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<jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Higher serum intact fibroblast growth factor 23 (iFGF23) was associated with disease progression in participants with autosomal dominant polycystic kidney disease (ADPKD) in the HALT-PKD Studies. PKD mutation is also an important determinant of progression. We hypothesized that serum levels of iFGF23 and vitamin D metabolites (1,25-dihydroxyvitamin D [1,25(OH)\n                      <jats:sub>2<\/jats:sub>\n                      D] and 25-hydroxyvitamin D [25[OH]D]) differ according to ADPKD mutation and differentially predict clinical end points according to genotype (significant interaction between genotype and mineral metabolites).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      A total of 864 individuals with ADPKD who participated in the HALT-PKD Study A or B and had measurements of mineral metabolites (1,25[OH]\n                      <jats:sub>2<\/jats:sub>\n                      D, 25[OH]D, iFGF23) were categorized by PKD mutation (PKD1 truncating, PKD1 nontruncating, PKD2, or no mutation detected [NMD]). The association of the interactions of genotype \u00d7 iFGF23, genotype \u00d7 1,25(OH)2D, and genotype \u00d7 25(OH)D with (\n                      <jats:italic toggle=\"yes\">1<\/jats:italic>\n                      ) annualized change in eGFR; (\n                      <jats:italic toggle=\"yes\">2<\/jats:italic>\n                      ) mean annualized percentage change in height-corrected total kidney volume (Study A only); and (\n                      <jats:italic toggle=\"yes\">3<\/jats:italic>\n                      ) time to a composite of 50% reduction in eGFR, ESKD, or death were evaluated using linear regression and Cox proportional hazards regression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Median (interquartile range) iFGF23 differed (PKD1 truncating, 55.8 [40.7\u201376.8]; PKD1 nontruncating, 49.9 [37.7\u201371.0]; PKD2, 49.0 [33.8\u201370.5]; NMD, 50.3 [39.7\u201367.4] pg\/ml;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.03) and mean\u00b1SD 1,25(OH)\n                      <jats:sub>2<\/jats:sub>\n                      D differed (PKD1 truncating, 32.8\u00b112.8; PKD1 nontruncating, 33.4\u00b112.5; PKD2, 34.1\u00b113.1; NMD, 38.0\u00b114.6 pg\/ml;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.02) according to PKD genotype. There was a significant interaction between iFGF23 and genotype (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.02) for the composite end point in fully adjusted models, but no significant interaction between 1,25(OH)\n                      <jats:sub>2<\/jats:sub>\n                      D or 25(OH)D and genotype for clinical end points.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>ADPKD genotype interacts significantly with FGF23 to influence clinical end points. Whereas the worst outcomes were in individuals with a PKD1-truncating or -nontruncating mutation and the highest iFGF23 tertile, risk of the composite end point differed according to iFGF23 the most in the PKD1-nontruncating and PKD2 groups.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.34067\/kid.0001692020","type":"journal-article","created":{"date-parts":[[2020,5,12]],"date-time":"2020-05-12T21:55:14Z","timestamp":1589320514000},"page":"648-656","source":"Crossref","is-referenced-by-count":8,"title":["Interactions between FGF23 and Genotype in Autosomal Dominant Polycystic Kidney Disease"],"prefix":"10.34067","volume":"1","author":[{"given":"Laura","family":"Grau","sequence":"first","affiliation":[{"name":"Department of Biostatistics and Informatics, University of Colorado Anschutz Medical Campus, Aurora, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Berenice","family":"Gitomer","sequence":"additional","affiliation":[{"name":"Division of Renal 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