Early posttransplant changes in circulating endothelial microparticles in patients with kidney transplantation

Abstract

Background Endothelial microparticles (EMP) are membrane vesicles shed from endothelial cell in response to injury, activation or apoptosis. Kidney transplantation (KTx) is the treatment of choice for patients with end stage kidney disease (ESKD). The aim of this study was to analyze changes in EMP and serum creatinine (SCr) in patients following KTx. Methods Blood was periodically collected from patients before (pre-KTx) and after KTx for two months. EMP were identified as CD31+/CD42b− microparticles and quantified by fluorescence-activated cell scanning. Results This study included 213 KTx, 14 kidney/pancreas (KPTx) recipients and 60 healthy donors prior to donation. The recipients were divided into 5 groups based on the cause of ESKD. No differences in the quantity of circulating EMP were seen in the pre-KPTx or KTx recipient sera and healthy donor sera. Patients with ESKD secondary to diabetes mellitus, obstructive/inherited kidney disease and autoimmune disease had a decrease in both circulating EMP and SCr by day 60 after KTx. Conclusion Reduction in both circulating EMP and SCr was seen after kidney KTx in patients with selective ESKD.

Factors Contributing to Kidney Allograft Loss and Associated Consequences among Post Kidney Transplantation Patients

“…Again, graft losses were also associated with fibrosis/atrophy [12]. Chronic allograft injury (CAI) remains one of the main causes for allograft failure [14][15][16]. Kidney allograft rejection may ultimately cause allograft loss.…”

“…Kidney allograft rejection may ultimately cause allograft loss. Kidney allograft rejection occurs via cellular, humoral or combined mechanisms of which in many cases, the endothelium is the main target of the recipient immune system [14]. Thomas [10] identifies three types of renal transplant rejection namely, hyperacute, acute and chronic rejection or chronic allograft nephropathy (CAN).…”

Extracellular vesicles as mediators of vascular inflammation in kidney disease

“…A detailed analysis determined that most plaque EVs are of leukocyte origin, including 29% macro phage (CD14 + ), 15% lymphocyte (CD4 + ), 8% granulocyte (CD66b + ) provenience [86] . No platelet, but erythrocyte and smooth muscle cell markers were detected in EVs from the plaque lysate, recent in vitro data providing first evidence of EV generation from smooth muscle cells in healthy controls at start of the trial [48] which may reflect that these patients represent a subgroup with relatively few comorbidities. In summary, chronic elevation of endothelial EVs currently appears to be significantly associated with vascular dysfunction and atherosclerosis in renal disease.…”

“…Counts and provenience of circulating EVs have been characterized in patients with chronic renal impairment with and without renal replacement therapy. Some studies found elevated serum concentrations of total and CD42 + platelet EV [4446] , total, endothelial (CD31 + , CD114 + ) [43,46] , platelet (CD41 + ), and erythrocyte (CD235 + ) EVs [43] in patients with end stage renal disease, while in others, total plasma EV concentrations were unaltered [47,48] or only endothelial EVs were increased [41] . Also, the effect of the hemodialysis procedure is controversial with an increase in some [47] but not other studies [44,45] .…”

“…A follow up study of 81 hemodialysis patients for a mean of 50 mo revealed that endothelial (CD31 + ) EV concentration in serum obtained after the long interval was a significant predictor of all cause and cardiovascular mortality, an association that was not observed for CD41 + platelet, CD11b + leukocyte or CD235 + erythrocyte EVs [59] . Another prospective study investigated endothelial EV counts (CD31 + ) in a cohort of 227 patients with end stage renal disease who were scheduled for kidney transplantation [48] . Endothelial EVs significantly decreased during 60 d of longitudinal follow up after kidney transplantation.…”