Journal
AMERICAN JOURNAL OF KIDNEY DISEASES
Volume 72, Issue 5, Pages S8-S16Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1053/j.ajkd.2018.06.020
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Funding
- Frank M. Norfleet Forum for Advancement of Health
- Community Foundation of Greater Memphis
- University of Tennessee Health Science Center
- Intramural Research Program, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), NIH
- NIH [R01 DK084149, R01 DK070941]
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Genetic methodologies are improving our understanding of the pathophysiology in diverse diseases. Breakthroughs have been particularly impressive in nephrology, for which marked disparities exist in rates and etiologic classifications of end-stage kidney disease between African Americans and European Americans. Discovery of the apolipoprotein L1 gene (APOL1) association with focal segmental glomerulosclerosis, human immunodeficiency virus (HIV)-associated nephropathy, lupus nephritis, sickle cell nephropathy, and solidified glomerulosclerosis, as well as more rapid failure of transplanted kidneys from donors with APOL1 renal-risk genotypes, has improved our understanding of nondiabetic nephropathy. Environmental factors acting through natural selection in sub-Saharan African populations likely underlie this association. This article describes the discovery of chromosome 22q renal-risk variants and their worldwide distribution, reviews the epidemiology and pathology of APOL1-associated nephropathies, and explores several proposed mechanisms of kidney injury identified in cell culture and animal models. Detection of APOL1 associations with kidney diseases and delineation of injury pathways brings hope for effective treatment for these kidney diseases.
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