The diminishing risk of acute renal scarring with urine infections (reflux nephropathy) after infancy is unexplained, but might reflect kidney maturation. The mechanisms of reflux nephropathy scarring are best explained by a piglet model in which vesicoureteric reflux allows infected urine to enter those segments of renal parenchyme that are drained by compound papillae. We carried out a similar study in adult pigs to determine whether protective maturation occurs. Adult pigs were exposed to urine infection after surgery to produce unilateral vesicoureteric reflux. The intravesical portion of one ureter was deroofed in six female adult Gottingen mini-pigs and the bladder and the ureteric mucosae stitched around the perimeter of the new orifice. One week later Escherichia coli was injected into the urinary bladder to produce cystitis. Three weeks later the animals were killed humanely and the urinary tracts were examined. The animals sustained persistent urine infections; the untreated ureters and kidneys remained normal. However, on the operated side, the ureters were thickened and dilated, vesicoureteric reflux was shown in four cases, and the kidneys had one or more flattened area overlying a renal segment, which showed severe inflammatory changes and early scar formation. The risk of reflux nephropathy scarring is not eliminated by maturation of the kidney in pigs. It is unlikely that the much-reduced risk of initiating scarring that is seen in older children with urine infections is due to a protective maturation of the human kidney. A possible explanation is that most children born with risk factors for developing scarring will have already sustained scars when very young.