Of FSGS initiation factors not yet elucidated, but most scholars believe that
thelymphocyte abnormal activation, release of lymphocyte factor, resulting in
abnormalglomerular permeability and sclerosing changes. But results in abnormal
glomerular capillary wall permeability and promote hardening factor remains
unclear. The reportwould permit the experimental animals the presence of
proteinuria lymphocyte-derivedfactor in FSGS patients. Some scholars believe
that this cycle can change vascularpermeability factor can cause glomerular
epithelial cell foot process fusion, resulting infoot process and basement
membrane separation, followed by the basement membranepermeability changes in
endothelial protein deposition, vascular loop necrosis, vascular loop and
balloon adhesion, typical glomerulosclerosis change to.
Oxide production may be another important pathogenic mechanism observed in
animal models of proteinuria, Mn - superoxide dismutase have increased the level
of gene transcription in rat renal artery perfusion oxide.
FSGS have different characteristics in different ethnic groups.
African-American andSpanish children from FSGS to terminal renal speed faster
than the Caucasian, and theratio of the number. Related kidney transplant
relapse rate than cadaveric renaltransplantation more, suggesting that
genetic background plays an important role of FSGS pathogenic, but the specific
genetic markers have not yet been confirmed.
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