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The role of hormone in the treatment of nephrotic syndrome

Dec 31, 2016
Hormone mainly through the inhibition of immune cells, macrophages, B cells, immune cell communication, the immune response is inhibited, so as to reduce the deposition of immune complexes on the natural cell injury. At the same time, glucocorticoid can balance between synthesis and degradation of polysaccharide balance protection cell matrix generation; inhibition of prostaglandin, inhibition of platelet factor activity, decreased synthesis and release induced renal toxicity factor, has anti-inflammatory effect. For the short term, especially in the acute phase of nephrotic syndrome, can effectively control the progress of the disease.
But glucocorticoids are not pathological in renal function cells caused by inflammatory reaction changes, such as: mesangial cell proliferation and mesangial matrix increased, glomerular basement membrane changes, glomerular fibrosis and sclerosis play a therapeutic role. Therefore, the process of renal fibrosis continues, and with a series of nephrotoxic cytokines and growth factors, the production and release of kidney injury.
In addition, irregular application of hormone drugs (random addition and withdrawal of the withdrawal, etc.) and is prone to repeated exacerbations, accelerate the process of renal fibrosis, and make the condition once again increased once again increased the difficulty of treatment and rehabilitation. And, in the process of accelerating the development of renal fibrosis, due to the damage or damage to the renal function cells, there will be a result of centripetal obesity, hypokalemia, edema, hypertension and other side effects caused by hormones.
To sum up, although the application of glucocorticoid can ease the symptoms, short-term effect is very good. However, it does not repair the damaged functional renal units, but also can not reach the role of renal fibrosis. On the contrary, the long-term use of glucocorticoids can also reduce the body's defense function, easy to induce a variety of infections and the potential spread of infectious lesions, accelerate the process of renal fibrosis.

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