It is impossible to understand the reasons for the development of PMR without understanding the normal structure of the PMR. Anatomically, the closure function of the PMS is achieved due to the ratio of the length and width of the intravesical ureter (5: 1), the oblique passage of the ureter through the bladder wall. The long submucosal tunnel is a passive element of the “ureterovesical valve”. The active element of the valve mechanism is represented by the musculo-ligamentous apparatus of the ureter and the Lietot triangle, which closes the orifice when the detrusor contracts.
The causes of non-physiological urine flow include pathological conditions leading to a violation of the PMS closure mechanism and high intravesical fluid (urine) pressure. The first include congenital malformations of the PMS and the inflammatory process in the area of the superficial or deep triangle of the bladder (cystitis), which disrupts the function of the detrusor or directly the PMS itself.
Anomalies of the vesicoureteral junction are often the result of abnormal development of the ureteral outgrowth of the Wolf’s duct at the 5th week of embryogenesis. Types of vesicoureteral anomaly:
- wide, constantly gaping shape of the ureteral orifice:
- the location of the orifice of the ureter outside the zone of the bladder triangle (lateroposition);
- complete absence or shortening of the submucosal tunnel of the vesicoureteral junction;
- violation of the morphological normal structure of the vesicoureteral junction (dysplasia).
Loss of the closure function of the vesicoureteral junction occurs with inflammation of the bladder wall or the PMS zone. Most often, secondary VUR is a consequence (complication) of a bullous (granular) or fibrinous form of cystitis. Urinary tract infection occurs in 1-2% of boys and 5% of girls. More often the urinary tract is colonized by conditionally pathogenic (intestinal) flora, among which the main place is occupied by Escherichia coli (40-70%).