renal vascular malformation
Introduction
Introduction Renal vascular malformation and compression refer to a series of arterial and venous changes in the kidneys of the bilateral kidneys and their branches in the number of origins, the direction of drainage, or the compression of the surrounding organs. Pathological damage. The bilateral renal artery of the normal person is emitted from both sides of the abdominal aorta at the level of the first lumbar vertebrae, slightly below the superior mesenteric artery, and the right renal artery is slightly longer than the left renal artery. The renal artery is divided into two parts before and after entering the renal hilum. The renal parenchyma enters the anterior and posterior part of the renal pelvis, and the anterior branch of the renal artery divides the four-segment arteries (tip, upper, middle, and lower). The posterior branch continues into the posterior segmental artery, and the branches of the renal segment form the leaves between the renal cones. The inter-arterial artery, which emits interlobular arteries, enters the renal cortex radially, and then branches into the small arterioles, forming capillaries in the glomeruli, and then collecting into small arteries and leaving the glomeruli. The small arterioles enter the medulla through the small arterioles of the kidneys, form the capillary network, and then enter the bilateral renal vein trunks in the veins of the same name accompanied by the arteries, and return to the inferior vena cava. Renal vascular malformation and compression refer to a series of arterial and venous changes in the kidneys of the bilateral kidneys and their branches in the number of origins, the direction of drainage, or the compression of the surrounding organs. Pathological damage.
Cause
Cause
The causes of renal vascular malformation and compression can be divided into congenital and acquired types. Congenital renal vascular malformations and mutations are difficult to distinguish. Usually "abnormality" refers to abnormalities in morphology and structure, accompanied by pathological changes in dysfunction; and variation refers to only abnormalities in morphological structure without affecting organ function, and no pathological changes. Some renal vascular variations may also have pathological changes under certain conditions, and renal vascular malformations may not constitute pathological changes. For example, some small branches of renal arteriovenous fistula do not generally affect health, and when a female patient is pregnant, due to increased blood flow, heart failure may result in high cardiac output. The etiology of congenital renal vascular malformation is unclear, probably due to chromosomal aberrations caused by certain viral infections during embryonic development, or DNA recombination errors during cell division. Acquired factors include trauma, tumors and so on.
Examine
an examination
Related inspection
Renin activity flank renal venous renin activity assay
The clinical manifestations of renal artery malformation and compression are not characterized, and the rate of missed diagnosis is high. Clinicians must be vigilant. If you have the following clinical manifestations, you should consider the possibility of varicocele to the disease:
1. Unexplained hematuria or proteinuria.
2. Abdominal vascular murmurs with high-displacement heart failure that cannot be explained.
3. Children or adolescents with high blood pressure.
4. Elderly hypertensive patients with abdominal vascular murmur.
5. Varicocele with left renal enlargement.
The only way to diagnose is renal angiography.
Laboratory inspection:
1. Blood test: Renal vascular malformation and compression In addition to the performance of the renin-angiotensin system in some patients, there is almost no abnormality in other biochemical tests. The renal function is generally impaired, only severe or advanced. Nitrogenemia can occur in cases.
2. Urine examination: common hematuria, may have proteinuria.
Other auxiliary examinations: The diagnosis of this disease mainly depends on imaging examination.
X-ray inspection
(1) There may be no abnormalities in the plain film. In the case of severe renal blood supply disorder, one side of the kidney may be reduced, and the left renal vein compression syndrome may have an enlarged left kidney.
(2) intravenous pyelography: generally no positive performance. In the kidney or near the renal hilum, the tumor mass may be deformed by the renal pelvis and the contrast agent is blocked.
(3) renal angiography: can directly display the location, extent, extent, pathological properties of the renal vascular malformation or compression, collateral circulation and abdominal aorta changes. Congenital renal arteriovenous fistula is often located in the central renal proximal renal hilum, showing a group of curly blood vessels, thickening of the blood supply artery, early renal vein, and even the inferior vena cava can be developed in the arterial phase. Acquired arteriovenous fistula, the thickening of the blood supply artery, early renal cystic dilatation; renal parenchymal phase, the renal parenchyma of the diseased side is a low-density area, indicating renal insufficiency in this area. In patients with renal vascular compression, the filling of the compressed vascular lumen can be seen. In the case of thrombosis, the lesion is interrupted. In the renal parenchyma, the renal parenchyma is the conical low-density area of the lesion. Patients with left renal vein compression syndrome may have abdominal aorta or renal artery angiography. In the arterial phase, the position of the abdominal aorta and the superior mesenteric artery and the position of the left renal vein are shown. In the venous phase, the left renal vein is compressed. Degree and location.
2. CT scan can show the shape of the kidney, the nature, location, size, shape of the kidney and perirenal mass and the compression of the kidney. It has a certain meaning for differential diagnosis.
3. Abdominal ultrasonography can detect abnormal blood flow by color Doppler examination of the kidney. B-mode ultrasound can show the size of the kidney and the condition of the tumor, but the sensitivity is not high.
4. Nuclear medicine examination Nuclide renal blood pool or renal parenchymal development is not specific for the diagnosis of renal arteriovenous fistula and renal vascular compression, but it has certain differential diagnostic value. In addition, if the 99mTc-RBC blood pool imaging showed a local high concentration, and the 99mTc-calcium gluconate renal imaging showed a local defect in the concentrated area, it has a qualitative significance for the diagnosis of renal aneurysms.
Diagnosis
Differential diagnosis
Need to be identified with the following symptoms:
Hematuria: Hematuria includes microscopic hematuria and gross hematuria. The former refers to normal urine color, which can be determined by microscopic examination. Usually, urine microscopy after centrifugation has more than 3 red blood cells per high power field. The latter means that the urine is washed with water or blood, and the naked eye can be seen as hematuria.
Proteinuria: The normal glomerular filtrate contains a small amount of small molecular protein, the content of 20mg/100ml. Reabsorption through the renal tubules, and finally the protein remaining in the urine is very small, no more than 70 ~ 100mg / 24h. It can not be detected by ordinary urine routine examination. When the protein content in the urine increases, the routine urine examination can be measured, which is called proteinuria.
Heart failure: Heart failure is not an independent disease, it is a serious stage of heart disease caused by various causes. The incidence is high and the five-year survival rate is similar to that of malignant tumors. Heart failure is due to initial myocardial damage and stress: including systolic or diastolic ventricular overload and/or changes in the number and quality of cardiomyocytes (segmental myocardial infarction, diffuse such as myocarditis), causing ventricles and (or Buxinfang hypertrophy and enlargement (ventricular remodeling, remodel-ing people followed by ventricular systolic and diminished function, gradually developed.
