Zahida Qamri1, Ronald Pelletier2, Jamison Foster2, Sunil Kumar2, Hammam Momani2, Kyle Ware1, Jon Von Visger2, Anjali Satoskar1, Tibor Nadasdy1, Sergey V Brodsky3. 1. Department of Pathology, The Ohio State University Wexner Medical Center, Columbus, OH, United States. 2. Comprehensive Transplant Center, The Ohio State University Wexner Medical Center, Columbus, OH, United States. 3. Department of Pathology, The Ohio State University Wexner Medical Center, Columbus, OH, United States. Electronic address: sergey.brodsky@osumc.edu.
Abstract
BACKGROUND: Endothelial microparticles (EMPs) 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. EMPs 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.
BACKGROUND: Endothelial microparticles (EMPs) 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. EMPs 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.
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