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1.
Artigo em Inglês | WPRIM (Pacífico Ocidental) | ID: wpr-922552

RESUMO

BK polyomavirus-associated nephropathy (BKPyVAN) is a common cause of allograft failure. However, differentiation between BKPyVAN and type I T cell-mediated rejection (TCMR) is challenging when simian virus 40 (SV40) staining is negative, because of the similarities in histopathology. This study investigated whether donor-derived cell-free DNA (ddcfDNA) can be used to differentiate BKPyVAN. Target region capture sequencing was applied to detect the ddcfDNAs of 12 recipients with stable graft function, 22 with type I TCMR, 21 with proven BKPyVAN, and 5 with possible PyVAN. We found that urinary ddcfDNA levels were upregulated in recipients with graft injury, whereas plasma ddcfDNA levels were comparable for all groups. The median urinary concentrations and fractions of ddcfDNA in proven BKPyVAN recipients were significantly higher than those in type I TCMR recipients (10.4 vs. 6.1 ng/mL,

2.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-755900

RESUMO

Objective To compare the clinical outcomes of low-dose rabbit antithymocyte globulin (rATG ) vs basiliximab as induction therapy in recipients of ABO-incompatible kidney transplantation (ABOi-KT) .Methods Retrospective analysis was conducted for e the clinical data of 40 ABOi-KT recipients between March 2017 and March 2019 .17 recipients of them received induction therapy with basiliximab (basiliximab group) while another 23 recipients received low-dose rATG (rATG group ,rATG 25 mg/d × 3 d) .During a median follow-up period of 282 days , the data of serum creatinine and eGFR at 1 week and 1 month ,graft survival rate and complication rate of two groups were compared .Results No significant difference existed in age ,gender ,dialytic modality/ duration , blood groups of recipients , HLA mis-match , blood group antibody titers , dose of rituximab ,blood groups of donors or donor age ( P > 0 .05 ) . The times of double filtration plasmapheresis in Basiliximab group were more (P< 0 .05) .No significant difference existed in serum creatinine and eGFR at 1 week or 1 month ( P > 0 .05 ) . No significant difference existed in graft survival rate . No significant difference existed in rate of acute rejection ,parvovirus B19 infection , urinary tract infection or hematoma .Conclusions Low-dose of rATG is as effective as basiliximab for ABOi-KT recipients .And rATG does not increase the rate of infection .

3.
Biomed Res Int ; 2018: 5484731, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30112400

RESUMO

VEGF-NO axis uncoupling is an important pathogenesis for DN. Reduced ß2GPI could play a part in VEGF signaling pathway and has a protective effect on diabetic vascular disease. This study investigates the effect of reduced ß2GPI on glomerular mesangial cells VEGF-NO axis uncoupling induced by high glucose. Compared to control group, glomerular mesangial cell line HBZY-1 cells treated with high glucose expressed higher levels of VEGF mRNA and protein and produced more ROS but less NO. The related proteins related to VEGF-NO axis were assayed. High glucose could significantly increase the expression of the level of VEGFR2 and obviously increase phosphorylation of Akt and eNOS but significantly decrease the expression of GTP cyclohydrolase 1 (GCH-1), reducing the production of eNOS dimer. Both ß2GPI and reduced ß2GPI partly reverse these effects caused by high glucose. Reduced ß2GPI had stronger effect than ß2GPI. GCH-1 is the speed limit of tetrahydrobiopterin (BH4) synthesis enzyme. As the key part of eNOS cofactors, BH4 could partly restore eNOS dimer induced by high glucose. Our results indicated that high glucose could interfere with eNOS dimer formation. ß2GPI and reduced ß2GPI can partly reverse the VEGF-NO axis uncoupling by restoring the GCH-1 expression level and then promote eNOS dimer formation.


Assuntos
Glucose/fisiologia , Óxido Nítrico Sintase Tipo III/metabolismo , Fator A de Crescimento do Endotélio Vascular/fisiologia , Animais , Humanos , Células Mesangiais , Coelhos , Ratos , beta 2-Glicoproteína I
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