We report three important findings in this study: (1) Chronic inflammation characterized by TLT formation in interstitium was common in both aged and post-AKI kidneys; (2) Treatment with young plasma after AKI could attenuate AKI-to-CKD transition but not the AKI severity; (3) Young plasma could inhibit angiotensin II-induced expression of pro-inflammatory chemokines in pericytes and possibly thereby attenuate TLT formation in the kidneys after AKI. This evidence concerns the gene AGT and acute kidney injury.