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Vesicoureteral reflux (VUR) refers to the retrograde passage of urine from the urinary bladder into the ureter and often to the renal collecting system. VUR mainly affects infants and young children with a prevalence of 25% to 40% ( Box 119.1 ). VUR is a risk factor for the development of pyelonephritis, with consequent renal scarring.
VUR is common in infants and young children.
African Americans have lower incidence of VUR.
VUR has a familial association (parent-child or sibling-sibling) with genetic heterogeneity.
Most VUR will resolve spontaneously within the first decade of life.
In utero VUR is associated with renal dysplasia.
The main indications to evaluate for VUR are UTI and antenatal hydronephrosis.
Children with VUR have increased incidence of pyelonephritis and renal scarring.
Initial management in most children with VUR is to await spontaneous resolution.
Children with VUR should be evaluated for bowel and bladder dysfunction.
Treatment of bowel and bladder dysfunction increases resolution of VUR and improves surgical outcomes.
Prophylactic antibiotic therapy decreases the risk of recurrent UTIs in children with VUR but not the risk of renal scarring.
Surgery for VUR is reserved for children with breakthrough infections and progressive scarring.
Current evidence suggests that the long-term risks associated with pyelonephritis and renal scarring are low and that preventive antibiotics and surgery may be useful in only a subset of patients. Therefore most children with an uncomplicated initial urinary tract infection (UTI) will not benefit from imaging, and the focus in the evaluation of VUR should be patients who have complicated or recurrent UTIs, as some of them may benefit from prophylactic antibiotics or surgery. Another common indication in the evaluation of VUR is prenatal hydronephrosis. VUR may also be associated with anomalies that require prompt surgical treatment to prevent renal damage.
The etiology of VUR is not entirely understood. It is possible that VUR in some infants is physiologic and will spontaneously resolve. VUR may be caused by abnormal ureteric budding or interaction with the metanephric mesenchyme, resulting in a lateralized ureteral orifice, with a subsequent shortened submucosal ureter that is deficient in longitudinal muscle fibers. Primary VUR has a familial association with genetic heterogeneity.
Secondary VUR is seen in patients with other urinary tract anomalies ( Box 119.2 ). In addition, increased bladder pressure from bladder outlet obstruction (e.g., posterior urethral valves), as well as increased detrusor muscle tone or uncoordinated bladder contraction (e.g., neurogenic bladder) can cause VUR.
Developmental, idiopathic, or immature urinary tract
Anomalous development at the ureterovesical junction
Bladder outlet obstruction, particularly posterior urethral valves
Neurogenic bladder
Bladder dyssynergia and dysfunctional voiding
Bladder diverticula
Prune-belly syndrome
Postoperative bladder, including ureterocele incision
The diagnostic imaging modalities preferred for the evaluation of VUR include voiding cystourethrogram (VCUG), radionuclide cystography (RNC), and ultrasound (US) ( Box 119.3 ). The optimal imaging modality in the assessment of VUR depends on the indication, radiologist preference and experience, and availability. VCUG is the gold standard for depicting VUR and is especially useful as the initial imaging examination for boys, while contrast-enhanced voiding urosonography (ce-VUS) involves no ionizing radiation and may be used as the first study in girls and in follow-up studies. In the past, RNC was considered to have lower levels of ionizing radiation compared with VCUG; however, with the use of modern fluoroscopy techniques, VCUG has been found to result in significantly lower radiation dose.
Gold standard study for grading of VUR
Defines anatomy (bladder, urethra, and refluxing ureters and ureterovesical junctions)
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