Endocan as a marker of microvascular inflammation in kidney transplant recipients

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

doi:10.1038/s41598-018-37975-9

Endocan as a marker of microvascular inflammation in kidney transplant recipients

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

Department of Medicine

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17 Scopus citations

Abstract

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.

Original language	English
Article number	1854
Journal	Scientific Reports
Volume	9
Issue number	1
DOIs	https://doi.org/10.1038/s41598-018-37975-9
State	Published - 1 Dec 2019

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Lee, Y. H., Kim, S. Y., Moon, H., Seo, J. W., Kim, D. J., Park, S. H., Kim, Y. G., Moon, J. Y., Kim, J. S., Jeong, K. H., Lim, S. J., Kim, C. D., Park, J. B., Chung, B. H., Kim, Y. H., Yang, J., Yang, H. I., Kim, K. S., & Lee, S. H. (2019). Endocan as a marker of microvascular inflammation in kidney transplant recipients. Scientific Reports, 9(1), Article 1854. https://doi.org/10.1038/s41598-018-37975-9

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title = "Endocan as a marker of microvascular inflammation in kidney transplant recipients",

abstract = "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.",

author = "Lee, {Yu Ho} and Kim, {Se Yun} and Haena Moon and Seo, {Jung Woo} and Kim, {Dong Jin} and Park, {Seon Hwa} and Kim, {Yang Gyun} and Moon, {Ju Young} and Kim, {Jin Sug} and Jeong, {Kyung Hwan} and Lim, {Sung Jig} and Kim, {Chan Duck} and Park, {Jae Berm} and Chung, {Byung Ha} and Kim, {Yeong Hoon} and Jaeseok Yang and Yang, {Hyung In} and Kim, {Kyoung Soo} and Lee, {Sang Ho}",

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AU - Kim, Se Yun

AU - Moon, Haena

AU - Seo, Jung Woo

AU - Kim, Dong Jin

AU - Park, Seon Hwa

AU - Kim, Yang Gyun

AU - Moon, Ju Young

AU - Kim, Jin Sug

AU - Jeong, Kyung Hwan

AU - Lim, Sung Jig

AU - Kim, Chan Duck

AU - Park, Jae Berm

AU - Chung, Byung Ha

AU - Kim, Yeong Hoon

AU - Yang, Jaeseok

AU - Yang, Hyung In

AU - Kim, Kyoung Soo

AU - Lee, Sang Ho

PY - 2019/12/1

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AB - 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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Endocan as a marker of microvascular inflammation in kidney transplant recipients

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