Vesicoureteral reflux

Physiology of the antireflux mechanism

In a healthy body, retrograde urine flow is effectively prevented by the valve apparatus of the vesicoureteral junction. The closing function of this barrier does not occur spontaneously, but strictly depends on three anatomical conditions:

• The oblique angle at which the ureter enters the muscular wall of the urinary bladder.
• Sufficient length of the submucosal (or intramural) segment of the ureter.
• The correct ratio of the total lumen of the ureter to its total length.

When these anatomical parameters are met, an increase in intravesical pressure leads to tight closure of the orifice, blocking the retrograde path for urine.

Causes of the pathology

Vesicoureteral reflux develops due to functional or anatomical incompetence of the ureteral orifice closing mechanism. All etiological factors are traditionally divided into three large groups:

1. Anatomical defects. These include congenital malformations of the muscle layer, shortening of the intramural segment, and ectopic (abnormal) location of the orifice.
2. Functional disorders in the operation of the structures of the vesicoureteral junction itself.
3. Secondary inflammatory changes. Chronic and frequently recurring infections of the lower urinary tract trigger the process of sclerosis in the tissues of the prevesical and terminal sections of the ureter. Due to scarring, the antireflux barrier is destroyed purely mechanically.

Note: modern medicine also assigns an important role to genetic predisposition in the development of this pathology.

Classification of VUR

Staging of the disease is based on the criteria of the International Reflux Study Committee. Physicians analyze the radiological picture (voiding cystography) according to two key features: the height of urine reflux and the severity of dilatation (dilation) of the upper urinary tract.

There are 5 consecutive degrees of severity:

• Grade I. The pathological process is limited exclusively to the ureter. The reflux does not reach the renal pelvis, and ureteral dilatation is absent (or minimal).
• Grade II. Total reflux: urine reaches the pelvicalyceal system (PCS). However, anatomy is preserved: there is no dilation of the passages, and the calyceal fornices have a normal sharp shape.
• Grade III. Structural deformation begins. Mild to moderate dilatation of the PCS and ureter is recorded. The fornices begin to flatten.
• Grade IV. Characterized by pronounced dilatation. The ureter becomes tortuous and wide. The PCS is significantly dilated, the calyces are rounded (blunted), but the contours of the renal papillae can still be traced on the radiograph.
• Grade V. Terminal stage. The ureter is severely dilated and tortuous (megaureter). The PCS is grossly deformed, the papillae are no longer visualized, and the calyces take on a characteristic club-like shape. Urine refluxes directly into the parenchyma (intrarenal reflux).

Consequences of the disease

Even mild reflux can initiate serious structural and functional disorders, which in children manifests as delayed physical growth of the affected kidney.

A specific and most dangerous outcome of VUR is reflux nephropathy. This process represents the formation of focal or widespread (diffuse) sclerosis of the renal parenchyma, leading to irreversible loss of organ function.

Class and exam questions

What else to study on this topic

• Mechanisms of delayed physical growth of the kidney in VUR during childhood.
• Differential diagnosis of functional and anatomical causes of vesicoureteral junction incompetence.
• Pathogenesis of intrarenal reflux in the terminal stage of the disease.
• The role of genetic predisposition in the formation of ureteral anomalies.
• Morphological differences between focal and diffuse sclerosis in reflux nephropathy.

Other topics in "Chapter 8. Kidney and Urinary Tract Diseases"

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