The biretropical cortex is a thinning of the cortex due to a series of lesions produced by chronic glomerulonephritis. Chronic glomerulonephritis is the end stage in the development of different types of glomerulonephritis. The lesion is characterized by vitreous degeneration and sclerosis of a large number of glomeruli, also known as chronic sclerosing glomerulonephritis. To the naked eye, both kidneys are reduced in size and have a diffuse, fine-grained surface. The cortex is thin and the medulla is not well defined. There is an increase in fat around the renal pelvis. The gross lesion of chronic nephritis is called secondary granular consolidation kidney. The etiology is as follows: 1. Intrarenal arteriosclerosis caused by glomerular lesions, which can further aggravate ischemic damage to the renal parenchyma; 2. Glomerular damage caused by compensatory changes in renal hemodynamics. When part of the glomerulus is involved, the glomerular filtration rate of the surviving kidney units is compensatingly increased, and this hyperperfusion and hyperfiltration state can cause sclerosis of the surviving glomerulus and eventually renal failure; 3. Hypertension causes small renal arteriosclerosis. Long-term hypertension causes ischemic changes, resulting in narrowing and occlusion of small renal arteries, which accelerates glomerulosclerosis. Hypertension can also cause glomerular hyperfiltration and accelerate glomerulosclerosis by increasing glomerular capillary hydrostatic pressure; 4. Overload state of glomerular thylakoid membrane. Normal glomerular thylakoid cells have the function of phagocytosis and removal of immune complexes, but when overloaded, it can cause proliferation of thylakoid stroma and cells, and eventually sclerosis.