to health disparities, conflating racial patterns of disease with genetic ancestry, and distracting attention from the large and compelling body of scientific evidence pointing to social determinants of health disparities. 2 For example, genomic research has emphasized discovery of genetic contributors to diabetes risk, but the recent increase in the prevalence of obesity and type 2 diabetes, which disproportionately affects minority populations, cannot be attributed to genetic changes and rather reflects social forces affecting diet, food access, and patterns in physical activity. The introduction of new genomic health technologies could also exacerbate disparities in access to high-quality health care, if specific genomic testing improved health and was only available to those who were affluent. Nonetheless, the claim persists that genomic research can reduce health disparities-if only participation by minority populations in genomic research could be increased. 3 The source of this claim is an idiosyncratic usage of the term health disparities that may result in missed opportunities for the nation's health research agenda. Health disparities are generally understood to refer to systematic differences in health effects resulting from social disadvantage, but the term is often used in genomics to refer to differing health outcomes associated with population genetic variation. This usage arguably stems from the US focus on the association of health disparities with race/ethnicity (vs socioeconomic status), together with a growing body of knowledge about population genetic variation. Compounding the problem is a tendency in the United States to conflate health disparities and health care disparities, perhaps based on the erroneous assumption that improved health care will resolve health disparities. 4 The misunderstanding about the causes of health disparities leads to confusion about fruitful lines of research and potential remedies.A causal association between social position and health is well established. 5 This association has been documented in both developed and developing countries and dates back to the earliest records, despite substantial change over time in the principal causes of disease. A broad array of health conditions across the lifespan follows a social gradient, wherein better health and longer lifespans track with increases in social advantage. This pattern holds whether measured by proxies of social class, such as education, income, and occupation, or by race/ethnicity. 5 In the United States, health disparities are significant and widening and have attracted

show abstract

APOL1 Genotype and Race Differences in Incident Albuminuria and Renal Function Decline

Cited by 124 publications

References 23 publications

APOL1 genetic variants are not associated with longitudinal blood pressure in young black adults

APOL1 genetic variants are not associated with longitudinal blood pressure in young black adults

Race, APOL1 Risk, and eGFR Decline in the General Population

Genomics, Health Disparities, and Missed Opportunities for the Nation’s Research Agenda

Contact Info

Product

Resources

About