Fibrotic infarction of renal arterioles
Introduction
Introduction A fibrous infarction in the renal arteriole is a symptom of primary malignant hypertension. In addition to the interlobular artery of the arcuate artery and the small arteriole, it can extend from the small artery to the glomerular capillaries. The occurrence of fibrinoid necrosis is related to severe hypertension itself. It has been found that the diastolic blood pressure needs to be as high as 150mmHg, and the small arterial wall necrosis is higher, the necrosis is more serious; and it is related to many vasoactive substances abnormalities at this time, including renin- Angiotensin-aldosterone (RAS) over-activation of vasopressin enhances prostacyclin reduction and decreased kinin levels; in addition, fibrinoid necrosis may also cause local coagulation and increased intracellular calcium levels due to vascular endothelial injury. Related.
Cause
Cause
Malignant arteriolar atherosclerosis is caused by acute or malignant hypertension. At this time, the arterial lesions are mainly fibrinous necrosis of the arterial wall and thickening of the endometrium.
1. Cellulose-like necrosis: This lesion is considered to be a characteristic lesion of malignant hypertension, except in the interlobular artery of the arcuate artery and the small arteriole, and can extend from the small artery to the glomerular capillaries. Hey.
The occurrence of fibrinoid necrosis is related to severe hypertension itself. It has been found that the diastolic blood pressure needs to be as high as 150mmHg, and the small arterial wall necrosis is higher, the necrosis is more serious; and it is related to many vasoactive substances abnormalities at this time, including renin- Angiotensin-aldosterone (RAS) over-activation of vasopressin enhances prostacyclin reduction and decreased kinin levels; in addition, fibrinoid necrosis may also cause local coagulation and increased intracellular calcium levels due to vascular endothelial injury. Related.
2. Intimal thickening: similar to benign small arteriosclerosis, the main mechanism of invasion of interlobular artery and arcuate artery wall is the same as that of benign small arteriosclerosis.
Examine
an examination
Related inspection
Anti-adrenal cortical antibody renal angiography apolipoprotein E genotyping
Laboratory examination: blood routine red blood cells and hemoglobin are generally no abnormalities, but acute hypertensive patients may have Coombs test negative microvascular hemolytic anemia, with red blood cells, high hemoglobin increased blood viscosity, prone to thrombosis complications (including brain Infarction) and left ventricular hypertrophy. Urine routine: Early patients have normal urine routine, and the urine specific gravity is gradually reduced when the renal concentrating function is impaired. There may be a small amount of urinary protein, red blood cells, and occasional casts. As the renal lesion progresses, the amount of urinary protein increases. In patients with benign renal cirrhosis, such as 24h urine protein above 1g, the prognosis is poor. Red blood cells and casts can also be increased, and the casts are mainly transparent and granules. Renal function: Blood urea nitrogen and creatinine are often used to estimate renal function. There was no abnormality in the early patient examination, and the renal parenchyma was damaged to a certain extent and began to rise. Adult creatinine >5mg / dl, the elderly and pregnant >1.2mg / dl suggest kidney damage. The phenol red excretion test, the urea clearance rate, and the endogenous creatinine clearance rate may be lower than normal. Systemic vasculitis, a group of diseases characterized by inflammation and necrosis of the vessel wall (mainly arteries), including nodular polyarteritis, allergic vasculitis, and granulomatosis (Churg-Strauss disease) Wegner granuloma, giant cell arteritis, Kawasaki disease and Takayasu arteritis, most of which are related to immune mechanisms, such as proteinuria, hematuria, hypertension, renal dysfunction and other kidney damage. Among them, nodular polyarteritis and Wegener's granulomatosis can also be secondary to malignant hypertension, but various systemic vasculitis have their own clinical features (especially extrarenal manifestations), and some difficult cases can be used as kidney The biopsy is clearly diagnosed. Clinical diagnosis of malignant hypertension and malignant small arteriosclerosis, such as the lack of essential hypertension and chronic glomerulonephritis history, hypertension and urinary abnormalities have been unclear, then judge this malignant hypertension and malignant arterioles Whether kidney cirrhosis is caused by primary hypertension or chronic glomerulonephritis is relatively difficult, younger (under 40 years old), anemia and kidney reduction are beneficial to the diagnosis of the latter, if necessary An open renal biopsy is needed to confirm the diagnosis.
If there is a history of chronic nephritis or a period of urinary abnormalities, and then malignant hypertension, chronic nephritis is more likely to have malignant hypertension, such as a history of primary benign hypertension, at the same time as malignant hypertension or Proteinuria, hematuria, and renal failure soon appear as malignant small arteriosclerosis caused by essential hypertension.
1. Video room examination: The chest X-ray examination shows the aorta, especially the ascending and arching, and the ascending, arching or descending part can be expanded. Left ventricular enlargement occurs in hypertensive heart disease, left ventricular enlargement is more pronounced in left heart failure, and left and right ventricles increase in whole heart failure, and signs of pulmonary congestion. When the pulmonary edema is seen, the hilar is obviously congested and has a butterfly-shaped blurred shadow. It should be checked by routine photography for comparison before and after inspection.
2. Fundus examination: The measurement of central arterial pressure in the retina is observed to increase, and the following fundus changes can be seen at different stages of the disease progression:
Grade I: Retinal artery spasm.
Grade II A: mild retinal arteriosclerosis, B: retinal arteries significantly hardened.
Grade III: Grade II retinopathy (bleeding or exudation).
Grade IV: Grade III plus optic disc edema.
Acute nephritis develops rapidly, and proteinuria and hematuria rapidly develop into oliguric acute renal failure, but acute nephritis is more common in young adults, and hypertension is not prominent [diastolic pressure rarely exceeds 16kPa (120mmHg)], no Hypertensive neuroretinopathy, B-ultrasound examination of both kidneys often increased, blood C3 can be reduced (type II), may have a history of pre-infection, no previous history of essential hypertension.
Diagnosis
Differential diagnosis
Renal arteriosclerosis: refers to a type of disease that affects renal vascular function due to the renal artery and branches and/or arterioles. 1. According to the progress of the disease, it is divided into benign small arteriosclerosis and malignant small arteriosclerosis. Often moderate to high blood pressure and its clinical symptoms. 2. May be associated with heart, brain, fundus arteriosclerosis and its performance. 3. There is mild proteinuria, the degree of which is positively correlated with hypertension. 4. There may be nocturia in the later stage, and the urine specific gravity and urine permeability will decrease, resulting in renal insufficiency.
Renal artery occlusion: Renal angiography, which is common in renal pelvis and ureteral tumors, can be found to be thin or obstructed in the intrarenal artery, often indicating infiltration.
Renal artery stenosis: lesions vary in severity, from obvious renal artery stenosis to small renal artery lesions that are not clinically detectable. Severe stenosis can cause renal perfusion damage, decreased glomerular filtration rate (GFR), resulting in sodium retention, increased extracellular fluid volume, hypertension and renal failure.
Signs: (1) Hypertension: blood pressure is often greater than 200/120mmHg, and the diastolic blood pressure is more obvious. (2) Asymmetry of blood pressure in the extremities. (3) Abdominal vascular murmur.
