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Studies of families with hereditary NL and NC have identified &amp;gt;30 causative genes that have increased our understanding of extracellular calcium homeostasis and renal tubular transport of calcium. However, these account for &amp;lt;20% of the likely genes that are involved, and to identify novel genes for renal calcification disorders, we investigated 1745 12-month-old progeny from a male mouse that had been treated with the chemical mutagen N-ethyl-N-nitrosourea (ENU) for radiological renal opacities. This identified a male mouse with renal calcification that was inherited as an autosomal dominant trait with &amp;gt;80% penetrance in 152 progeny. The calcification consisted of calcium phosphate deposits in the renal papillae and was associated with the presence of the urinary macromolecules osteopontin and Tamm-Horsfall protein, which are features found in Randall's plaques of patients with NC. Genome-wide mapping located the disease locus to a \u223c30\u2009Mbp region on chromosome 17A3.3-B3 and whole-exome sequence analysis identified a heterozygous mutation, resulting in a missense substitution (Met149Thr, M149T), in the bromodomain-containing protein 4 (BRD4). The mutant heterozygous (Brd4+\/M149T) mice, when compared with wild-type (Brd4+\/+) mice, were normocalcemic and normophosphatemic, with normal urinary excretions of calcium and phosphate, and had normal bone turnover markers. BRD4 plays a critical role in histone modification and gene transcription, and cDNA expression profiling, using kidneys from Brd4+\/M149T and Brd4+\/+ mice, revealed differential expression of genes involved in vitamin D metabolism, cell differentiation, and apoptosis. Kidneys from Brd4+\/M149T mice also had increased apoptosis at sites of calcification within the renal papillae. Thus, our studies have established a mouse model, due to a Brd4 Met149Thr mutation, for inherited NC. \u00a9 2019 American Society for Bone and Mineral Research.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jbmr.3695","type":"journal-article","created":{"date-parts":[[2019,3,4]],"date-time":"2019-03-04T19:04:16Z","timestamp":1551726256000},"page":"1324-1335","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Mice with a Brd4 Mutation Represent a New Model of Nephrocalcinosis"],"prefix":"10.1093","volume":"34","author":[{"given":"Caroline M","family":"Gorvin","sequence":"first","affiliation":[{"name":"Academic Endocrine UnitOxford Centre for Diabetes, Endocrinology, and MetabolismRadcliffe Department of MedicineUniversity of OxfordOxfordUK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nellie Y","family":"Loh","sequence":"additional","affiliation":[{"name":"Academic Endocrine UnitOxford Centre for 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