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The authors demonstrate that crystal formation, deposition, and clearance, as well as the resulting renal tubular injury, inflammation, fibrosis, and loss of kidney function, are virtually identical in experimental rodent models induced by an adenine-enriched diet and in patients with adenine phosphoribosyltransferase deficiency. These models are thus suitable to study cellular mechanisms, such as crystal clearance (\n                      <jats:italic toggle=\"yes\">via<\/jats:italic>\n                      a reparative process the authors call extratubulation), or to identify relevant molecular pathways, such as TNF receptor 1\u2013dependent crystal retention, that might inform the development of novel treatments.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Hereditary deficiency of adenine phosphoribosyltransferase causes 2,8-dihydroxyadenine (2,8-DHA) nephropathy, a rare condition characterized by formation of 2,8-DHA crystals within renal tubules. Clinical relevance of rodent models of 2,8-DHA crystal nephropathy induced by excessive adenine intake is unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Using animal models and patient kidney biopsies, we assessed the pathogenic sequelae of 2,8-DHA crystal-induced kidney damage. We also used knockout mice to investigate the role of TNF receptors 1 and 2 (TNFR1 and TNFR2), CD44, or alpha2-HS glycoprotein (AHSG), all of which are involved in the pathogenesis of other types of crystal-induced nephropathies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Adenine-enriched diet in mice induced 2,8-DHA nephropathy, leading to progressive kidney disease, characterized by crystal deposits, tubular injury, inflammation, and fibrosis. Kidney injury depended on crystal size. The smallest crystals were endocytosed by tubular epithelial cells. Crystals of variable size were excreted in urine. Large crystals obstructed whole tubules. Medium-sized crystals induced a particular reparative process that we term\n                      <jats:italic toggle=\"yes\">extratubulation<\/jats:italic>\n                      . In this process, tubular cells, in coordination with macrophages, overgrew and translocated crystals into the interstitium, restoring the tubular luminal patency; this was followed by degradation of interstitial crystals by granulomatous inflammation. Patients with adenine phosphoribosyltransferase deficiency showed similar histopathological findings regarding crystal morphology, crystal clearance, and renal injury. In mice, deletion of\n                      <jats:italic toggle=\"yes\">Tnfr1<\/jats:italic>\n                      significantly reduced tubular CD44 and annexin two expression, as well as inflammation, thereby ameliorating the disease course. In contrast, genetic deletion of\n                      <jats:italic toggle=\"yes\">Tnfr2<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">Cd44<\/jats:italic>\n                      , or\n                      <jats:italic toggle=\"yes\">Ahsg<\/jats:italic>\n                      had no effect on the manifestations of 2,8-DHA nephropathy.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Rodent models of the cellular and molecular mechanisms of 2,8-DHA nephropathy and crystal clearance have clinical relevance and offer insight into potential future targets for therapeutic interventions.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2019080827","type":"journal-article","created":{"date-parts":[[2020,2,21]],"date-time":"2020-02-21T15:29:22Z","timestamp":1582298962000},"page":"799-816","source":"Crossref","is-referenced-by-count":94,"title":["Cellular and Molecular Mechanisms of Kidney Injury in 2,8-Dihydroxyadenine Nephropathy"],"prefix":"10.1681","volume":"31","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1566-7129","authenticated-orcid":false,"given":"Barbara Mara","family":"Klinkhammer","sequence":"first","affiliation":[{"name":"Institute of Pathology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sonja","family":"Djudjaj","sequence":"additional","affiliation":[{"name":"Institute of Pathology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Uta","family":"Kunter","sequence":"additional","affiliation":[{"name":"Division of Nephrology and 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Iceland;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sverrir","family":"Hardarson","sequence":"additional","affiliation":[{"name":"Department of Pathology Landspitali\u2013The National University Hospital of Iceland, Reykjavik, Iceland;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7548-4327","authenticated-orcid":false,"given":"Orestes","family":"Foresto-Neto","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Klinikum der Universit\u00e4t, LMU M\u00fcnchen, Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shrikant R.","family":"Mulay","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Klinikum der Universit\u00e4t, LMU M\u00fcnchen, Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcus Johannes","family":"Moeller","sequence":"additional","affiliation":[{"name":"Division of Nephrology and 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