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Published on: October 12, 2017
Physiopathology of vesico-ureteral reflux
Salvatore Arena1, Roberta Iacona2, Pietro Impellizzeri3
1Department of Human Pathology in Adult and Developmental Age "Gaetano Barresi" - Unit of Paediatric Surgery, University of Messina, 98125, Messina, Italy. salarena@unime.it.
Insights
Vescico-ureteral reflux (VUR) in children stems from congenital issues at the vesico-ureteral junction (VUJ). Abnormalities in ureteral endings, including muscle structure and Sarcoglycan complex modifications, contribute to VUJ incompetence.
Area of Science:
- Pediatric Urology
- Developmental Biology
- Cellular Biology
Background:
- Vescico-ureteral reflux (VUR) is a common congenital anomaly in children.
- It originates from abnormalities at the vesico-ureteral junction (VUJ), likely due to abnormal fetal development.
- Refluxing ureteral endings exhibit structural and functional deficits.
Purpose of the Study:
- To investigate the causes of functional alterations in refluxing ureteral ends.
- To explore the role of Sarcoglycan (SG) complex modifications, Cajal cells, and tunnel length to diameter ratio in VUJ incompetence.
Main Methods:
- Review of existing literature on VUR pathophysiology.
- Analysis of structural and functional anomalies in refluxing ureteral endings.
- Focus on smooth muscle cells, Cajal cells, Connexin 43, and Sarcoglycan expression.
Main Results:
- Decreased smooth muscle actin, myosin, and desmin content in refluxing ureters.
- Evidence of muscular atrophy, degeneration, and disorganized fibers.
- Modified Sarcoglycan (SG) sub-complex configuration, including ε-SG deficiency and α-SG overexpression, is implicated.
Conclusions:
- Congenital muscular deficiency and altered Sarcoglycan expression are key factors in VUR.
- The roles of Cajal cells and the ureteral tunnel configuration are critical for VUJ function.
- These factors contribute to the functional alterations leading to VUJ incompetence.
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.
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