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Publication Information
Affiliation
Department of Biostatistics and Informatics, University of Colorado Anschutz Medical Campus, Aurora, Colorado.; Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus, Aurora, Colorado.; Department of Biostatistics and Informatics, University of Colorado Anschutz Medical Campus, Aurora, Colorado.; Division of Nephrology, Duke University, Durham, North Carolina.; Division of Nephrology & Hypertension, Mayo Clinic, Rochester, Minnesota.; Department of Biostatistics and Informatics, University of Colorado Anschutz Medical Campus, Aurora, Colorado.; Division of Nephrology & Hypertension, Mayo Clinic, Rochester, Minnesota.; Renal Division, Beth Israel Deaconess Medical Center, Boston, Massachusetts.; Division of Nephrology and Hypertension, University of Kansas Medical Center, Kansas City, Kansas.; Section of Nephrology, University of Chicago, Chicago, Illinois.; Department of Biostatistics and Informatics, University of Colorado Anschutz Medical Campus, Aurora, Colorado.; Department of Biostatistics and Informatics, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
Authors
Grau Laura, Gitomer Berenice, McNair Bryan, Wolf Myles, Harris Peter, Brosnahan Godela, Torres Vicente, Steinman Theodore, Yu Alan, Chapman Arlene, Chonchol Michel, Nowak Kristen L
Studies
Abstract
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)2D] 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).