Skip to main content
. 2017 Dec 7;2(23):e92896. doi: 10.1172/jci.insight.92896

Figure 4. CRELD2 levels in the urine correlate with the duration of renal ischemia.

Figure 4

Mice were exposed to sham treatment or either 10 or 30 minutes of bilateral ischemia. (A) After 24 hours of reperfusion, paraffin sections of control and I/R-injured kidneys were stained with H&E and PAS. Note acute tubular necrosis (arrows) at 24 hours of reflow following 30 minutes of kidney ischemia. Scale bars: 40 μm. (B) BUN levels for the indicated groups: sham-operated mice (n = 10), mice with 10 minutes of bilateral ischemia followed by 24 hours of reperfusion (n = 5), and mice with 30 minutes of bilateral ischemia followed by 24 hours of reperfusion (n = 7). Data represent mean ± SEM, **P < 0.01 by 1-way ANOVA. (C–E) Representative WBs of CRELD2 (C), KIM-1 (D) and NGAL (E) in unprocessed urine samples obtained at reperfusion periods (3, 6 and 24 hours) as shown, after 10 or 30 minutes of bilateral renal vascular pedicles clamping. The urinary excretion of CRELD2 (C), KIM-1 (D), or NGAL (E) was normalized to 1 μg of urine Cr excretion and quantified. I, Ischemia. The average urinary biomarker excretion in mice subjected to bilateral renal ischemia for 10 minutes was set as 1. *P < 0.05, **P < 0.01, and ***P < 0.001 by 2-way ANOVA. PAS, periodic acid-Schiff; BUN, blood urea nitrogen; CRELD2, cysteine-rich with EGF-like domains 2; KIM-1, kidney injury molecule-1; NGAL, neutrophil gelatinase-associated lipocalin.