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. 2018 Jun 4;128(7):2894–2913. doi: 10.1172/JCI96640

Figure 1. CI-AKI is dependent on Nlrp3.

Figure 1

WT (Nlrp3+/+) and Nlrp3–/– mice were treated with vehicle control or ioversol (IVRS) and assessed at 1–3 days. (A) Renal function as determined by serum creatinine (day 3, Nlrp3+/+ vs. Nlrp3–/–, ***P = 0.0001, n = 6/group, ANOVA). Volume depletion demonstrated an effect on serum creatinine (ref. values 0.04–0.08 mg/dl) (Nlrp3+/+, day –2 vs. day 0, ***P = 0.001, n = 3–4/group, ANOVA), but it returned to baseline on day 3 (Nlrp3+/+ day 3, no IVRS vs. IVRS, **P = 0.0023, n = 3–6/group, ANOVA). (B) Fixed kidney tissue was analyzed for tissue injury using KIM-1 (red). Images were taken with a fluorescence confocal microscope. Labels: nuclei, DAPI (blue); tubules, LTL (green); E-cadherin (E-Cad; white); KIM-1 (red). Image is representative of 3 independent experiments. Scale bars: 50 μm. (C) Real-time PCR for KIM-1 mRNA expression (Nlrp3+/+ vs. Nlrp3–/–, 6 hours: ***P = 0.0005, day 1: ***P = 0.001, n = 3–5/group, ANOVA). (D) Cellular injury in Nlrp3+/+ and Nlrp3–/– mice determined by multiphoton intravital microscopy and SYTOX positivity of kidney TECs. Image is representative of 3 independent experiments. Scale bars: 200 μm. (E) Quantitation of SYTOX-positive cells at indicated time points (Nlrp3+/+ vs. Nlrp3–/–, day 1: ***P = 0.001, day 3: ***P < 0.001, n = 7–15/group, ANOVA).