Endocan as a marker of microvascular inflammation in kidney transplant recipients

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作者
Yu Ho Lee
Se-Yun Kim
Haena Moon
Jung-Woo Seo
Dong-Jin Kim
Seon Hwa Park
Yang-Gyun Kim
Ju-Young Moon
Jin Sug Kim
Kyung-Hwan Jeong
Sung-Jig Lim
Chan-Duck Kim
Jae Berm Park
Byung Ha Chung
Yeong Hoon Kim
Jaeseok Yang
Hyung-In Yang
Kyoung Soo Kim
Sang-Ho Lee
机构
[1] Kyung Hee University,Division of Nephrology, Department of Internal Medicine
[2] Kyung Hee University,Department of Pathology
[3] Kyungpook National University Hospital,Division of Nephrology, Department of Internal Medicine
[4] Samsung Medical Center,Department of Surgery
[5] The St. Mary’s Hospital of Catholic University of Korea,Division of Nephrology, Department of Internal Medicine, College of Medicine
[6] Inje University College of Medicine,Division of Nephrology, Department of Internal Medicine
[7] Seoul National University Hospital,Transplantation Center
[8] Kyung Hee University Hospital at Gangdong,East
[9] College of Medicine,West Bone & Joint Disease Research Institute
[10] Kyung Hee University,Department of Clinical Pharmacology and Therapeutics
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摘要
Endocan is a water-soluble proteoglycan exclusively secreted by vascular endothelium. Endocan levels may be elevated in kidney transplant recipients experiencing antibody-mediated rejection (ABMR), which is characterized by vascular inflammation in transplanted kidney. We evaluated the clinical relevance of endocan as markers of microvascular inflammation in patients who underwent kidney transplantation. Plasma and urinary endocan levels were measured in 203 kidney transplant recipients and were compared across different etiologies of allograft dysfunction and various pathologic scores. Both plasma and urinary endocan levels were significantly higher in patients with acute ABMR than those in patients with normal pathology, acute tubular necrosis (ATN), acute pyelonephritis, BK virus associated nephropathy (BKVN), and T-cell mediated rejection (TCMR). Patients with chronic active ABMR also exhibited significantly higher plasma and urinary endocan levels than patients with long-term graft survival. Scores of glomerulitis and peritubular capillaritis, which are typical features of microvascular inflammation, were significantly elevated in patients with higher plasma and/or urinary endocan levels. Furthermore, plasma and urinary endocan levels could effectively discriminate ABMR from ATN, BKVN, and TCMR. Finally, patients exhibiting high urinary and plasma endocan levels in acute ABMR group showed significantly worse renal survival. Altogether, plasma and urinary endocan levels may serve as potential markers of microvascular inflammation in kidney transplant recipients.
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