Most clinical and experimental evidence suggests that renal scarring occurs following urinary tract infections in those patients with an abnormality of the urinary tract or kidney function. Experimentally, bacterial multiplication within the kidney occurs only in the presence of obstruction, leading rapidly to acute exudative pyelonephritis and invariably to kidney scars within weeks. Various manipulations of the bacterial load and/or of the inflammatory response during acute pyelonephritis have demonstrated that the inflammatory processes, not the bacterial component of pyelonephritis, are responsible for permanent renal tissue damage. Polymorphonuclear leucocytes (PMNLs) infiltrating the kidney tissue during acute pyelonephritis appear to release metabolites that are toxic to the parenchyma. Indeed, both the prevention of PMNL influx into renal tissue, by means of colchicine or cyclophosphamide, and the inactivation of some of their toxic metabolites, by means of dapsone, have led to the prevention of tissue damage and kidney scars. However, the most potent protective activity was observed with early antibiotic treatment, which stopped bacterial multiplication and prevented the early influx of PMNLs, thus preventing tissue damage and scar formation. Similar observations have been made in children with acute pyelonephritic episodes, in whom early and aggressive antibiotic treatment prevented subsequent kidney scars, while delayed treatment did not.