The pathogenesis of vesicoureteral reflux and reflux nephropathy is multifactorial, but certain known interconnections between different factors have been established. There exists an age-dependent anatomy and function of the ureterovesical junction, and this is of absolute importance for the presence of vesicoureteral reflux. Also, bladder urethral dysfunction with formation of high bladder pressures, urinary tract infections, and ureteric peristaltic properties seem to be of major importance for the development and maintenance of reflux. Vesicoureteral reflux combined with normal bladder-urethral function induces no change in the dynamic function of the upper urinary tract. In cases of bladder-urethral dysfunction that lead to high-pressure reflux, dilatation of the upper urinary tract is produced with irreversible damage of the peristaltic rhythm, frequency, and propagation. Such changes are aggravated by simultaneous infection. Reflux nephropathy most often occurs in cases of pyelorenal backflow with infected urine but can be aggravated by bladder-urethral dysfunction producing high pelvic pressures. Bacteria ascend from the bladder to the kidney, and maximal bladder pressures and the peristaltic conditions in the ureter have an impact on this. The maximal bladder pressure and the compiled pressure load transmitted without hindrance from the bladder to the kidney are presumably mandatory for the formation of nephropathy in cases of sterile reflux.This survey is based on earlier work performed in this laboratory [see 32, 50, 76-78, 94, 95, loo].