Abstract
Chronic kidney disease (CKD) is one of the clinical features characterized by progressive and irreversible loss of renal function. The incidence of this pathology is constantly increasing globally, due to the growing number of patients diagnosed with diabetes and hypertension, both diseases generating tubular fibrosis and kidney dysfunction. Through experimental models for the production of tubulo-interstitial fibrosis (TIF), we try to understand deeply and comprehensively the main pathogenic mechanisms that govern the onset, progression and worsening of CKD. Understanding the mechanisms underlying the production of this pathology, one can try therapeutic methods to produce an evolutionary slowdown in CKD and also translate the main benefits in clinical practice, based on these experimental models of basic research.