The long-term presence of hypertension, the first to be affected is renal arterioles, and then injury of vascular endothelial cells, epithelial cells, mesangial cells and renal tubular epithelial cells, leading to cell proliferation and extracellular matrix hyperplasia of mesangial cell secretion, promote glomerular sclerosis.
Renal arteriole injury and glomerulosclerosis leads to ischemia and hypoxia, ischemia, hypoxia and long-term in turn stimulate the cells to attract the infiltration of inflammatory cells and the release of inflammatory mediators, transdifferentiation of fibroblasts into myofibroblasts, release of extracellular matrix increased, the degradation function, excessive extracellular matrix deposition that leads to renal tubule and renal interstitial fibrosis, thus forming a chain deterioration of renal fibrosis.
In the early stage of renal injury, usually is the stage of inflammation, only slight proteinuria occurs. With the progression of the disease, glomerular fibrosis and renal function gradually decline, and renal hypertension appears. If the disease develops rapidly, it is characterized by headache, accompanied by nausea, vomiting, anorexia, enlargement of the heart, heart failure, blurred vision, even blindness and nervous system abnormalities. A urine test can appear urinary protein increased, and red blood cells, white blood cells, a few patients had hematuria and other symptoms, to protect the kidney, one of the core problem is to control blood pressure.
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