Suppression of the renin-angiotensin system during lactation causes irreversible renal structural changes. In this study we investigated 1) the time course and the mechanisms underlying the chronic kidney disease caused by administration of the AT1 receptor blocker, losartan, during lactation, and 2) whether this untoward effect can be used to engender a new model of chronic kidney disease. Male Munich-Wistar pups were divided into two Groups: C, whose mothers were untreated; and L_Lact, whose mothers received oral Losartan, 250 mg/kg/day, during the first 20 days after delivery. At 3 months of life, both nephron number and the GFR were reduced in L_Lact rats, whereas glomerular pressure was elevated. Unselective proteinuria and decreased expression of the ZO-1 protein were also observed, along with modest glomerulosclerosis, significant interstitial expansion and inflammation, and wide glomerular volume variation, with a stable subpopulation of exceedingly small glomeruli. In addition, the urine osmolality was persistently lower in L_Lact rats. At 10 months of age, L_Lact rats exhibited systemic hypertension, heavy albuminuria, substantial glomerulosclerosis, severe renal interstitial expansion and inflammation, and creatinine retention. Conclusions: 1) Oral losartan during lactation can be used as a simple and easily reproducible model of chronic kidney disease in adult life, associated with low mortality and no arterial hypertension until advanced stages; 2) The mechanisms involved in the progression of renal injury in this model include glomerular hypertension, glomerular hypertrophy, podocyte injury and interstitial inflammation.