title: Renal and Cardiovascular Morbidities Associated withAPOL1Status among African-American and Non-African-American Children with Focal Segmental Glomerulosclerosis.
abstract: OBJECTIVE
  African-American (AA) children with focal segmental glomerulosclerosis (FSGS) have later onset disease that progresses more rapidly than in non-AA children. It is unclear howAPOL1genotypes contribute to kidney disease risk, progression, and cardiovascular morbidity in children.
  We examined the prevalence ofAPOL1genotypes and associated cardiovascular phenotypes among children with FSGS in the Chronic Kidney Disease in Children (CKiD) study; an ongoing multicenter prospective cohort study of children aged 1-16 years with mild to moderate kidney disease.
  
  
  RESULTS
  A total of 140 AA children in the CKiD study were genotyped. High risk (HR)APOL1genotypes were present in 24% of AA children (33/140) and were associated with FSGS,p< 0.001. FSGS was the most common cause of glomerular disease in children with HRAPOL1(89%; 25/28). Of 32 AA children with FSGS, 25 (78%) had HRAPOL1. Compared to children with low riskAPOL1and FSGS (comprising 36 non-AA and 7 AA), children with HRAPOL1developed FSGS at a later age, 12.0 (IQR: 9.5, 12.5) vs. 5.5 (2.5, 11.5) years,p= 0.004, had a higher prevalence of uncontrolled hypertension (52 vs. 33%,p= 0.13), left ventricular hypertrophy (LVH) (53 vs. 12%,p< 0.01), C-reactive protein > 3 mg/l (33 vs. 15%,p= 0.12), and obesity (48 vs. 19%,p= 0.01). There were no differences in glomerular filtration rate, hemoglobin, iPTH, or calcium-phosphate product.
  
  
  CONCLUSIONS
  AA children with HRAPOL1genotype and FSGS have increase prevalence of obesity and LVH despite a later age of FSGS onset, while adjusting for socioeconomic status. Treatment of obesity may be an important component of chronic kidney disease and LVH management in this population.
authors.affiliation: Stony Brook Children's Hospital , Stony Brook, NY , USA.
authors.forename: Robert P
authors.initials: RP
authors.lastname: Woroniecki
authors.affiliation: Johns Hopkins Bloomberg School of Public Health , Baltimore, MD , USA.
authors.forename: Derek K
authors.initials: DK
authors.lastname: Ng
authors.affiliation: Basic Research Laboratory, Frederick National Laboratory, NCI, NIH, Leidos Biomedical , Frederick, MD , USA.
authors.forename: Sophie
authors.initials: S
authors.lastname: Limou
authors.affiliation: Basic Research Laboratory, Frederick National Laboratory, NCI, NIH, Leidos Biomedical , Frederick, MD , USA.
authors.forename: Cheryl A
authors.initials: CA
authors.lastname: Winkler
authors.affiliation: Pediatric Nephrology, Children's Hospital at Montefiore , Bronx, NY , USA.
authors.forename: Kimberly J
authors.initials: KJ
authors.lastname: Reidy
authors.affiliation: Division of Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center , Cincinnati, OH , USA.
authors.forename: Mark
authors.initials: M
authors.lastname: Mitsnefes
authors.affiliation: Division of Pediatric Nephrology, University of Michigan School of Medicine , Ann Arbor, MI , USA.
authors.forename: Matthew G
authors.initials: MG
authors.lastname: Sampson
authors.affiliation: Pediatric Nephrology, University of New Mexico , Albuquerque, NM , USA.
authors.forename: Craig S
authors.initials: CS
authors.lastname: Wong
authors.affiliation: Division of Pediatric Nephrology, Children's Mercy Hospital , Kansas City, MO , USA.
authors.forename: Bradley A
authors.initials: BA
authors.lastname: Warady
authors.affiliation: University of Pennsylvania , Philadelphia, PA , USA.
authors.forename: Susan L
authors.initials: SL
authors.lastname: Furth
authors.affiliation: NIDDK, NIH , Bethesda, MD , USA.
authors.forename: Jeffrey B
authors.initials: JB
authors.lastname: Kopp
authors.affiliation: Pediatric Nephrology, Children's Hospital at Montefiore , Bronx, NY , USA.
authors.forename: Frederick J
authors.initials: FJ
authors.lastname: Kaskel
keywords: FSGS; cardiovascular; children; chronic renal disease; left ventricular hypertrophy