Understand the root cause of why kidney disease patients need to use glucocorticoids!

Understand the root cause of why kidney disease patients need to use glucocorticoids!

Glucocorticoids are hormones naturally secreted by the adrenal glands that regulate metabolism of substances and water and salt metabolism. They have a wide range of complex effects and have been used in the treatment of kidney disease for more than half a century. They still play an important role in the treatment of many immune-mediated kidney diseases. So why can this substance normally secreted by the human body be used in the treatment of kidney disease? This is because glucocorticoids have definite and powerful anti-inflammatory, immunosuppressive and cytoprotective effects. Therefore, they can significantly inhibit active lesions, reduce kidney damage, reduce proteinuria, and delay the progression of kidney disease.

Immune abnormality is an important pathogenesis of many kidney diseases, and its pathological basis is immune complex deposition that triggers inflammatory response, inflammatory cell infiltration, cell proliferation, etc. The immunosuppressive effect of glucocorticoids runs through all links of the immune process. First, it can inhibit the phagocytosis and processing of antigens by macrophages; secondly, glucocorticoids can temporarily inhibit peripheral lymphocytes, reducing their absolute number, and the reason is mostly related to the migration of lymphocytes to tissues outside the blood, not caused by the destruction of lymphocytes. In addition, glucocorticoids can inhibit the process of B cells transforming into plasma cells, resulting in less antibody production and inhibiting antibody-mediated humoral immune response.

Glucocorticoids have a powerful anti-inflammatory effect and can inhibit inflammatory reactions caused by infectious, immune, chemical, and aseptic inflammation. First, glucocorticoids can change the tension and permeability of blood vessels, reduce capillary permeability, and thus alleviate inflammatory symptoms. In addition, glucocorticoids can inhibit the aggregation of inflammatory cells such as macrophages, monocytes, and neutrophils to the site of inflammation; at the same time, glucocorticoids can enhance the stability of lysosomal membranes and reduce the release of lysosomal hydrolases and proteases; in the late stage of inflammation, glucocorticoids can inhibit fibroblasts, reduce the production of collagen and aminopolysaccharides, and reduce the formation of adhesions and scars.

Although glucocorticoids can treat kidney disease by inhibiting inflammation, regulating immunity and protecting cells, we patients need to be aware that not all kidney diseases require glucocorticoid treatment. So, under what circumstances are glucocorticoids used to treat kidney disease? The basic principle is to fully understand the cause, pathogenesis and clinical characteristics of the disease, and at the same time, combine the information of kidney pathological biopsy to decide on the use of glucocorticoids.

Although glucocorticoid therapy is the basic medication for the treatment of kidney disease, different patients respond differently to glucocorticoid therapy, and care should be taken to judge and evaluate its efficacy during treatment. Some patients are sensitive to glucocorticoids, and proteinuria is relieved within 8 weeks of adequate hormone treatment. Some patients are effective at the beginning of glucocorticoid treatment, but proteinuria reappears within 2 weeks after hormone reduction or discontinuation, which we call hormone dependence. Similarly, some patients still have persistent proteinuria after hormone treatment, which is hormone resistance. After hormone treatment, the urine protein has disappeared, and the urine protein increases significantly again after hormone discontinuation for more than 4 weeks, which is called relapse. Therefore, during hormone treatment of kidney disease, its efficacy needs to be closely monitored, and the next treatment plan should be formulated according to the patient's response to hormones.

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