TY - JOUR
T1 - APOL1 Risk Variants and Subclinical Cardiovascular Disease in Incident Hemodialysis Patients
AU - Chen, Teresa K.
AU - Fitzpatrick, Jessica
AU - Winkler, Cheryl A.
AU - Binns-Roemer, Elizabeth A.
AU - Corona-Villalobos, Celia P.
AU - Jaar, Bernard G.
AU - Sozio, Stephen M.
AU - Parekh, Rulan S.
AU - Estrella, Michelle M.
N1 - Funding Information:
TKC was previously supported by the Extramural Grant Program by Satellite Healthcare (a not-for-profit renal care provider) and a Clinician Scientist Career Development Award from Johns Hopkins University and is currently supported by the National Institutes of Health and the National Institute of Diabetes and Digestive and Kidney Diseases NIH/NIDDK K08DK117068. The project has been supported in part by the National Institutes of Health and the National Cancer Institute Intramural Research Program (CAW) and under contract HHSN26120080001E. The Predictors of Arrhythmic and Cardiovascular Risk in End-Stage Renal Disease (PACE) study was supported by NIH/NIDDK R01DK72367, the National Center for Research Resources (NCRR) UL1 RR 025005, the Doris Duke Foundation, and the National Kidney Foundation of Maryland. The content of this publication does not necessarily reflect the view or policy of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the government. We thank the participants of the PACE study. We also thank the PACE Study Endpoint Committee: Bernard G. Jaar, MD, MPH (Chair); Michelle M. Estrella MD, MHS; Stephen M. Sozio MD, MHS; Rulan S. Parekh MD, MS; N'Dama Bamba MD; Wei Tsai MD, MS, MPH; Geetha Duvuru, MD; Julia Scialla, MD, MHS; Teresa K. Chen, MD, MHS; Jose Manuel Monroy Trujillo, MD; Frances-LLena Capili, MD; Ijaz Anwar, MD; Lili Zhang, MD; Manisha Ghimire, MD; Raghotham Narayanaswamy, MD; Ramya Ravindran, MD; Svetlana Chembrovich, MD; and Stefan Hemmings, MD. Portions of this work were presented at the 2019 American Society of Nephrology Kidney Week in Washington, DC (November 5–10, 2019). Conception or design (TKC, RSP, MME); Genotyping (CAW, EAB-R); Analysis and interpretation of data, or both (all authors); Drafting of manuscript (TKC) or critical revision of manuscript (all authors); Providing intellectual content of critical importance to the work described (all authors); Supervision (MME).
Funding Information:
TKC was previously supported by the Extramural Grant Program by Satellite Healthcare (a not-for-profit renal care provider) and a Clinician Scientist Career Development Award from Johns Hopkins University and is currently supported by the National Institutes of Health and the National Institute of Diabetes and Digestive and Kidney Diseases NIH/NIDDK K08DK117068. The project has been supported in part by the National Institutes of Health and the National Cancer Institute Intramural Research Program (CAW) and under contract HHSN26120080001E. The Predictors of Arrhythmic and Cardiovascular Risk in End-Stage Renal Disease (PACE) study was supported by NIH/NIDDK R01DK72367, the National Center for Research Resources (NCRR) UL1 RR 025005 , the Doris Duke Foundation, and the National Kidney Foundation of Maryland. The content of this publication does not necessarily reflect the view or policy of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the government. We thank the participants of the PACE study. We also thank the PACE Study Endpoint Committee: Bernard G. Jaar, MD, MPH (Chair); Michelle M. Estrella MD, MHS; Stephen M. Sozio MD, MHS; Rulan S. Parekh MD, MS; N’Dama Bamba MD; Wei Tsai MD, MS, MPH; Geetha Duvuru, MD; Julia Scialla, MD, MHS; Teresa K. Chen, MD, MHS; Jose Manuel Monroy Trujillo, MD; Frances-LLena Capili, MD; Ijaz Anwar, MD; Lili Zhang, MD; Manisha Ghimire, MD; Raghotham Narayanaswamy, MD; Ramya Ravindran, MD; Svetlana Chembrovich, MD; and Stefan Hemmings, MD. Portions of this work were presented at the 2019 American Society of Nephrology Kidney Week in Washington, DC (November 5–10, 2019).
Publisher Copyright:
© 2020 International Society of Nephrology
PY - 2021/2
Y1 - 2021/2
N2 - Introduction: To better understand the impact of APOL1 risk variants in end-stage renal disease (ESRD) we evaluated associations of APOL1 risk variants with subclinical cardiovascular disease (CVD) and mortality among African Americans initiating hemodialysis and enrolled in the Predictors of Arrhythmic and Cardiovascular Risk in ESRD cohort study. Methods: We modeled associations of APOL1 risk status (high = 2; low = 0/1 risk alleles) with baseline subclinical CVD (left ventricular [LV] hypertrophy; LV mass; ejection fraction; coronary artery calcification [CAC]; pulse wave velocity [PWV]) using logistic and linear regression and all-cause or cardiovascular mortality using Cox models, adjusting for age, sex, and ancestry. In sensitivity analyses, we further adjusted for systolic blood pressure and Charlson Comorbidity Index. Results: Of 267 African American participants successfully genotyped for APOL1, 27% were high-risk carriers, 41% were women, and mean age was 53 years. At baseline, APOL1 high- versus low-risk status was independently associated with 50% and 53% lower odds of LV hypertrophy and CAC, respectively, and 10.7% lower LV mass. These associations were robust to further adjustment for comorbidities but not systolic blood pressure. APOL1 risk status was not associated with all-cause or cardiovascular mortality (mean follow-up 2.5 years). Conclusion: Among African American patients with incident hemodialysis, APOL1 high-risk status was associated with better subclinical measures of CVD but not mortality.
AB - Introduction: To better understand the impact of APOL1 risk variants in end-stage renal disease (ESRD) we evaluated associations of APOL1 risk variants with subclinical cardiovascular disease (CVD) and mortality among African Americans initiating hemodialysis and enrolled in the Predictors of Arrhythmic and Cardiovascular Risk in ESRD cohort study. Methods: We modeled associations of APOL1 risk status (high = 2; low = 0/1 risk alleles) with baseline subclinical CVD (left ventricular [LV] hypertrophy; LV mass; ejection fraction; coronary artery calcification [CAC]; pulse wave velocity [PWV]) using logistic and linear regression and all-cause or cardiovascular mortality using Cox models, adjusting for age, sex, and ancestry. In sensitivity analyses, we further adjusted for systolic blood pressure and Charlson Comorbidity Index. Results: Of 267 African American participants successfully genotyped for APOL1, 27% were high-risk carriers, 41% were women, and mean age was 53 years. At baseline, APOL1 high- versus low-risk status was independently associated with 50% and 53% lower odds of LV hypertrophy and CAC, respectively, and 10.7% lower LV mass. These associations were robust to further adjustment for comorbidities but not systolic blood pressure. APOL1 risk status was not associated with all-cause or cardiovascular mortality (mean follow-up 2.5 years). Conclusion: Among African American patients with incident hemodialysis, APOL1 high-risk status was associated with better subclinical measures of CVD but not mortality.
KW - APOL1
KW - ESRD
KW - cardiovascular disease
KW - hemodialysis
KW - mortality
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U2 - 10.1016/j.ekir.2020.11.006
DO - 10.1016/j.ekir.2020.11.006
M3 - Article
C2 - 33615058
AN - SCOPUS:85099477500
SN - 2468-0249
VL - 6
SP - 333
EP - 341
JO - Kidney International Reports
JF - Kidney International Reports
IS - 2
ER -