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How much do you know about the clinical symptoms of hypertensive nephropathy?
In hypertensive nephropathy occurred just before this period: Patients with hypertensive nephropathy has no clinical symptoms of proteinuria and nocturia in hypertensive patients, routine blood and urine tests are normal, but the application of sensitive examination means you can still find some abnormal. That is, early renal damage in primary hypertension, including increased urinary sediment red cell technology. The morphological aberration of erythrocytes was observed by phase contrast microscopy, which was caused by the glomerular capillary filtration barrier caused by hypertension. Urinary albumin excretion increased. This is especially true in patients with primary hypertension who are not adequately controlled and newly developed severe hypertension, which can be reduced after blood pressure control. Urinary NAG excretion increased. The renal tubule and urinary tract epithelial cells contain NAG, and the urinary excretion can be up to 1200 times during renal damage, and the blood pressure control can be reduced. Urinary beta 2 microspheres excretion increased. Beta 2 microspheres have been recognized as sensitive indicators for glomerular filtration rate and renal tubular absorption function. Newly discovered hypertensive patients and elderly patients with hypertension can increase the level of urine beta 2 microspheres, and decrease after blood pressure control.
In the early stages of hypertensive nephropathy, nocturia is usually a typical manifestation of hypertension in the early stages of kidney disease. Increased nocturia is associated with chronic hypertension that causes impairment of the renal arterioles and dysfunction of urine in the tubules. These patients often urinate at least two or three times, more than five or six times. At this point, if the patient routine urine test, you can often find microalbuminuria. Following the occurrence of proteinuria in patients with hypertensive nephropathy, inpidual hypertensive nephropathy may also suffer from transient gross hematuria due to rupture of the capillaries, but without significant low back pain. Clinically, hypertensive nephropathy patients are complicated with arteriosclerotic retinopathy, left ventricular hypertrophy, coronary heart disease, heart failure, cerebral arteriosclerosis and / or cerebrovascular accident history. Discoloration of urine. Urine is thick brown, wash meat, water samples, soy sauce color or muddy, such as Taomi shui. Urine foam, long does not disappear. It shows that the proteins excreted in urine are more. Nocturia. Normal people, less than 60 years of age, should not have nocturia, and if young people develop nocturia, it is likely to be an early manifestation of kidney dysfunction. Excessive or scanty urine. The average daily urine volume of normal persons is 1500 ml, 4-8 times a day. If there is no fever, sweating a lot, drinking water and so on, the amount of urine has fallen sharply or suddenly increased, it is necessary to go to the hospital for examination, to see if it is kidney disease. Lumbago。 No definite reason for backache should be checked kidneys. Spinal and lumbar back muscles, etc.. Edema. Wake up in the morning, eyelids or facial edema, afternoon more subsided, tired after the increase, rest after the relief. Severe edema can occur on both sides of the ankle, lower extremities, lumbosacral, and so on.
The clinical symptoms of hypertensive nephropathy are severe edema. Edema is usually the first symptom, presenting with systemic edema and marked by depression. Severe patients and hydrothorax, ascites, pleural effusion and ascites when more can cause breathing difficulties, umbilical hernia or inguinal hernia. High edema, often accompanied by oliguria, hypertension, mild hypoxemia. Massive proteinuria. Proteinuria and nephrotic syndrome is the main manifestation, qualitative urine protein is + + ~ + + + +, adult daily urine protein excretion than 3.5g/d, as the most selective proteinuria. Hyperlipidemia. Blood cholesterol and triglyceride levels increased significantly. Hypoproteinemia. Plasma protein decreased, serum protein <30g/L, seriously less than 10g/L. Digestive symptoms. Hypertension causes nausea, vomiting and other digestive symptoms, mostly caused by hypertensive encephalopathy. The cause of the disease is the serious and persistent spasm of the small cerebral artery, which causes the cerebral blood circulation disorder and causes the brain edema and the increase of intracranial pressure. Brain symptoms. Headache and dizziness are common symptoms of the disease. It can also have a heavy head or tight neck. Dizziness caused by hypertension occurs more frequently in the morning than in the forehead, occiput or temporal region. Hypertension induced dizziness can be temporary or persistent, blood pressure decreased after the loss, but sometimes excessive drop in blood pressure or cause dizziness. Heart complication. The most common is hypertensive left ventricular hypertrophy, the patient can appear palpitations or exertional dyspnea, paroxysmal nocturnal dyspnea, pulmonary edema, severe left heart failure can occur, or complicated with ischemic heart disease, clinical symptoms of angina pectoris and myocardial infarction. Retinopathy. Blurred vision, optic disc edema, retinal hemorrhage and oozing of blood. Urinary volume change. Some people believe that the first clinical symptoms are nocturia, followed by proteinuria and hematuria, and even uremia. Complications of the brain. Cerebral vascular structure is relatively weak, sclerosis is more fragile, easy to cause cerebral hemorrhage when the blood pressure fluctuates. In addition, small sclerosis is conducive to thrombosis and cerebral infarction.
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