primary vesicoureteral reflux
Introduction
Introduction to primary vesicoureteral reflux Primary vesicoureteral reflux is due to weakness in the development of the ureteric bladder. The urinary bladder junction is not functioning properly due to various reasons, and the phenomenon that the bladder urine returns to the ureter is called vesicoureteral reflux. The disease can be divided into congenital and acquired two, children are mostly congenital, the incidence rate is higher than adults. Adults are mostly caused by urethral and bladder lesions, more women than men, vesicoureteral reflux caused by ureter and hydronephrosis, secondary infections and stones, damage to kidney function. The treatment effect of this disease is better, and the surgical cure rate is above 95%. Bladder ureteral reflux can cause bacterial infection of the upper urinary tract, occasionally increased intra-renal pressure, damage to the kidney function, causing reflux is mainly due to congenital developmental defects in the ureteral junction of the bladder. Reflux can also occur in children with anatomy at the junction, normal function but with bladder outlet obstruction, increased intravesical pressure, and neurogenic bladder. The bacteria in the lower urinary tract easily pass through the reflux to the upper urinary tract, causing renal parenchymal infection, renal scar formation and renal dysfunction. Chronic bladder storage and increased urination pressure (>40cmH2O) can cause an increase in intrarenal pressure to cause reflux. Bladder ureteral reflux can produce pain in the waist and abdomen, persistent or repeated urinary tract infections, difficulty urinating or low back pain during urination, frequent urination, urgency, and symptoms of renal insufficiency. Pyuria, hematuria, proteinuria, and bacteriuria can also occur. Perfusion and urinary bladder urethrography can clarify reflux and determine if there is bladder outlet obstruction, which can be surgically resolved. Direct isotope angiography with isotope can also determine the presence or absence of reflux, long-term use of preventive antibacterial therapy, reflux will naturally disappear after several months to several years. Prophylactic antibacterial therapy is ineffective, and the best development of renal scarring is ureteral bladder replantation. Reflux combined with bladder storage and high urinary urination requires medication and/or behavioral therapy to reduce intravesical pressure. Sometimes reflux will be solved, otherwise surgery must be replanted. Replantation almost always cures reflux and reduces the incidence of pyelonephritis, reducing the incidence and mortality of kidney diseases secondary to reflux and infection. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: anemia, hydronephrosis
Cause
Primary vesicoureteral reflux etiology
Primary
The most common, congenital vesicoureteral valve insufficiency, including congenital bladder submucosal ureteral short or horizontal position, ureteral opening abnormalities, bladder deltoid tissue thinning, weakness, Waldeyer, s sheath congenital anomalies. 53% of the cases were reflux caused by abnormal bladder detrusor function.
Pathophysiology
Pathogenesis: The pathogenesis of RN has not yet been elucidated, and renal damage caused by VUR may be caused by multiple factors.
Bacterio
Urine reflux brings bacteria into the kidney, and kidney damage is thought to be a direct violation.
Urodynamic changes
Because the ureteral orifice is fish-like, the reverse flow is large. Even if there is no infection, when the pressure in the renal pelvis increases to 40 mmHg, IRR may occur and cause kidney damage. Participation in urine is one of the most important outcomes of VUR, and residual urine volume may play an important role in the etiology of UTI recurrence.
Urine input into kidney tissue
The urine leaks into the renal interstitium through the renal pelvis, the rupture of the Bellin tube or the humerus of the kidney nipple, and the urine can be directly stimulated by the renal interstitial or through the autoimmune reaction (the antigen may be bacteria in the urine or Tamm-Horsfall) Protein) causes inflammation or fibrosis.
Intrarenal vascular stenosis
Intrarenal vascular occlusion and stenosis due to inflammatory muscle fibrosis caused by leakage of urine into the interstitium outside the renal tubules and capillaries and small blood vessels. Further cause intrarenal ischemic lesions and secondary hypertension. In addition, when functional urinary tract obstruction exists, bladder urethral pressure increases, resulting in increased renal tubular pressure and IRR, followed by decreased glomerular filtration rate, decreased blood flow to the parietal arteries, leading to renal defects and interstitial nephritis .
Glomerulosclerosis
In recent years, attention has been paid to the focal segmental glomerulosclerosis of RN. Lotran (1982) summarized its pathogenesis as: immune damage, mesangial insufficiency after ingestion of macromolecular substances, intrarenal vascular disease, glomerular hyperfiltration.
genetic factors
Some people think that 10%-20% of the incidence of VUR is related to heredity, and 40% of first-degree relatives in the susceptible family have reflux.
Pathology: the nipple tube and the collecting tube with reflux were obviously dilated, the interstitial congestion and edema around the wall, lymphocytes and neutrophils infiltrated, followed by atrophy of the kidney to the tube, focal and fibrosis around the glomerulus. Renal pelvis, renal pelvis dilatation, renal parenchyma thinning, severe VUR with repeated UTI scar management, generally upper and lower poles of the kidney (ie, the tendency of polarity distribution). Small arteries can have thickened stenosis.
Prevention
Primary vesicoureteral reflux prevention
1. Mild vesicoureteral reflux has a natural regression trend, congenital vesicoureteral reflux in childhood, if the condition is mild or stable, it is advisable to observe treatment, because with the increase of age, the reflux has the possibility of natural regression.
2. Mild (I ~ II) patients can be treated with medical treatment
1 long-term treatment of small doses of antibiotics, the course of treatment should be more than half a year until the urine culture is negative. 2 urinary training: multiple urination, shortening the interval between urination. Patients with middle (grade III) and severe (IV to V) should undergo surgical treatment, ie vesicoureteral reflux surgery.
3. Patients with unilateral reflux, if the renal function of the affected side is seriously impaired, and the contralateral renal function is good, the affected side nephrectomy is feasible.
4. According to the bacteria and drug susceptibility test of urine culture, and should be early and sufficient, it is necessary to control the infection.
5. Use drugs with low nephrotoxicity whenever possible.
6. Adjust dose changes based on indicators of renal function.
Complication
Primary vesicoureteral reflux complications Complications anemia, hydronephrosis
1. Frequent urination, urgency, dysuria and back pain, fever.
2. Physical examination of unilateral or bilateral renal area tenderness, snoring pain; if the hydronephrosis is more, you can touch the abdominal mass.
3. If bilateral ureteral ureteral reflux, renal function has been seriously damaged, there may be symptoms of uremia: anemia, edema, stomach anorexia and so on.
Symptom
Primary vesicoureteral reflux symptoms Common symptoms Urinary tract infection fever with frequent urination, urine... Abdominal mass in the kidney area snoring pain nephropathy edema face stomach symptoms
In the examination, the bladder ureteral forced flow can be divided into five degrees:
I degree: reflux only reaches the lower ureter.
II degree: reflux caused by renal pelvis, renal pelvis, but no expansion.
III degree: reflux and mild to moderate pyelectasis.
Grade IV: The renal pelvis and renal pelvis are obviously dilated and the ureter is bent.
V degree: severe expansion of the renal pelvis, renal pelvis lost papillary morphology, ureteral distortion.
Clinically, it is often found in urinary tract infections: manifestations of fever, frequent urination, urgency, renal pelvis, severe renal dilatation, and impaired renal function. Renal hypertension is often a bilateral severe reflux disease, accounting for about 18% of the incidence, and some individuals also have unilateral pyelonephritis and scar.
Due to the low degree of reflux, there are no symptoms. When the reflux is severe or there is infection, the following symptoms may occur.
1. Repeated episodes of urinary tract infection and pyelonephritis: frequent urination, urgency, dysuria and back pain, fever.
2. Physical examination of unilateral or bilateral renal area tenderness, sputum pain. If there is more hydronephrosis, you can touch the abdominal mass.
3. If bilateral ureteral ureteral reflux, renal function has been seriously damaged, there may be symptoms of uremia: anemia, edema, stomach anorexia and so on.
Examine
Primary vesicoureteral reflux examination
1, laboratory inspection
UTI routine urine examination has pyuria and urinary bacterial culture positive. Urine tests at RN can reveal proteins, red blood cells, white blood cells, and various casts. Renal function tests were normal or abnormal.
2, ultrasound examination
B-ultrasound can be used to estimate the function of the ureteral junction, observe the ureteral dilatation, peristalsis and continuity of the basal part of the bladder, observe the renal pelvis, kidney morphology and substantial changes. Someone inserts a catheter in time B and injects a gas (such as CO2). If the gas enters the ureter, VUR can be diagnosed. The function of the junction and the position of the ureteral opening were observed by color Doppler ultrasound. However, B-ultrasound has limitations on the detection of upper pole scars, and it cannot classify VUR.
3, X-ray inspection
(1) Urinary bladder urography (MCU): This is the basic method for the diagnosis of VUR commonly used and the classification of the "fund standard" International Reflex Committee proposed by the five-level classification: Grade I: urinary reflux is limited to the ureter, Grade II: urinary reflux to the ureter, renal pelvis, but no dilatation, normal renal pelvis, grade III: ureteral light, moderate dilatation and (or) distortion, moderate renal dilatation, no paralysis of the iliac crest, or mild dullness, Grade IV: moderate dilatation and distortion of the ureter, moderate dilatation of the renal pelvis and renal pelvis, complete disappearance of the humerus, most pelvis maintained nipple compression, grade V: severe dilatation and distortion of the ureter, severe enlargement of the renal pelvis and renal pelvis, most The renal pelvis does not show nipple pressure.
(2) intravenous pyelography (IVP): can further confirm the presence of renal atrophy and renal scar formation. In recent years, it is believed that high-dose intravenous pyelography plus X-ray layer photos can show scars.
4. Radionuclide inspection
(1) Radionuclide bladder imaging: direct and indirect assays for the determination of VUR.
(2) DMSA scanning technology: For hotels with urinary sterility, it is the only "gold standard" for diagnosing children's RN, especially for children over 5 years old. Coldraich divides renal scars into four grades according to DMSA scan photographic signs: grade I: one or two scars, grade II: two or more scars, but the renal parenchyma is normal between scars, grade III: diffuse damage throughout the kidney, Types of obstructive nephropathy, ie, renal atrophy, with or without scarring of the kidney, grade IV: terminal, atrophic kidney, almost no or no DMSA uptake (less than 10% of total renal function).
Diagnosis
Diagnosis and diagnosis of primary vesicoureteral reflux
Diagnostic criteria
Because the symptoms of clinical diagnosis of VUR are not obvious or only non-specific, the diagnosis depends on imaging.
1. The following situations should consider the possibility of reflux
1 repeated recurrence and prolonged UTI;
2 long-term urinary frequency, urinary dripping or enuresis;
3 younger, <2 years old and/or boy UTI;
4 middle urine culture continued to be positive;
5UTI with urinary tract malformation;
6 family first-degree relatives have VUR, RN patients;
7 fetal or infancy with hydronephrosis.
2, RN diagnosis
Diagnosis depends on imaging examination, clinical manifestations and renal biopsy pathological changes can help diagnose.
Primary VUR is a congenital disease that is part of the immature development of children. As the age gradually increases and the development matures, VUR gradually disappears. Many growing children with grade 1 to 3 reflux can heal themselves. Level 5 is difficult to heal. If the infection can be controlled without other complications, 80% grade 1~2 reflux, 50% grade 3 reflux and 30% grade 4 reflux can heal itself.
3, the main symptoms of this disease are repeated urinary tract infections. Late kidney may have symptoms of chronic renal insufficiency.
4, laboratory inspection
There are white blood cells and pus cells in the urine. The mid-stage urine quantitative bacteria cultured long pathogenic bacteria above 105/ml. When the advanced renal function is seriously damaged, the blood urea nitrogen is increased.
5, intravenous urography
Can show renal pelvis and renal pelvis expansion, ureter thickening, distortion, but no obvious obstruction.
6, urinary bladder urethra angiography
Can show vesicoureteral reflux, but no lower urinary tract obstruction.
