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Genome-Wide Association of CKD Progression: The Chronic Renal Insufficiency Cohort Study

  1. Author:
    Parsa, A.
    Kanetsky, P. A.
    Xiao, R.
    Gupta, J.
    Mitra, N.
    Limou, Sophie
    Xie, D.
    Xu, H.
    Anderson, A. H.
    Ojo, A.
    Kusek, J. W.
    Lora, C. M.
    Hamm, L. L.
    He, J.
    Sandholm, N.
    Jeff, J.
    Raj, D. E.
    Boger, C. A.
    Bottinger, E.
    Salimi, S.
    Parekh, R. S.
    Adler, S. G.
    Langefeld, C. D.
    Bowden, D. W.
    Groop, P. H.
    Forsblom, C.
    Freedman, B. I.
    Lipkowitz, M.
    Fox, C. S.
    Winkler, C. A.
    Feldman, H. I.

  2. Author Address

    Division of Nephrology and Department of Medicine, Baltimore Veterans Affairs Medical Center, Baltimore, Maryland; aparsa@medicine.umaryland.edu. Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida. Department of Biostatistics and Epidemiology and. Department of Health Sciences, College of Health Professions and Social Work, Florida Gulf Coast University, Fort Myers, FL. Molecular Genetic Epidemiology Section, Basic Research Laboratory, Center for Cancer Research, National Cancer Institute and Basic Science Program, Leidos Biomedical Research, Inc., Frederick National Laboratory, Frederick, Maryland. Departments of Medicine and. Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia, Pennsylvania. Division of Nephrology, University of Michigan, Ann Arbor, Michigan. Division of Kidney, Urologic and Hematologic Diseases, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. Department of Medicine, Division of Nephrology, University of Illinois at Chicago, Chicago, Illinois. Department of Medicine, Section of Nephrology, Tulane University, New Orleans, Louisiana. Folkhalsan Institute of Genetics, Folkhalsan Research Center, Helsinki, Finland; Abdominal Center Nephrology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland; Research Programs Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland. Department of Medicine, The Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine Mount Sinai, New York, New York. Department of Medicine, The George Washington University School of Medicine, Washington, DC. Department of Nephrology, University Hospital Regensburg, Regensburg, Germany. Epidemiology and Public Health, University of Maryland School of Medicine, Baltimore, Maryland. Division of Nephrology, Department of Pediatrics and Medicine, Hospital for Sick Children, University Health Network and the University of Toronto, Toronto, Ontario, Canada. Department of Medicine, Division of Nephrology and Hypertension, Harbor-University of California, Los Angeles Medical Center, Los Angeles, California. Departments of Biostatistical Sciences and. Biochemistry and. Department of Internal Medicine, Section on Nephrology, Wake Forest School of Medicine, Winston-Salem, North Carolina. Department of Medicine, Georgetown University Medical Center, Washington, DC; and. Division of Intramural Research, National Heart, Lung and Blood Institute's Framingham Heart Study, National Heart, Lung and Blood Institute, Framingham, Massachusetts.
    1. Year: 2017
    2. Date: Mar
    3. Epub Date: 10/11/2016
  2. Journal: Journal of the American Society of Nephrology : JASN
    1. 28
    2. 3
    3. Pages: 923-934
  4. Type of Article: Article
  5. ISSN: 1046-6673
  1. Abstract:

    The rate of decline of renal function varies significantly among individuals with CKD. To understand better the contribution of genetics to CKD progression, we performed a genome-wide association study among participants in the Chronic Renal Insufficiency Cohort Study. Our outcome of interest was CKD progression measured as change in eGFR over time among 1331 blacks and 1476 whites with CKD. We stratified all analyses by race and subsequently, diabetes status. Single-nucleotide polymorphisms (SNPs) that surpassed a significance threshold of P< 1x10-6 for association with eGFR slope were selected as candidates for follow-up and secondarily tested for association with proteinuria and time to ESRD. We identified 12 such SNPs among black patients and six such SNPs among white patients. We were able to conduct follow-up analyses of three candidate SNPs in similar (replication) cohorts and eight candidate SNPs in phenotype-related (validation) cohorts. Among blacks without diabetes, rs653747 in LINC00923 replicated in the African American Study of Kidney Disease and Hypertension cohort (discovery P=5.42x10-7; replication P=0.039; combined P=7.42x10-9). This SNP also associated with ESRD (hazard ratio, 2.0 (95% confidence interval, 1.5 to 2.7); P=4.90x10-6). Similarly, rs931891 in LINC00923 associated with eGFR decline (P=1.44x10-4) in white patients without diabetes. In summary, SNPs in LINC00923, an RNA gene expressed in the kidney, significantly associated with CKD progression in individuals with nondiabetic CKD. However, the lack of equivalent cohorts hampered replication for most discovery loci. Further replication of our findings in comparable study populations is warranted.

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External Sources

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  2. DOI: 10.1681/asn.2015101152
  3. PMID: 27729571
  4. View record in Web of Science®
  5. WOS: 000395049000022

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