{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T16:09:58Z","timestamp":1787069398486,"version":"build-2736575974"},"reference-count":22,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2018,10,15]],"date-time":"2018-10-15T00:00:00Z","timestamp":1539561600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Clinical Apheresis"],"published-print":{"date-parts":[[2018,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Angiotensin II type\u20101 receptor antibody (AT1RAb) has been reported to cause antibody mediated rejection (AMR) in kidney transplant recipients possibly by contraction of renal arteries. We here report 2 kidney transplant recipients with elevated AT1RAbs and negative HLA donor specific antibodies (DSA) and anti\u2010major histocompatibility complex class I chain\u2010related gene A (MICA) Abs who received therapeutic plasma exchange (TPE) treatment followed by IVIG.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Case 1<\/jats:title>\n                    <jats:p>Thirty\u2010eight\u2010year\u2010old patient received second kidney transplant for end stage renal disease (ESRD) with chronic rejection. Three years post\u2010transplant, she developed AMR with AT1RAb level &gt;40\u2009U\/mL. She received 5 TPE and AT1RAb decreased by 20%, and biopsy showed improvement of AMR. She received another 3 TPE and AT1RAb decreased by 60%. Her creatinine (Cr) was stabilized at around 1.4 mg\/dL.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Case 2<\/jats:title>\n                    <jats:p>Twenty\u2010four\u2010year\u2010old patient received kidney transplant for ESRD with unclear etiology. Two weeks post\u2010transplant, her Cr rose with AT1RAb level at 18\u2009U\/mL and biopsy showed possible AMR. She received 6 TPE treatments and AT1RAb decreased by 55% and biopsy showed improvement of AMR. She received weekly TPE for subsequently rising AT1RAb but TPE was discontinued because of unsuccessful decrease of AT1RAb. Her Cr was stabilized at around 1.7 mL\/dL.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>We reported 2 patients who received TPE treatments to decrease AT1RAbs. A course of TPE treatment successfully decreased AT1RAb. Histological improvement was observed quickly and Cr was also stabilized following the TPE treatment. Further study is necessary to determine the optimal use of TPE in renal transplant recipients with AT1RAbs.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jca.21657","type":"journal-article","created":{"date-parts":[[2018,10,15]],"date-time":"2018-10-15T12:25:31Z","timestamp":1539606331000},"page":"673-677","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Efficacy of therapeutic plasma exchange on angiotensin II type\u20101 receptor antibodies on two kidney transplant recipients"],"prefix":"10.1002","volume":"33","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1968-2385","authenticated-orcid":false,"given":"Chisa","family":"Yamada","sequence":"first","affiliation":[{"name":"Division of Transfusion Medicine, Department of Pathology University of Michigan Ann Arbor Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yihung","family":"Huang","sequence":"additional","affiliation":[{"name":"Section of Transplant Nephrology, Department of Internal Medicine University of California, Davis Davis California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Silas","family":"Norman","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine University of Michigan Ann Arbor Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abhijit","family":"Naik","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine University of Michigan Ann Arbor Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Omar","family":"Moussa","sequence":"additional","affiliation":[{"name":"Division of Histocompatibility Laboratory, Department of Pathology University of Michigan Ann Arbor Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Milagros","family":"Samaniego","sequence":"additional","affiliation":[{"name":"Department of Medicine Henry Ford Transplant Institute Detroit Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0216-1599","authenticated-orcid":false,"given":"Laura","family":"Cooling","sequence":"additional","affiliation":[{"name":"Division of Transfusion Medicine, Department of Pathology University of Michigan Ann Arbor Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2018,10,15]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.14107"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/ajt.14625"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.humimm.2016.05.021"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.trre.2016.06.001"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.4.1047"},{"key":"e_1_2_5_7_1","doi-asserted-by":"crossref","first-page":"415","DOI":"10.1016\/S0031-6997(24)01458-3","article-title":"International union of pharmacology. 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