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Front Pediatr. 2016 Nov 17;4:122. eCollection 2016.

Renal and Cardiovascular Morbidities Associated with APOL1 Status among African-American and Non-African-American Children with Focal Segmental Glomerulosclerosis.

Author information

1
Stony Brook Children's Hospital , Stony Brook, NY , USA.
2
Johns Hopkins Bloomberg School of Public Health , Baltimore, MD , USA.
3
Basic Research Laboratory, Frederick National Laboratory, NCI, NIH, Leidos Biomedical , Frederick, MD , USA.
4
Pediatric Nephrology, Children's Hospital at Montefiore , Bronx, NY , USA.
5
Division of Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center , Cincinnati, OH , USA.
6
Division of Pediatric Nephrology, University of Michigan School of Medicine , Ann Arbor, MI , USA.
7
Pediatric Nephrology, University of New Mexico , Albuquerque, NM , USA.
8
Division of Pediatric Nephrology, Children's Mercy Hospital , Kansas City, MO , USA.
9
University of Pennsylvania , Philadelphia, PA , USA.
10
NIDDK, NIH , Bethesda, MD , USA.

Abstract

BACKGROUND AND OBJECTIVES:

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 how APOL1 genotypes contribute to kidney disease risk, progression, and cardiovascular morbidity in children.

DESIGN SETTING PARTICIPANTS AND MEASUREMENTS:

We examined the prevalence of APOL1 genotypes 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) APOL1 genotypes 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 HR APOL1 (89%; 25/28). Of 32 AA children with FSGS, 25 (78%) had HR APOL1. Compared to children with low risk APOL1 and FSGS (comprising 36 non-AA and 7 AA), children with HR APOL1 developed 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.

CONCLUSION:

AA children with HR APOL1 genotype 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.

KEYWORDS:

FSGS; cardiovascular; children; chronic renal disease; left ventricular hypertrophy

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