{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"medRxiv"}],"indexed":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T12:41:58Z","timestamp":1768567318906,"version":"3.49.0"},"posted":{"date-parts":[[2024,11,5]]},"group-title":"Genetic and Genomic Medicine","reference-count":112,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2024,11,5]],"date-time":"2024-11-05T00:00:00Z","timestamp":1730764800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.medrxiv.org\/about\/FAQ#license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2024,11,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                <jats:p>\n                  The disproportionate risk for idiopathic proteinuric podocytopathies in Black people is explained, in part, by the presence of two risk alleles (G1 or G2) in the\n                  <jats:italic>APOL1<\/jats:italic>\n                  gene. The pathogenic mechanisms responsible for this genetic association remain incompletely understood. We analyzed glomerular RNASeq transcriptomes from patients with idiopathic nephrotic syndrome of which 72 had inferred African ancestry (AA) and 152 did not (noAA). Using gene coexpression networks we found a significant association between\n                  <jats:italic>APOL1<\/jats:italic>\n                  risk allele number and the coexpression metamodule 2 (MM2), even after adjustment for eGFR and proteinuria at biopsy. Unadjusted Kaplan-Meier curves showed that unlike noAA, AA with the highest tertile of MM2 gene activation scores were less likely to achieve complete remission (p\u22640.014). Characteristic direction (ChDir) identified a signature of 1481 genes, which separated patients with\n                  <jats:italic>APOL1<\/jats:italic>\n                  risk alleles from those homozygous for reference\n                  <jats:italic>APOL1<\/jats:italic>\n                  . Only in AA, the tertile with the highest activation scores of these 1481 genes was less likely to achieve complete remission (p\u22640.022) and showed a trend to faster progression to the composite event of kidney failure or loss of 40% eGFR (p\u22640.099). The MM2 and ChDir genes significantly overlapped and were both enriched for Epithelial Mesenchymal Transition and inflammation terms. Finally, MM2 significantly overlapped with a parietal epithelial cell (PEC)-identity gene signature but not with a podocyte identity signature. Podocytes expressing variant APOL1s may generate inflammatory signals that activate PECs by paracrine mechanisms contributing to\n                  <jats:italic>APOL1<\/jats:italic>\n                  nephropathy.\n                <\/jats:p>","DOI":"10.1101\/2024.11.05.24316766","type":"posted-content","created":{"date-parts":[[2024,11,6]],"date-time":"2024-11-06T00:20:12Z","timestamp":1730852412000},"source":"Crossref","is-referenced-by-count":0,"title":["Analysis of Glomerular Transcriptomes from Nephrotic Patients Suggest\n                  <i>APOL1<\/i>\n                  Risk Variants Impact Parietal Epithelial Cells"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3682-0815","authenticated-orcid":false,"given":"Agustin","family":"Gonzalez-Vicente","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dana C.","family":"Crawford","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William S.","family":"Bush","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhenzhen","family":"Wu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Leslie A.","family":"Bruggeman","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Viji","family":"Nair","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Felix","family":"Eichinger","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Oliver","family":"Wessely","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthias","family":"Kretzler","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John F.","family":"O\u2019Toole","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John R.","family":"Sedor","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"name":"Kidney Precision Medicine Project","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"name":"Nephrotic Syndrome Study Network","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"54368","reference":[{"key":"2024110818201740000_2024.11.05.24316766v1.1","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-023-43020-9"},{"key":"2024110818201740000_2024.11.05.24316766v1.2","doi-asserted-by":"publisher","DOI":"10.1016\/j.kint.2019.07.010"},{"key":"2024110818201740000_2024.11.05.24316766v1.3","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2022020213"},{"issue":"1","key":"2024110818201740000_2024.11.05.24316766v1.4","first-page":"75","article-title":"APOL1 and APOL1-Associated Kidney Disease: A Common Disease, an Unusual Disease Gene - Proceedings of the Henry Shavelle Professorship","volume":"3","year":"2023","journal-title":"Glomerular Dis"},{"key":"2024110818201740000_2024.11.05.24316766v1.5","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1522913113"},{"key":"2024110818201740000_2024.11.05.24316766v1.6","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2020010079"},{"key":"2024110818201740000_2024.11.05.24316766v1.7","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.51185"},{"key":"2024110818201740000_2024.11.05.24316766v1.8","doi-asserted-by":"crossref","unstructured":"Datta, S. , et al., APOL1-mediated monovalent cation transport contributes to APOL1-mediated podocytopathy in kidney disease. 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