ETIOLOGY AND EPIDEMIOLOGY
Vesicoureteral reflux (VUR) is the retrograde flow of urine from the bladder to the ureter or up to the kidney. Most VUR results from congenital incompetence of the ureterovesical (UV) junction that matures through early childhood. In a significant minority of children, structural UV abnormalities exist that never resolve. VUR may be familial; 30% to 40% of siblings of a child with VUR also have VUR. VUR may also be secondary to distal bladder obstruction or other urinary tract anomalies.
VUR exposes the kidney to increased hydrodynamic pressure during voiding and increases the likelihood of renal infection due to incomplete emptying of the ureter and bladder (see Chapter 114). Reflux nephropathy refers to development and progression of renal scarring. This is a particular risk if VUR is associated with infection or obstruction. Even though a single urinary tract infection (UTI) may result in renal scarring, the incidence is higher in children with recurrent UTIs. Renal scars noted in newborns, screened because of familial VUR, along with genetic studies, suggest that renal dysplasia is associated with congenital VUR. Because of the increasing use of maternal-fetal ultrasonography, a number of newborns are now identified with VUR before UTI has occurred, creating opportunities for early intervention and UTI prevention strategies. Duplication of the ureters, with or without an associated ureterocele, may obstruct the upper collecting system. Often the ureter draining the lower pole of a duplicated renal unit has VUR. Neurogenic bladder, with or without myelomeningocele, is accompanied by VUR in up to 50% of affected children. VUR may also be due to increased intravesicular pressure when the bladder outlet is obstructed from inflammation of the bladder (cystitis) or by acquired bladder obstruction.
VUR is most often identified during radiologic evaluation following a UTI The younger the patient with a UTI, the more likely VUR is present. No clinical signs are reliable in differentiating children with UTI with and without VUR.
A voiding cystourethrogram (VCUG) or radionuclide cystogram (NCG) should be performed in all infants and children up to 6 years of age with a documented first UTI, regardless of gender. An imaging study should be performed after initiation of UTI treatment, but there is no need to wait days or weeks before performing the test. The VCUG provides additional anatomic detail, but the NCG may detect a higher percentage of children with mild VUR and involves less radiation exposure. An international grading system has been used to describe reflux (Fig. 167-1). The incidence of renal scarring in patients with low-grade VUR is low (15%) and increases with grade IV or V reflux (65%). Grade I or II VUR is likely to resolve without surgical intervention, but VUR resolves in less than 50% grade IV or V. Nuclear renal scanning best identifies renal scars.
The presence of VUR is generally an indication for long-term prophylactic antibiotic therapy (trimethoprim-sulfamethoxazole or nitrofurantoin). Pivotal studies are under way to define the best evidence for appropriate observation versus prophylactic antibiotics versus corrective procedures in affected children. Complications of reflux nephropathy are hypertension and chronic kidney disease (CKD). CKD is typically heralded by mild proteinuria and involves development of focal and segmental glomerulosclerosis and interstitial scarring. Indications for surgical repair of VUR are controversial and have been made more complex by the development of dextranomer/hyaluronic acid copolymer (Deflux procedure), which appears to be a very successful minimally invasive correction of mild to moderate VUR.