{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T16:10:25Z","timestamp":1790266225787,"version":"4.1.0"},"reference-count":29,"publisher":"Springer Science and Business Media LLC","issue":"11","license":[{"start":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T00:00:00Z","timestamp":1781222400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T00:00:00Z","timestamp":1781222400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Pediatr Nephrol"],"published-print":{"date-parts":[[2026,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      <jats:italic>APOL1<\/jats:italic>\n                      variants confer increased risk for kidney disease in individuals of African ancestry, particularly in homozygous or compound heterozygous states. A missense variant, p.N264K, has been shown to attenuate this risk when co-inherited with the G2 allele. While these associations are established in adults, data in pediatric populations remain limited. Using the University of Tennessee Health Science Biorepository and Integrative Genomics initiative, we assessed chronic kidney disease (CKD) risk by\n                      <jats:italic>APOL1<\/jats:italic>\n                      high-risk genotype and the potential protective effect of p.N264K in a diverse pediatric cohort.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      This is a case\u2013control study of African American children enrolled in the BIG initiative at Le Bonheur Children\u2019s Hospital (2014\u20132022). Composite CKD was defined by eGFR\u2009&lt;\u200990\u00a0mL\/min\/1.73 m\n                      <jats:sup>2<\/jats:sup>\n                      or albuminuria (UACR\u2009&gt;\u200930\u00a0mg\/g) on two occasions\u2009\u2265\u200990\u00a0days apart. The p.N264K variant status was assessed in patients with\n                      <jats:italic>APOL1<\/jats:italic>\n                      high-risk (HR). Logistic regression models adjusted for age, sex, and five principal components of ancestry assessed associations with CKD and albuminuria.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      CKD cases had 8% higher odds of\n                      <jats:italic>APOL1<\/jats:italic>\n                      HR status (Odds Ratio (OR): 1.08, 95% Confidence Interval (CI): 0.88\u20131.33). Stronger associations were observed in cases with albuminuria and\n                      <jats:italic>APOL1<\/jats:italic>\n                      HR status (OR: 1.41, 95% CI: 1.02\u20131.92, p\u2009=\u20090.03). The p.N264K variant was detected in 4.3% of cases and 4.5% of controls, and appeared to attenuate CKD risk among HR individuals, though sample size limited statistical power.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      <jats:italic>APOL1<\/jats:italic>\n                      HR genotypes were associated with albuminuria in African American children. The p.N264K variant may modify this risk, warranting further study.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s00467-026-07385-5","type":"journal-article","created":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T14:15:58Z","timestamp":1781273758000},"page":"4057-4063","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["APOL1 and chronic kidney disease in pediatrics: a study from the Biorepository and Integrative Genomics Initiative"],"prefix":"10.1007","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3631-7195","authenticated-orcid":false,"given":"Rima S.","family":"Zahr","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lokesh","family":"Chinthala","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akram","family":"Mohammed","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Csaba P.","family":"Kovesdy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert L.","family":"Davis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,6,12]]},"reference":[{"key":"7385_CR1","doi-asserted-by":"publisher","first-page":"215","DOI":"10.1097\/PAP.0000000000000221","volume":"26","author":"JB Kopp","year":"2019","unstructured":"Kopp JB, Rosenberg AZ (2019) One actor, many roles: histopathologies associated with APOL1 genetic variants. 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