Vesicoureteral Reflux

Descriptive text is not available for this imageBASICS

DESCRIPTION

  • Vesicoureteral reflux (VUR) occurs when urine passes retrograde from the bladder to the upper urinary tract (ureters, kidneys).
  • VUR is classified into two types, primary or secondary, based on underlying etiology.
    • Primary VUR results from aberrant anatomy at the ureterovesical junction (UVJ) leading to valvular incompetence.
    • Secondary VUR occurs due to functional or anatomic bladder obstruction overwhelming an anatomically normal UVJ (e.g., dysfunctional elimination, neurogenic bladder, posterior urethral valves [PUVs]).
  • VUR is usually detected in two clinical scenarios: the evaluation of an infant with prenatal hydronephrosis (HN) or during imaging evaluation after a febrile urinary tract infection (fUTI).
  • Children with VUR are at an increased risk of fUTIs and renal scarring (RS); thus, treatment goals include prevention of fUTI and RS and minimization of morbidity of treatment and follow-up.

EPIDEMIOLOGY

  • VUR occurs in ~1% of children.
  • In those detected in the postnatal evaluation of an infant with prenatal HN:
    • 10–20% of patients with prenatal HN have VUR. Screening this population for VUR is controversial (see “Diagnostic Tests & Interpretation” section).
    • Overall, females are twice as likely to have VUR compared to males. In younger patients, male-to-female prevalence of 3:1 (0 to 6 months), which may be due to higher voiding pressures in male infants.
  • In those detected during imaging evaluation of a urinary tract infection (UTI), up to 40% of children with fUTI will have VUR.

RISK FACTORS

  • Primary VUR (see “Pathophysiology” section)
    • Younger age (Low-grade VUR commonly resolves spontaneously with growth.)
    • Ureteropelvic junction obstruction (UPJO) (prevalence for VUR of 8.2%; bilateral or contralateral in 5.7%)
    • Ureteral duplication (lower pole VUR in 30–40%)
    • Multicystic dysplastic kidney (contralateral VUR in 26%)
    • Renal agenesis (contralateral VUR in 24–28%)
    • Bladder diverticula, especially periureteral location
    • Prune belly (Eagle-Barrett) syndrome
    • Megacystis–megaureter association
    • Congenital anomalies, including bladder exstrophy and cloacal anomalies, VACTERL (vertebral defects, anal atresia, cardiac defects, tracheoesophageal fistula, renal anomalies, and limb abnormalities), CHARGE (colobomas, heart abnormalities, atresia of nasal choanae, retardation of growth, genitourinary anomalies, ear anomalies), and imperforate anus
  • Secondary VUR (see “Pathophysiology” section)
    • Bladder neck and/or urethral obstruction (e.g., prolapsing ureterocele, PUVs, urethral atresia)
    • Neurologic conditions predisposing to neuropathic bladder (e.g., spina bifida, tethered cord)
    • Bladder and bowel dysfunction (BBD)

Genetics

  • Primary VUR demonstrates genetic predisposition, likely multigenic.
  • Higher VUR rate in identical versus fraternal twins (80% vs. 35%).
  • Parents with VUR have a 60% chance of having a child with VUR.
  • 27% of siblings will have VUR with the majority low grade. Screening siblings is controversial. Low-grade VUR usually resolves without sequelae.

PATHOPHYSIOLOGY

  • UVJ is characterized by oblique entry of the ureter into the bladder through the detrusor muscle. The intramural portion of the ureter creates a flap valve mechanism, whereby preventing VUR.
    • High ratio of tunnel length to ureteral diameter confers valvular competence.
  • During storage and voiding, bladder filling leads to increased bladder pressure that compresses the intramural segment against detrusor to prevent retrograde flow of urine.
  • VUR can result from either abnormal anatomy, abnormal ureteral function, abnormal voiding dynamics, or a combination of the three.
  • Primary VUR results from a short and perpendicularly oriented ureteral tunnel leading to UVJ incompetence.
    • Spontaneous resolution or improvement is seen over time as bladder growth elongates submucosal tunnel and bladder dynamics stabilize.
  • Secondary VUR results from abnormally high bladder pressures that overcome an anatomically normal UVJ because of bladder outlet obstruction or bladder dysfunction.
    • The distinction between primary and secondary reflux is important as treatment is dependent on underlying etiology of VUR.
  • The International Reflux Study in Children described a VUR grading scale (I to V) based on voiding cystourethrogram (VCUG) findings:
    • Grade I: reflux into ureter
    • Grade II: reflux to renal pelvis without calyceal dilation
    • Grade III: mild to moderate dilation of the ureter and renal pelvis and calyces; fornices minimally blunted
    • Grade IV: gross ureteral dilatation with tortuosity, moderate calyceal dilation, papillary impressions maintained
    • Grade V: gross urinary tract dilatation with tortuosity, loss of papillary impressions
  • VUR does not cause UTI but can facilitate pyelonephritis in those with UTI.
  • Renal injury in VUR is primarily a consequence of postinfectious RS.
    • VUR without UTI does not cause RS in primary reflux.
    • Children <2 years of age have higher risk of RS following fUTI.
    • Higher grade VUR associated with increased RS

COMMONLY ASSOCIATED CONDITIONS

  • Prenatal HN
  • fUTIs
    • VUR is more likely to be detected in those with recurrent fUTI.
    • fUTI is not thought to cause VUR, although some data suggest high-grade VUR may be a risk for fUTI.
  • It is unknown whether some pathologies of the urinary tract are associated with VUR (e.g., UPJO), reflect a single event (e.g., ureteral bud defect), or represent separate abnormalities.

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