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The clinical implication of inhibiting platelet activation on chronic renal allograft dysfunction: a prospective cohort study.

Abstract：

INTRODUCTION:Clinically chronic renal allograft dysfunction (CRAD) manifests as a progressive elevation of serum creatinine (Cr) with an associated deterioration in proteinuria and decrease in glomerular filtration rate (GFR) following the first year after transplantation. Currently, how to delay or reverse CRAD and improve the long-term survival of transplanted kidneys is an intensively researched topic in the transplantation field. OBJECTIVE:The objective of this study was to examine the therapeutic efficacy and safety profile of inhibiting platelet activation on living related donor renal transplant recipients with CRAD. METHODS:We performed a prospective cohort study to examine the effects of inhibiting platelet activation on the expression of platelet activation markers, namely platelet surface glycoprotein IIIa (CD61), lysosomal enzyme glycoprotein (CD63), and fibrinogen receptor monoclonal antibody (PAC-1); we also studied platelet-derived growth factor-BB (PDGF-BB) and transforming growth factor β(1) (TGF-β(1)) in the peripheral blood of renal graft recipients with CRAD. In addition, we correlated this metrics with the function of transplanted kidneys, peripheral blood platelet counts and trough concentrations of immunosuppressants. RESULTS:Inhibiting platelet activation decreased the expression of platelet activation markers in peripheral blood: CD61 (P < .001), CD63 (P = .031), PAC-1 (P = .002), PDGF-BB (P = .013), and TGF-β(1) (P = .030). Cr and urea nitrogen remained stable compared with the control group, which showed progressive increases. The GFR of transplanted kidneys was improved (P = .033); however, there was no difference before versus after treatment in the platelet count (P = .991) or the trough concentration of immunosuppressants (cyclosporine, P = .071; tacrolimus, P = .984). CONCLUSION:Inhibition of platelet activation, which was effective and safe, seemed to treat CRAD probably through improving the microcirculation of transplanted kidneys, down-regulating the expression of TGF-β, and thereby delaying fibrosis.

journal_name

Transplant Proc

journal_title

Transplantation proceedings

authors

Zhang Y,Zong HT,Yang CC,Zhang XD

doi

10.1016/j.transproceed.2011.05.047

subject

Has Abstract

pub_date

2011-09-01 00:00:00

pages

2596-600

issue

7

eissn

0041-1345

issn

1873-2623

pii

S0041-1345(11)00849-9

journal_volume

43

pub_type

杂志文章

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