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BMC Nephrol. 2015 Feb 10;16:14. doi: 10.1186/s12882-015-0008-6.

Apolipoprotein L1, income and early kidney damage.

Author information

1
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. rtamrat1@jhmi.edu.
2
Department of Medicine, University of California, San Francisco, CA, USA. carmenalicia.peralta@ucsf.edu.
3
San Francisco VA Medical Center, San Francisco, CA, USA. carmenalicia.peralta@ucsf.edu.
4
Laboratory of Epidemiology and Population Sciences, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA. salman.tajuddin@nih.gov.
5
Laboratory of Epidemiology and Population Sciences, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA. evansm@grc.nia.nih.gov.
6
Laboratory of Epidemiology and Population Sciences, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA. zondermana@mail.nih.gov.
7
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. dcrews1@jhmi.edu.
8
Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Medical Institutions, Baltimore, MD, USA. dcrews1@jhmi.edu.
9
Center on Aging and Health, Johns Hopkins Medical Institutions, Baltimore, MD, USA. dcrews1@jhmi.edu.
10
Division of Nephrology, Johns Hopkins University School of Medicine, Johns Hopkins Bayview Medical Center, 301 Mason F. Lord Drive, Suite 2500, Baltimore, MD, 21224, USA. dcrews1@jhmi.edu.

Abstract

BACKGROUND:

The degree to which genetic or environmental factors are associated with early kidney damage among African Americans (AAs) is unknown.

METHODS:

Among 462 AAs in the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) study, we examined the cross-sectional association between apolipoprotein L1 (APOL1) risk variants and income with: 1) mildly reduced eGFR (<75 mL/min/1.73 m(2), creatinine-cystatin C equation) and 2) elevated urine albumin-to-creatinine ratio (ACR) (≥17 in men and ≥25 mg/g in women). High risk APOL1 status was defined by 2 copies of high-risk variants; low risk if 0 or 1 copy. Income groups were dichotomized as < $14,000/year (lowest income group) or ≥ $14,000/year. Logistic regression models were adjusted for age, sex, and % European ancestry.

RESULTS:

Overall, participants' mean age was 47 years and 16% (n = 73) had high risk APOL1 status. Mean eGFR was 99 mL/min/1.73 m(2). Mildly reduced eGFR was prevalent among 11% (n = 51). The lowest income group had higher adjusted odds (aOR) of mildly reduced eGFR than the higher income group (aOR 1.8, 95% CI 1.2-2.7). High-risk APOL1 was not significantly associated with reduced eGFR (aOR 1.5, 95% CI 0.9-2.5). Among 301 participants with ACR data, 7% (n = 21) had elevated ACR. Compared to low-risk, persons with high-risk APOL1 had higher odds of elevated ACR (aOR 3.8, 95% CI 2.0-7.3). Income was not significantly associated with elevated ACR (aOR 1.8, 95% CI 0.7-4.5). There were no significant interactions between APOL1 and income.

CONCLUSIONS:

Both genetic and socioeconomic factors may be important determinants of early kidney damage among AAs.

PMID:
25884165
PMCID:
PMC4361142
DOI:
10.1186/s12882-015-0008-6
[Indexed for MEDLINE]
Free PMC Article

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