Glomerulosclerosis Diabetic

**Glomerulosclerosis**. The basis of the disease is a decrease in the number of functioning nephrons due to damage to the glomeruli and the walls of the Shumlyansky-Henle capsule, as well as due to dystrophy and atrophy of the tubules and intrarenal vessels. Morphologically it is characterized by the replacement of the stromal elements of the glomerulus with connective tissue with compression of the capillary loops; inflammatory, degenerative-dystrophic and sclerotic changes in the wall and medulla of the renal arteries. There is atrophy of the cortex and shrinkage of the kidneys. Microscopic examination mainly reveals homogeneous tubular-medullary atrophy, hyaline and funicular necrosis of the tubular epithelium, compaction and thickening of the basement membrane with the appearance of vacuoles in it. The function of the kidney is also impaired - the amount of glomerular fluid secreted by goblet cells decreases and its viscosity increases. With pathological processes in the tubules, sodium reabsorption stops, its concentration in the urine increases and, as a result, dehydration of the body.

Glomeruloskerosis is a severe immunoinflammatory process that occurs in the kidneys and leads to dysfunction. In this case, it is glomerulosclerosis of the diabetic type, that is, it is a consequence of the development of diabetes mellitus. The causes of this pathology are not fully understood, however, it is generally accepted that the development of this process is caused by various viruses and

Diabetic glomerulsclerosis is a progressive disease that affects the filtering structures of the kidneys, leading to loss of function and ability to clear toxins from the blood. One of the main causes of the disease is diabetes, but it can also be associated with other diseases such as atherosclerosis, hypertension, etc.

Diabetic glomerular sclerosis is characterized by the replacement of functional kidney tissue with a mass of collagen fibers and connective tissue, which leads to a decrease in the size and functionality of the glomerular walls. This is accompanied by a decrease in renal filtration, a decrease in the volume of urine produced and the development of azotemia. The disease may proceed