title: Target organ damage in African American hypertension: role of APOL1.
abstract: Apolipoprotein L1 (APOL1) gene association studies and results of the African American Study of Kidney Disease and Hypertension are disproving the longstanding concept that mild to moderate essential hypertension contributes substantially to end-stage renal disease susceptibility in African Americans. APOL1 coding variants underlie a spectrum of kidney diseases, including that attributed to hypertension (labeled arteriolar or hypertensive nephrosclerosis), focal segmental glomerulosclerosis, and HIV-associated nephropathy. APOL1 nephropathy risk variants persist because of protection afforded from the parasite that causes African sleeping sickness. This breakthrough will lead to novel treatments for hypertensive African Americans with low-level proteinuria, for whom effective therapies are lacking. Furthermore, APOL1 nephropathy risk variants contribute to racially variable allograft survival rates after kidney transplantation and assist in detecting nondiabetic forms of nephropathy in African Americans with diabetes. Discovery of APOL1-associated nephropathy was a major success of the genetics revolution, demonstrating that secondary hypertension is typically present in nondiabetic African Americans with nephropathy.
authors: Section on Nephrology, Wake Forest School of Medicine, Winston-Salem, NC 27157-1053, USA. bfreedma@wakehealth.edu
authors: Barry I
authors: BI
authors: Freedman
authors: Mariana
authors: M
authors: Murea
mesh_terms: D001741:Black or African American / Q000235:genetics*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000075944:Apolipoprotein L1; D001053:Apolipoproteins / Q000235:genetics*; D015331:Cohort Studies; D005192:Family Health; D020022:Genetic Predisposition to Disease; D055106:Genome-Wide Association Study; D005919:Glomerular Filtration Rate; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy / Q000208:ethnology / Q000235:genetics / Q000503:physiopathology; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics; D007676:Kidney Failure, Chronic / Q000150:complications / Q000208:ethnology / Q000235:genetics / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000473:pathology / Q000503:physiopathology; D008075:Lipoproteins, HDL / Q000235:genetics*; D008565:Membrane Proteins / Q000235:genetics; D020409:Molecular Motor Proteins / Q000235:genetics; D018995:Myosin Heavy Chains / Q000235:genetics; D020641:Polymorphism, Single Nucleotide; D011507:Proteinuria / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D012307:Risk Factors; D017211:Treatment Failure
chemical_list: C108666:APOL1 protein, human; D000806:Angiotensin-Converting Enzyme Inhibitors; D000075944:Apolipoprotein L1; D001053:Apolipoproteins; D047908:Intracellular Signaling Peptides and Proteins; D008075:Lipoproteins, HDL; C103814:MYH9 protein, human; D008565:Membrane Proteins; D020409:Molecular Motor Proteins; C407223:NPHS2 protein; D018995:Myosin Heavy Chains