The so-called refractory nephrotic syndrome, the medical field to explain this concept: After a standard regimen of hormone medicine, or ineffective, or hormone-dependent, or to have effect and later relapse cases.
Hormone-dependent refers to hormone therapy has some effect, but in the course of hormone withdrawal or hormone withdrawal relapse within 14 days; hormone is ineffective standard hormone therapy for non-responders. Often relapsing forms of mechanized means of renal relapse within six months after remission for more than 2 or 2 times, or more than three times the recurrence or 3 times a year; these patients renal comprehensive, traveling the disease has not been controlled, and even deteriorating. Many people ask: Why are these renal comprehensive so "refractory" refractory renal comprehensive in the end how to cure??
Found in the clinical treatment of refractory refractory renal comprehensive reasons why are the following:
1, infection factors:
Infection is now generally considered the primary factor in renal comprehensive relapse. Patients with renal comprehensive general decline in immune capacity, reduce defense capabilities, such as bacteria, fungi, bacteria, or other factors, can easily cause repeated infections, a large number of immune complex formation, deposition in the kidney inherent cells, increased kidney damage, leading to renal ball further fibrosis, sclerosis.
If the infection is not controlled factors have been constantly increased inflammatory response, the disease from inflammation of (induction phase) into inflammatory matrix synthesis phase, when the damaged intrinsic cells induced nephrotoxicity in a series of cytokines and growth factors Next, the occurrence of phenotypic transformation, secrete large amounts of collagen fibers protein (extracellular matrix-ECM), the destruction itself ECM degradation and synthesis balancing mechanism, resulting in a healthy kidney to replace ECM units, rapid progression of renal fibrosis. At this simple anti-infective therapy, has been unable to effectively control the disease.
2, hypercoagulable state
The results in patients with nephrotic syndrome exists hypercoagulable states, both renal parenchymal damage, but also further promote kidney disease, one of the leading refractory renal comprehensive factors.
Nephrotic syndrome due to (1) the vascular wall damage starts exogenous coagulation system, as well as promote platelet adhesion and aggregation; (2) the hepatic synthesis of Fbg (an important coagulation factors involved in platelet aggregation and adhesion between, can induce thrombosis formation) increases; (3) long-term glucocorticoid, so factor ⅷ activity increased, while inhibiting monocyte - macrophage system, it swallowed, clear activation function to reduce clotting factors, resulting in the accumulation of activated coagulation factors, coagulation system activation; (4) antithrombin Ⅲ (AT-Ⅲ) is the most important in vivo anticoagulant protein S (PS) is a vitamin K-dependent anticoagulant protein. Once suffering from nephrotic syndrome, protein S, antithrombin Ⅲ and lost a lot of urine, which led to reduced anticoagulant function. (5) enhanced platelet adhesion and aggregation functions, easily lead to thrombosis, microcirculation. (6) Since plasminogen missing from the urine, and plasminogen activator inhibitor (PAI) activity increased, thrombin-activated fibrinolysis inhibitor (TAFI) antigen and activity increased, so decreased fibrinolytic activity , can easily lead to a hypercoagulable state, thrombosis.
Hypercoagulable state of nephrotic syndrome cause kidney further ischemia and hypoxia, can easily result in the formation of blood clots, kidney lumen becomes narrow, contracted kidney inherent cells continue to be damaged, more severe ischemia and hypoxia, thus forming a kind of vicious circle, leading to inflammatory cell infiltration, increased inflammatory response, accelerate the process of renal fibrosis.
3, hyperlipidemia
Hyperlipidemia and hypercoagulable state as a result of kidney damage also nephrotic syndrome, and its persistence will cause more damage the kidneys, increase the difficulty of treatment of nephrotic syndrome.
Persistent hyperlipidemia, hyperlipidemia make LDL (low density lipoprotein) increased it by mesangial cell receptor-mediated endocytosis and intracellular release of free cholesterol, promote mesangial cell proliferation; Secondly LDL and OX-LDL (oxLDL) stimulate mesangial cells to produce ECM and induce apoptosis of mesangial cells; again LDL and OX-LDL stimulated monocytes - macrophages to release a variety of inflammatory mediators and cytokines and growth factor prompting ECM generation and deposition.
Persistent hyperlipidemia likely to cause damage to endothelial cells, thereby activating the deterioration caused by the process of renal fibrosis, the disease gradually progress to deteriorate more and more difficult to treat!
In addition, leading refractory renal comprehensive there other reasons why it is difficult to treat pathological type, and use of hormone medication is not standardized, and so on.
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