IgA Nephropathy is an immune-complex-medicated glomerulonephritis defined by
the presence of IgA deposits in the mesangial area of the kidney.
The onset of IgA Nephropathy can be associated with the upper respiratory
tract infection, and the disease may occur due to the hyperactivity of the
mucosal immune system.If you need the overview list of IgA Nephropathy, please email to kidneyask@hotmail.com or consult free online service!
What are the Causes of IgA Nephropathy?
1. Infection and Inflammatory reaction
The attack of IgA Nephropathy is often followed by an infection, especially
infection of the upper respiratory tract.
2. Genetic predisposition
Some patients show familial aggregation of the disease, which indicated that
IgA Nephropathy may inherit.
3. IgA deposition in the mesangial area
Deposition of IgA Nephropathy and other immune complexes in the mesangial
area destroy the normal structure of certain renal intrinsic cells, thus causing
kidney damage. If you need the detailed cause of IgA Nephropathy, please email to kidneyask@hotmail.com or consult the free online service.
What is the Pathology of IgA Nephropathy?
When you get an infection, antigens (a virus, bacteria, or toxin) can easily
invade into your body, the body produce more antibodies, which are
immunoglobulins produced by the immune system, to fight against these
invaders.
However, antibodies fail to fight off these antigens, but lock onto the
surfaces of foreign substances, forming antigen-antibody aggregates known as
immune complexes. These deposits don't belong to our body, so the body will try
to eliminate them. The immune complexes are too stubborn to be cleared away, so
the inflammatory response will become more and more tense, eventually resulting
in hypersensitivity. The renal intrinsic cells and tissues will be impaired if
the hypersensitivity is out of control. Symptoms will occur over time.
What is the Lee Classification of IgA Nephropathy?
IgA nephropathy can be divided into 5 stages according to the severity of
mesangial proliferation, cresent and tubulointerstitium changes.
Level I: Most glomeruli are normal; occasional moderate mesangial broadening
with or without cell proliferation; the tubulointerstitium is normal.
Level II: Focal glomerular proliferation and sclerosis(50%), cresent is
rarely seen; the tubulointerstitium is normal.
Level III: Diffuse glomerular filtration; more cresents; interstitial edema,
cell infiltration is occasionally seen and tubular atrophy is rare.
Level IV: Severe diffuse mesangial proliferation with focal or total
glomerular sclerosis; cresents (<45%); tubular atrophy, interstitial
infiltration and interstitial foam cells can be occasionally seen.
Level V: cresents is more than 45%, the tubulointerstitium changes are
similar with level VI, but more serious.
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