Vesicoureteral Reflux



  • Vesicoureteral reflux (VUR) occurs when urine passes from the bladder to the ureters or kidneys. VUR is either a primary (congenital) or acquired process secondary to bladder dysfunction (congenital, acquired, or behavioral) or outlet obstruction (e.g., posterior urethral valves [PUVs]).
  • VUR can be subgrouped according to presentation type. It is usually detected in two scenarios: the postnatal evaluation of an infant with prenatal hydronephrosis (HN) or during imaging evaluation after urinary tract infection (UTI).
  • Children in the latter category are at higher risk for recurrent UTI (rUTI) and renal scarring (RS). RS is primarily a risk after febrile UTI (fUTI). Breakthrough UTI (btUTI) is a UTI that occurs while on continuous antibiotic prophylaxis (CAP).



  • VUR occurs in ~1% of children.
  • In those detected in the postnatal evaluation of an infant with prenatal HN:
    • ~20–30% of patients with prenatal HN have VUR. Screening this population for VUR is controversial (see “Diagnostic Tests & Interpretation” section).
    • Ratio of males to females in this group is 3:1, which is believed to reflect a period of high-pressure voiding in boys that resolves by 18 months.
  • In those detected during imaging evaluation of a UTI:
    • Up to 30–50% of children with fUTI will have VUR.


It is important to distinguish between associations that increase risk for VUR and conditions in which VUR is more commonly found.

  • VUR is more likely to be detected in those with prenatal HN and/or r/fUTI. fUTIs are 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 associated with VUR (e.g., ureteropelvic junction obstruction [UPJO]) reflect a single event (e.g., ureteral bud defect) or represent separate abnormalities.
  • Primary VUR (see “Pathophysiology”)
    • Young age (There is debate whether normal infant voiding patterns may predispose to VUR.)
    • UPJO (ipsilateral VUR in 10–20%)
    • Ureteral duplication (see “Pathophysiology”)
    • Dysplastic kidney (contralateral VUR in 30–40%)
    • Bladder diverticula, especially periureteral location
    • Prune belly (Eagle-Barrett) syndrome
    • Severe congenital anomalies, including bladder exstrophy and cloacal anomalies, VACTERL and CHARGE, and imperforate anus
  • Secondary VUR (see “Pathophysiology”)
    • Bladder neck and/or urethral obstruction (e.g., prolapsing ureterocele, PUV, urethral atresia)
    • Neurologic conditions predisposing to neuropathic bladder (e.g., spina bifida, tethered cord)
    • Bladder and bowel dysfunction (BBD)


  • 30% of siblings will have VUR (usually low grade). The majority will be asymptomatic with only rare RS.
  • Parents with VUR have a 60% chance of having a child with VUR.
    • Screening siblings is controversial. Low-grade VUR usually resolves without sequelae.
    • Consider screening siblings with history of febrile illnesses, even in absence of definitive UTIs.
    • Siblings of children with VUR are more likely to show renal cortical abnormalities if diagnosed after a previous UTI than after screening.


  • The ureterovesical junction (UVJ) is a flap valve. During storage and voiding, pressure within the bladder compresses the intramural ureter against detrusor backing to prevent flow of urine up the ureter.
  • VUR can result from either abnormal anatomy, abnormal storage, abnormal voiding pressure, or a combination of the three.
  • Primary VUR results from either a short ureteral tunnel through the bladder wall or transient high-pressure voiding, which occurs normally in the first 18 months of life (particularly in boys).
    • Patients with primary VUR generally improve and even resolve with time as the ureteral tunnel grows or bladder pressures decrease.
  • In complete ureteral duplication, an early forming ureteric (refluxing in 30–40%) bud drains the lower pole renal moiety, and a late forming ureteric bud drains the upper pole renal moiety.
  • Any circumstance that increases pressure storage of urine and/or impairs or obstructs urine outflow can overwhelm the UVJ and create secondary VUR.
    • The distinction between primary and secondary reflux is important because large prospective trials have been conducted on patients with primary reflux and it is not appropriate to extend those findings to patients with secondary reflux.
  • VUR is classified as five grades by the International Reflux Study based on the voiding cystourethrogram (VCUG):
    • Grade I: reflux into ureter
    • Grade II: reflux to renal pelvis without calyceal dilation
    • Grade III: calyceal blunting, mild dilatation of ureter
    • Grade IV: gross ureteral dilatation, moderate calyceal dilation, papillary impressions maintained
    • Grade V: gross urinary tract dilatation, loss of papillary impressions
  • General consensus is that VUR alone does not damage kidneys, but renal damage results from reflux of infected urine.
    • As VUR grade increases, risk of spontaneous resolution decreases and risk of rUTI, RS increases.
    • To this end, in the literature, VUR is often classified as either (i) low (I to II), moderate (III), or high grade (IV to V) or (ii) nondilating (I to II) versus dilating (≥III).
    • From the perspective of preventing r/btUTI and RS, dilating and high-grade VUR are more concerning than low-grade and nondilating VUR (ndVUR).

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