ON RENAL FUNCTION AND STRUCTURE IN URETEROVESICAL JUNCTION ANOMALIES WITH PARTICULAR REFERENCE TO THE GENESIS OF RENAL DYSPLASIA

Abstract

Renal function and morphology of the various congenital ureterovesical junction (UVJ) anomalies were investigated to provide further insight into the genesis of associated renal dysplasia.
I) (A) In the single ectopic ureter, 4 of 14 kidneys (28.6%) opening into the urinary tract were functionless and all the 4 proved to be severely dysplastic. All of 13 kidneys opening into the genital tracts were functionless and all proved to be dysplastic as well. It was noted that dysplasia was milder in female patients comparing to male counterparts. Although the occurrence of renal dysplasia was easily explicable by the “bud theory”, its severity seemed to be modified by other factors such as back pressure effect, growth of müllerian duct and unknown factors responsible for associated ureteral muscle dysplasia. (B) In the duplex system, all 11 upper segments opened ectopically into the G-zone of the urinary tract. Nine (81.8%) were functionless and 8 showed renal dysplasia. Genesis of renal dysplasia in the duplex system appeared to be similar to the single system. Renal function and morphology seemed to be more correlated with the type of the ureteral hiatus rather than its ectopic orifice per se.
II) (A) In the simple ureterocele (singe 14, duplex 9), only one kidney (7.1%) was functionless without histological confirmation. (B) In the ectopic ureterocele (all duplex but one), 10 of 14 kidneys (71.4%) were functionless, and 9 showed mild (i. e. focal or partial) dysplasia, except an aplastic one which belonged to the single system. The embryogenesis of the renal dysplasia seemed to be explained by the “bud theory”. Here again renal function and morphology seemed to be more correlated with the type of the ureteral hiatus rather than its ectopic orifice per se.
III) In the non-refluxing megaloureter (all single except one incomplete duplex), 8 of 58 kidneys (13.8%) were functionless and 2 proved to be dysplastic. In both cases their corresponding ureters showed muscle dysplasia or fetal ureter-like appearance. An unknown factor causing embryonal arrest of the ureter seemed to be respondible for the renal dysplasia.
IV) In the distal ureteral atresia (single one, duplex one), all 2 kidneys were functionless and showed aplastic dysplasia. No ureteral muscle dysplasia was proved. Back pressure seemed to be responsible for the renal dysplasia.
V) (A) In the refluxing megaloureter (all single but one), 4 of 49 kidneys (8.2%) were functionless and 3 showed mild dysplasia. (B) In the paraureteral diverticulum (single 23, duplex 5), 2 of single system (8.7%), 2 of upper segments and 3 of lower segments of duplex system (40% and 60%, respectively) were functionless. As for the renal morphology, the lower segments were more severely affected (one aplastic dysplasia and 2 agenesis). Because the position of the ureteral orifices seemed to be correlated with the severity of the renal morphology, it was indicated that the renal dysplasia in these cranial ectopic ureter could be more readily accounted for by the “bud theory” in both single and duplex cases.
It was concluded that abnormality in the ureteral bud would explain for the genesis of renal dysplasia as long as the adjoining ureter was ectopic (I, II, V), no matter whether the abnormality was single or duplex, with or without cele and cranial or caudal ectopia. Influences of back pressure and/or unknown factor responsible for concurrent ureteral muscle dysplasia appeared to play only a modifying role. In the non-refluxing megaloureter (III), unknown factor causing embryonal arrest of the ureter seemed to be responsible for the ureterorenal dysplasia. In the distal ureteral atresia (IV), the classical back pressure theory still seemed to be valid.