Physiopathology of vesico-ureteral reflux.

Salvatore Arena,Tiziana Russo,Pietro Impellizzeri,Roberta Iacona,Carmelo Romeo,Lucia Marseglia,Eloisa Gitto

doi:10.1186/s13052-016-0316-x

Abstract

Vescico-Ureteral Reflux (VUR) is a common condition in childhood, caused by a congenital anomaly at the Vescico-Ureteral Junction (VUJ) level. It seems that the main cause could be an abnormal embryological development occurred during the early stage of fetal life.Refluxing ureteral endings show structural and functional anomalies: previous studies have shown a significant decrease in alfa actin, miosin and desmin contents as well as an high rate of atrophy and muscular degeneration with disorganized muscular fibres. The roles played by Cajal cells and Connexin 43 in generating peristaltic waves appears to be fundamental for the physiological VUJ function and activity. Attention was focused also on the congenital muscular deficiency of the RUs, on regard to general morphology, smooth muscle cells architecture, inflammatory markers and the distribution of collagen composition.This review will discuss and investigate the importance of the modified configuration of Sarcoglycan (SG) sub complex (particularly the deficiency of the ε-SG and the increased expression of the α-SG), the role played by Cajal Cells, the intravescical tunnel length to ureteral diameter ratio as possible causes of the functional alterations in the refluxing ureteral ends leading towards the VUJ incompetence.

Highlights

Primary Vescico-Ureteral Reflux (VUR) is a common condition likely related to a congenital anomaly of the Vescico-Ureteral Junction (VUJ) caused by its abnormal embryological development [1]
It is noteworthy that the depletion of c-kit positive Interstitial cells of Cajal (ICCs) in refluxing ureteral ends (RUs) might be the consequence of the disruption of smooth muscle cells, progenitors of ICCs, or secondary to mechanical stress, affecting the expression of developmental genes, during episodes of VUR [12, 26]
Several studies have shown how the reduction of smooth muscle fascicles and the defective configuration at VUJ level, creates an uncoordinated muscular contraction accompanied by the loss of c-kit-positive ICCs

Summary

Introduction

Primary Vescico-Ureteral Reflux (VUR) is a common condition likely related to a congenital anomaly of the Vescico-Ureteral Junction (VUJ) caused by its abnormal embryological development [1]. Functional and structural alterations of ureteric ends seem to impair the active valve mechanism of the VUJ, causing VUR [8, 9]. A study conducted on 36 distal refluxing ureteral ends (RUs), showed an increased expression of MMP1 in CD68 cells in the smooth muscle cells and in the fibroblasts as well as a significant decrease of the neural cells S-100 in the positive RUs [6].

Results

Conclusion