Endothelial PI3Kβ loss sensitizes mice to TMA. (A) Kaplan-Meier survival plot of Tie2-CreER^T2+/−/p110β^flox/flox mice treated with vehicle (β^fl/fl) or tamoxifen to induce endothelial Cre recombinase activity and excision of Pik3cb (β^ECKO). As indicated, the animals received PBS (n = 6) or 200 μg/kg lectin-saporin cytotoxin conjugate to selectively injure the glomerular microvascular endothelium (n = 10 mice/group; toxin-treated β^ECKO vs β^fl/fl, P < .01). Kidney glomerular injury and function is worsened by endothelial PI3Kβ loss after TMA injury. (B-C) Quantification of histologic scoring of injured glomeruli (B) and acute tubular necrosis (C) among the groups at day 3 after cytotoxin exposure. (D-E) Quantification of serum creatinine (D) and urea concentration (E) among the groups. The data represent mean ± SEM; n ≥ 5 animals per group; *P < .05, **P < .01, toxin-treated group vs PBS group.