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Additional treatments included perfusion with triglycerides with 20 mM of \u03b2\u2010hydroxybutyrate and 2 mM of acetoacetate (<jats:italic>n<\/jats:italic> = 5) and perfusion with triglycerides with 70 mM of glucose (<jats:italic>n<\/jats:italic> = 1). Basal vacuolization was produced in all groups, but differed in morphology to that reported in postmortem studies. There was no further increase in vacuolization after 2 h of perfusion compared to 1 h (<jats:italic>p<\/jats:italic> = 0.24), and the addition of ketones did not alter the morphology or extent of vacuolization. This study using an <jats:italic>ex vivo<\/jats:italic> model has confirmed that isolated hypertriglyceridemia is sufficient to cause basal lipid vacuolization in renal tubular epithelial cells, but with different morphology to vacuoles observed in lethal ketoacidosis at autopsy.<\/jats:p>","DOI":"10.1111\/1556-4029.13354","type":"journal-article","created":{"date-parts":[[2016,12,17]],"date-time":"2016-12-17T15:03:22Z","timestamp":1481987002000},"page":"915-920","source":"Crossref","is-referenced-by-count":4,"title":["The Etiology of Basal Vacuolizations in Renal Tubular Epithelial Cells Evaluated in an Isolated Perfused Kidney Model"],"prefix":"10.1111","volume":"62","author":[{"given":"Chong","family":"Zhou","sequence":"first","affiliation":[{"name":"The University of Adelaide Medical School Frome Road Adelaide SA 5005"},{"name":"Forensic Science SA 21 Divett Place Adelaide SA 5000 Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrea 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