After experimental ischemic or obstructive kidney injury, Tet2-CHIP and Jak2V617F-CHIP mice displayed more severe kidney injury and impaired recovery after kidney injury when compared to mice with intact Tet2 and Jak2, respectively, as evidenced by higher serum levels of markers of impaired kidney function and injury (creatinine and BUN; KIM-1 and NGAL), as well as structural kidney damage, including higher and more pronounced initial tubular injury and kidney interstitial fibrosis 28 days after kidney injury. This evidence concerns the gene LCN2 and urogenital neoplasm.