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Basal Renal Tubular Epithelial Cell Vacuolization and Alcoholic Ketoacidosis

Authors

  • Chong Zhou,

    1. The University of Adelaide Medical School, Frome Road, Adelaide, SA 5005, Australia.
    2. Forensic Science SA, 21 Divett Place, Adelaide, SA 5000, Australia.
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  • Roger W. Byard M.D.

    1. The University of Adelaide Medical School, Frome Road, Adelaide, SA 5005, Australia.
    2. Forensic Science SA, 21 Divett Place, Adelaide, SA 5000, Australia.
    Search for more papers by this author

Additional information and reprint requests:
Prof. Roger W. Byard, M.B.B.S., M.D.
Discipline of Anatomy and Pathology
Level 3 Medical School North Building
The University of Adelaide
Frome Road
Adelaide 5005, SA
Australia
E-mail: roger.byard@sa.gov.au

Abstract

Abstract:  Subnuclear renal tubular epithelial cell vacuolization is a marker for diabetic ketoacidosis. Whether it is because of hyperglycemia or of ketoacidosis is unclear. To examine the effect of ketoacidosis on renal cells in isolation, five cases of lethal alcoholic ketoacidosis without hyperglycemia were examined (vitreous humor β-hydroxybutyrate: 6.42–8.75 mM, mean 7.66 mM; and glucose: 0.1–4.2 mM, mean 1.46 mM). Microscopic examination of the kidneys revealed basal vacuoles in three cases (60%). Seven control cases with acute alcohol toxicity without ketoacidosis (blood alcohol: 0.18–0.43%, mean 0.31%; and β-hydroxybutyrate: 0.12–0.42 mM, mean 0.21 mM) did not have these changes. In this study, basal epithelial vacuolization was found only in cases with significant ketoacidosis. Although the numbers are small, the finding of basal renal tubular epithelial vacuolization in normoglycemic cases with elevated β-hydroxybutyrate levels provide further evidence that disordered lipid metabolism may be involved in the pathogenesis of this phenomenon.

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