AUTHOR=Woroniecki Robert P. , Ng Derek K. , Limou Sophie , Winkler Cheryl A. , Reidy Kimberly J. , Mitsnefes Mark , Sampson Matthew G. , Wong Craig S. , Warady Bradley A. , Furth Susan L. , Kopp Jeffrey B. , Kaskel Frederick J. 

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

JOURNAL=Frontiers in Pediatrics

VOLUME=4

YEAR=2016

URL=https://www.frontiersin.org/journals/pediatrics/articles/10.3389/fped.2016.00122

DOI=10.3389/fped.2016.00122

ISSN=2296-2360

ABSTRACT=<sec id="ST1"><title>Background and objectives</title><p>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 <italic>APOL1</italic> genotypes contribute to kidney disease risk, progression, and cardiovascular morbidity in children.</p></sec><sec id="ST2"><title>Design, setting, participants, and measurements</title><p>We examined the prevalence of <italic>APOL1</italic> 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.</p></sec><sec id="ST3"><title>Results</title><p>A total of 140 AA children in the CKiD study were genotyped. High risk (HR) <italic>APOL1</italic> genotypes were present in 24% of AA children (33/140) and were associated with FSGS, <italic>p</italic> &lt; 0.001. FSGS was the most common cause of glomerular disease in children with HR <italic>APOL1</italic> (89%; 25/28). Of 32 AA children with FSGS, 25 (78%) had HR <italic>APOL1</italic>. Compared to children with low risk <italic>APOL1</italic> and FSGS (comprising 36 non-AA and 7 AA), children with HR <italic>APOL1</italic> developed FSGS at a later age, 12.0 (IQR: 9.5, 12.5) vs. 5.5 (2.5, 11.5) years, <italic>p</italic> = 0.004, had a higher prevalence of uncontrolled hypertension (52 vs. 33%, <italic>p</italic> = 0.13), left ventricular hypertrophy (LVH) (53 vs. 12%, <italic>p</italic> &lt; 0.01), C-reactive protein &gt; 3 mg/l (33 vs. 15%, <italic>p</italic> = 0.12), and obesity (48 vs. 19%, <italic>p</italic> = 0.01). There were no differences in glomerular filtration rate, hemoglobin, iPTH, or calcium–phosphate product.</p></sec><sec id="ST4"><title>Conclusion</title><p>AA children with HR <italic>APOL1</italic> 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.</p></sec>