Interpretation of IGA Nephropathy six doubts

What is IgA nephropathy?

IgA nephropathy (kidney disease IgA) is a group of mainly IgA or IgA immune complex deposition in the mesangial area or deposition along the glomerular capillary wall is characterized by clinical and pathological manifestations of kidney disease, IgA nephropathy ( kidney disease IgA) is the world's most common form of primary glomerular disease.

What type of IgA nephropathy? IgA nephropathy What are the symptoms of various types of performance?

Clinically of IgA nephropathy (kidney disease IgA) based on pathological types are divided into five types:

Type I: mild disease type. Light microscope: Most glomerular normal, a few areas may have increased mesangial matrix or mesangial cell proliferation, not associated with tubulointerstitial changes. The main symptoms of the onset of gross hematuria.

Type II: mild disease type. Mesangial proliferation, sclerosis, adhesions of less than 50% glomerular involvement, rare crescent. No tubule interstitial damage. Urine test showed abnormal symptoms, patients with persistent microscopic hematuria or with mild to moderate proteinuria (<2.5g / 24h).

Type III: focal segmental glomerulonephritis type. Diffuse mesangial cell proliferation with matrix increase, and more with focal segmental worse, occasionally blocking the crescent formation. Clinical manifestations of nephrotic syndrome or macroalbuminuria.

Type IV: diffuse mesangial proliferative glomerulonephritis type. All were diffuse glomerular mesangial proliferation and sclerosis, with varying degrees of cell proliferation and irregular distribution. It was seen abandoned glomerular, tubular atrophy, interstitial inflammation apparent. Also known as rapidly progressive glomerulonephritis type.

V type: diffuse sclerosing glomerulonephritis type. It may be in the stage or global sclerosis, hyalinization, balloon adhesion, more than 50% crescent formation, qualitative change small tube heavier. Clinical manifestations of chronic renal insufficiency symptoms.

IgA nephropathy is how did it happen? Why are some people predisposed to IgA nephropathy?

IgA nephropathy (kidney disease IgA) can occur at any age, but young people are common, more men than women. Wherein 10--15 years into end-stage renal failure accounted for 35-40%. Similarly young people, also has a cold, fever history, why some people do not suffer from IgA nephropathy, the incidence of some people it is easy to do?

IgA nephropathy (kidney disease IgA) patients had mucosal immune dysfunction. Many patients with IgA nephropathy, often before the onset of respiratory or gastrointestinal symptoms or urinary tract infection symptoms, after systemic immune, poly mucosal IgA synthesis from this type of secretory IgA plasma cells in peripheral blood from a patient and bone marrow.

New research: an increase in the molecular structure of IgA IgA nephropathy (kidney disease IgA) in patients with IgA antibody itself an exception rather than the amount. Healthy kidney transplanted into the body IgA nephropathy patients, also suffering from the same a few years later IgA nephropathy.

Renal fibrosis played a considerable influence in the pathogenesis of IGA nephropathy patients.

First, since the abnormal immune deficiencies or mucosal IgA nephropathy IgA1 molecular structure, the immune complex deposition in the mesangial area or glomerular capillary wall as a direct result of glomerular mesangial cell injury.

Mesangial cell damage after the change: contraction and proliferation. After mesangial cell contraction can reduce the glomerular filtration area, lower filtration fraction, resulting in glomerular capillary blood disorders, microcirculation blocked, causing further glomerular ischemia and hypoxia, which can damage glomerular capillary endothelial cells. Capillary endothelial cell damage, attracting inflammatory cells, so that the release of inflammatory mediators, thereby starting the process of renal fibrosis. At this stage it may exhibit pathological inflammation, increased mesangial cells, mesangial matrix increase.

Glomerular basement membrane pathological changes: larger pore filtration or atresia, or basement membrane rupture; charge barrier damaged filtration membrane permeability enhancement. There may be hematuria, proteinuria clinically. Continued development and evolution, and gradually developed into glomerulosclerosis.

How IgA nephropathy should be treated?

Conventional Western medicine IgA nephropathy (kidney disease IgA), more by hormones, immunosuppressants inhibit the inflammatory response, but could not prevent glomerular microcirculation, can not improve ischemia, hypoxia. Dipyridamole, aspirin and other platelet adhesion to improve function, reduce the formation of micro-thrombosis, but can not improve the function of renal artery smooth muscle cells.

Kidney areas in recent years developed a micro-based traditional Chinese medicine to block renal fibrosis therapy made great achievements in the treatment of IgA nephropathy. Micro-Chinese by blood, stasis, dilation of the renal arteries at all levels to improve within the damaged kidney tissue ischemia and hypoxia. By inactivating reverse, apoptosis, degradation of four measures to block the process of renal fibrosis, thereby improving the structure of the glomerular filtration membrane. Fundamentally blocking protein, occult blood leakage, thereby restoring normal renal function, treatment of IgA nephropathy patients achieved satisfactory results.


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