Study On The Relationship Between Transforming Growth Factor-β1and Intimal Hyperplasia Of Arteriovenous Fistula

Internal arteriovenous fistula, is the most common vascular access in patientswith uremia in maintenance hemodialysis, while phlebostenosis and thrombopoiesisin stomas rank primarily in the dysfunction of internal fistula in patients with uremia.However, phlebostenosis, whose pathological characteristics is endo-membranehyperplasia, its pathogenesis is still unclear, and there is no effective therapy to cureand prevent it. The recent research reveals that cellular migration, differentiation,proliferation and extracellular matrix apposition are main cause of endo-membranehyperplasia, while TGF-β1has the above-mentioned biology activity.but therelationship between endo-membrane hyperplasia and A-V fistula dysfunction hasnot been reported in nation so far.Purpose: To investigate the pathologic changes of endo-membrane hyperplasia viamorphology observation of venous vessel specimen of dysfunctional AV fistula;Toinvestigate the relationship between TGF-β1and endo-membrane hyperplasia in AVfistula dysfunction via researching on the relationship between TGF-β1andexpression of TGF-β1in vessels.Methods: We collected clinical data of35patients(20in male,15in female) withuremia. The hyperplasia group included10patients in our department as internalfistula failure; The control group A included10cases planed to be under the Internalarteriovenous fistula operattion; control group B included15cases who hadundergone successful primary Internal arteriovenous fistula up to now andperformed dialysis in clinics. We took one section of hyperplastic vein from eachpatients in hyperplasia group during the Internal fistula neoplasty, meanwhile, wetook a section of vein(not hyperplasia by naked eyes) as control when ligated thecollateral branches in the operation. During Internal fistula neoplasty, we took asection of vein(not hyperplasia by naked eyes) as control group A when ligated thecollateral branches in the operation. All of the vein specimens were observed underlight microscope in HE stain, double stain(collagen fiber and elastic fiber),immunohistochemistry stain. We collected all the patients blood on an empty stomach in the morning thencentrifuged to collect the serum and measured the serum level of TGF-β1by ELISA.Result:(1) HE stain: Under the light microscope, we could observe an evidentproliferation of the vein membrane in hyperplasia group and infiltration ofinflammatory cells in endo-and medial membrane and vacuole like denaturation, butno inflammatory cells in self-controlling group and control group A; The thicknessof vein endo-and medial membrane increased significantly than self-controllinggroup and control group A(P<0.05), but no significant difference in self-controllinggroup and control group A(P>0.05).(2)Double stain(collagen fiber and elastic fiber):An evident rupture and dissolution had been found in endocornea and extrcornea butno positive founding in self-controlling group and control group A.(3)Immun-ochemistry stain: TGF-β1located in cytoplasm and expressed strong positive inhyperplasia and weak positive in self-controlling group and control group A. Theexpression of TGF-β1in hyperplasia group was higher than self-controlling groupand control group A(P<0.01), no significant difference between self-controllinggroup and control group A.(4)Detection by ELISA: There is no significant differencein comparison among hyperplasia group and self-controlling group and controlgroup A(P=0.809).(5)The expression of TGF-β1in serum and blood vessels had nocorrelation with gender, age and primary diseases of kidney failure(P>0.05).Spearman rank correlation analysis indicated that localized expression of TGF-β1had no relationship with serum TGF-β1.Conclusion: Our research draws that Internal arteriovenous fistula is a localizedinflammatory process; Serum TGF-β1has no relationship with its expression inproliferative vasculars; The localized expression of TGF-β1has a relationship withhyperplasia of vein endomembrane in Internal arteriovenous fistula, restraining thelocalized expression of TGF-β1may become the aim of therapy.