Vesicoureteral reflux and bladder dysfunction

The relationship between vesicoureteral reflux and bladder dysfunction is inseparable and has long been emphasized. However, the primary concern of all physicians treating patients with vesicoureteral reflux is the prevention of renal scarring and eventual deterioration of renal function. Bladder dysfunction, urinary tract infection and vesicoureteral reflux are the three important factors which are closely related to each other and contribute to the formation of renal scar. Especially, there is ongoing discussion regarding the role of bladder dysfunction in the prognosis of both medically and surgically treated vesicoureteral reflux. The effect of bladder dysfunction on VUR is mostly via inadequate sphincter relaxation during infancy which is closer to immature bladder dyscoordination rather than true dysfunction. But after toilet training, functional obstruction caused by voluntary sphincter constriction during voiding is responsible through elevation in bladder pressure, thus distorting the architecture of bladder and ureterovesical junction. Reports suggest that voiding phase abnormalities in lower urinary tract dysfunction contributes to lower spontaneous resolution rate of VUR. However, filling phase abnormalities such as involuntary detrusor contraction can also cause VUR even in the absence of dysfunctional voiding. With regards to the effect of bladder dysfunction on treatment, meta-analysis reveals that the cure rate of VUR following endoscopic treatment is less in children with bladder bowel dysfunction but there is no difference for open surgery. The pathophysiology of bladder dysfunction associated with UTI can be explained by the 'milk-back' of contaminated urine back into the bladder and significant residual urine resulting from functional outlet obstruction. In addition, involuntary detrusor contraction can decrease perfusion of the bladder mucosa thus decreasing mucosal immunity and creating a condition prone to UTI. In terms of renal scarring, dysfunctional voiding seems to be more closely related to renal damage in association with VUR than overactive bladder. However, studies show that UTI can induce renal scarring even without VUR present and urodynamic abnormalities are quite often detected in these cases. Whether reflux of sterile urine in bladder dysfunction can cause significant renal scarring, especially when intrarenal reflux is present remains controversial. Another issue that warrants further research is the direct relationship between bladder dysfunction and renal scarring, since some reports suggest that these two conditions share a common genotype. Recently some studies have suggest VUR as a causal factor of bladder dysfunction, supported by the fact that bladder dysfunction resolves after injection therapy of VUR. Further study with more objective evaluation of bladder dysfunction may be needed.