Patient's question:
Problem Description:Doctor's answer:
IgA nephropathy has been clinically recognized for nearly 40 years. With the continuous deepening of research, people's understanding of IgA nephropathy has undergone significant changes, especially with the progress in genetic and hereditary research. It is no longer viewed as an independent disease entity. The clinical manifestations, pathological findings, or disease progression speed of IgA nephropathy are complex and are the result of the combined action of multiple genetic factors. In the early stages of IgA nephropathy, symptoms are often similar to those of nephritis or nephrotic syndrome, and a definitive diagnosis can only be made after a kidney biopsy. Once a patient is diagnosed with IgA nephropathy, clinical hospitalization and treatment are required. Based on the symptoms of "proteinuria and hematuria" associated with IgA nephropathy and the pathological study of immune complex deposition and damage, Western medicine primarily focuses on the use of hormones and cytotoxic drugs, while also combining anti-inflammatory and anticoagulant treatments. So, how do hormones, Tripterygium wilfordii, and cyclophosphamide work? High-dose hormone therapy is the most common approach, using larger doses of hormones mainly to suppress B-cell antibody production and promote antibody catabolism, thereby inhibiting the antigen-antibody reaction. The use of cyclophosphamide and other cytotoxic drugs primarily inhibits DNA replication and mainly targets B cells, suppressing the production of immunoglobulins and reducing antibody levels. At the same time, it suppresses T cells, interfering with the release of inflammatory mediators. Clinical data shows that simply relying on Western medicine treatment and regulating immune responses can achieve good results in reducing protein, occult blood, and hypertension, but this is only a temporary suppression of complications. If the patient encounters external adverse factors such as colds or infections later, symptoms may reappear. Once symptoms reappear, further treatment becomes necessary, with repeated increases in hormone doses and the rotation of Tripterygium wilfordii, cyclophosphamide, and the currently "popular" mycophenolate mofetil. What are the factors or causes behind the repeated, unresolved nature of IgA nephropathy treatment?The clinical recognition of IgA nephropathy has been nearly 40 years, and with the continuous deepening of research, people's understanding of IgA nephropathy has undergone significant changes, especially with the progress in genetic and hereditary research. It is no longer viewed as an independent disease entity. The clinical manifestations, pathological findings, or disease progression speed of IgA nephropathy are complex and are the result of the combined action of multiple genetic factors. Renal biopsy suggests poor prognosis factors include glomerular sclerosis, interstitial fibrosis, invasion of glomerular capillaries, diffuse proliferation, and diffuse crescent formation. In pathological analysis, IgA nephropathy is characterized by the deposition of IgA antibodies or immune complexes in the mesangial area of the glomerulus, leading to mesangial cell damage and a series of inflammatory reactions. Excessive proliferation or contraction of mesangial cells causes microcirculatory disorders, resulting in ischemia and hypoxia. Ischemia and hypoxia lead to damage to renal capillary endothelial cells, epithelial cells, and interstitial fibroblasts, along with phenotypic transformation, forming renal fibrosis. Damage to endothelial or epithelial cells alters the function of the basal membrane and charge barrier, leading to the leakage of large amounts of protein and red blood cells, forming proteinuria and hematuria. As mentioned above, the leakage of protein and red blood cells in kidney disease is primarily caused by damage to the glomerular filtration membrane, resulting in increased permeability. Currently, if only hormones, Tripterygium wilfordii, cyclophosphamide, and other drugs are used to suppress IgA antibodies and immunoglobulin production, this can only address the primary disease but cannot clear deposited IgA receptors and immune complexes, nor improve the ischemia and hypoxia within the kidneys. Without resolving these issues, it is impossible to completely treat and eliminate the series of reactions caused by mesangial cell damage or to effectively repair the glomerular filtration membrane and restore its normal filtration function.
It is clear that the use of hormones, Tripterygium wilfordii, or cyclophosphamide only temporarily suppresses the production of various receptors and controls the damage and progression of "inflammatory" reactions, leading to a reduction or even disappearance of proteinuria and occult blood for a period. However, the fundamental cause remains unresolved. Once the drug effects wear off or under certain factors or causes, how can proteinuria and occult blood not return? This is like the saying "stir the water to stop the boil." If the fire intensifies or the "stirring" is insufficient, the water will boil again. Treating the root cause of IgA nephropathy is far more complex than "stirring the water to stop the boil." Therefore, in the early stages of the disease, when the condition is urgent, it is necessary to quickly "stir the water to stop the boil" while also "removing the firewood at the bottom of the pot" (i.e., treating both the symptoms and the root cause). This makes it easier to treat the disease at its root. If "stirring the water to stop the boil" becomes ineffective, it is essential to quickly increase "removing the firewood at the bottom of the pot" while also combining "stirring the water to stop the boil."
The use of hormones, Tripterygium wilfordii, cyclophosphamide, and other drugs undeniably has excellent "stirring the water to stop the boil" effects. In the early stages of the disease, they can indeed effectively control the progression of the condition, even curing some patients when the "fire" is not yet intense. Therefore, not only should the role of these drugs not be ignored, but they should also be used accurately and reasonably. Through years of clinical validation, the theory of blocking renal fibrosis provides a clinical basis for treating IgA nephropathy by "removing the firewood at the bottom of the pot." This hospital has successfully pioneered the "Micro-Traditional Chinese Medicine Permeation Therapy for Blocking Renal Fibrosis" based on the theory of blocking renal fibrosis. It has been widely applied in clinical practice and has achieved excellent results. The micro-Traditional Chinese Medicine treatment for IgA nephropathy targets the "source" by expanding blood vessels, dilating all levels of renal arteries, and directly improving the ischemia and hypoxia in diseased renal tissues. This reduces further damage to various renal cells and restores the function of cells damaged by ischemia and hypoxia. At the same time, the active components in micro-Traditional Chinese Medicine can inactivate the activity of various "cytotoxic factors" released during the inflammatory response. This effectively blocks the "chain reaction" damage to renal cells. Unlike the mere "control" effects of hormones, Tripterygium wilfordii, cyclophosphamide, and other drugs, this treatment transforms the approach into a fundamental "elimination."