Renal parenchymal defects may be congenital, usually associated with dilated vesicoureteric reflux (VUR), or they may appear in previously normal kidneys and be caused by reflux nephropathy due to VUR combined with urinary tract infection (UTI). A piglet model defined that the 70% of children with VUR and vulnerable pyramids would scar rapidly with their first UTI. Because most defects are present at first imaging after a UTI, and from the lack of benefit from apparently reasonable clinical interventions, many now believe that most defects are congenital, their association with VUR being a shared dysplasia rather than causal. Consequently, guidelines now argue for less assiduous management. These conclusions ignore adult human transplant evidence, adult pig studies, and clinical anecdotes, which indicate that scars may develop in infant kidneys quicker than urine culture can confirm the diagnosis, and that reflux nephropathy has no age limit. Its rarity over 4 years suggests that most vulnerable children develop scars before then, despite all medical efforts. I argue that preventing such scarring will require better diagnosis of infant UTI, quicker treatment, reliable imaging of scars and VUR, and subsequent protection until VUR resolves. To make a difference, we need more assiduous management, not less, and cannot afford to consider VUR to be a benign condition.