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. 2017 Feb 28;21(8):1619–1635. doi: 10.1111/jcmm.13091

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© 2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Characterization of the Vil‐Cre;Pkd2 ^f3/f3 kidney. (A) The kidney/body weight ratio for Vil‐Cre;Pkd2 ^f3/f3 newborns and for mice at ½, 1, 2, 3 and 4 months of age, compared to that of age‐matched control mice (Pkd2 ^f3/f3). (B) The renal cystic index of Pkd2 ^f3/f3 mice with or without the Vil‐Cre transgene allele at the ages shown. (C) The Vil‐Cre;Pkd2 ^f3/f3 kidney showed gross cysts (arrows) at 1 month of age (b) and massive gross cysts at 2–4 months (c‐e); histological results (f‐j) of the same kidneys were consistent with the gross examination. (D) BUN levels of Vil‐Cre;Pkd2 ^f3/f3 mice at ½, 1, 2, 3 and 4 months of age: BUN values rose significantly above those in control (Pkd2 ^f3/f3) mice at 2 months of age and continued to worsen with age. (E) Cr levels showed a similar pattern, starting at 1 month of age. *P < 0.05; **P < 0.01; ***P < 0.001. Bar: 3 mm in Ca‐e; 600 μm in Cf‐j; 100 μm in boxed areas. M: months.