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. 2010 Oct 18;120(11):4055–4064. doi: 10.1172/JCI43721

Figure 2. Development of ADR nephropathy in mice with independent mutations in Prkdc.

Figure 2

(A–C) (BALB × B6) F1 hybrid mice are resistant to ADR nephropathy. (D–F) Prkdc+/– mice develop a mild version of ADR nephropathy with tubulointerstitial dilation, cast formation (D), and glomerular mesangial sclerosis (E and F). (G–I) The Prkdc–/– mice develop severe ADR nephropathy, with more abundant casts (G), acute tubular injury (H), and progression to focal global glomerulosclerosis (I). (J) Kidney injury scores in mice with independent Prkdc mutations compared with those of resistant B6 and (BALB × B6) F1 mice. *P < 0.05, **P < 1 × 10–5, respectively, (t test) as compared with B6 and (BALB × B6) F1 groups. Original magnification: ×200 (top row); ×400 (middle row); ×600 (bottom row).