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While the role of AT<jats:sub>1<\/jats:sub>R-Ab for ABMR and graft failure is increasingly recognized, there is little information available on the management of these patients for re-transplantation over the barrier of persisting AT<jats:sub>1<\/jats:sub>R-Ab.<\/jats:p><\/jats:sec><jats:sec><jats:title>Case<\/jats:title><jats:p>We report on a male patient with kidney failure in infancy due to obstructive uropathy who had lost his first kidney transplant due to AT<jats:sub>1<\/jats:sub>R-Ab-mediated chronic ABMR. Because this antibody persisted during 4 years of hemodialysis, for the 2nd kidney transplantation (living-related transplantation from his mother), he underwent a desensitization regimen consisting of 15 plasmapheresis sessions, infusions of intravenous immunoglobulin G and thymoglobulin, as well as pharmacological blockade of the Angiotensin II (AT II) pathway by candesartan. This intense desensitization regimen transiently decreased elevated AT<jats:sub>1<\/jats:sub>R-Ab titers, resulting in stable short-term kidney allograft function. The subsequent clinical course, however, was complicated by acute cellular rejection and chronic ABMR due to persistent AT<jats:sub>1<\/jats:sub>R-Ab and de novo HLA-DSA, which shortened allograft survival to a period of only 4 years.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>This case highlights the difficulty of persistently decreasing elevated AT<jats:sub>1<\/jats:sub>R-Ab titers by a desensitization regimen for re-transplantation and the detrimental effect of the interplay between AT<jats:sub>1<\/jats:sub>R-Ab and HLA-DSA on kidney transplant survival.<\/jats:p><\/jats:sec>","DOI":"10.1007\/s00467-020-04879-8","type":"journal-article","created":{"date-parts":[[2020,12,23]],"date-time":"2020-12-23T05:12:44Z","timestamp":1608700364000},"page":"725-729","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Kidney re-transplantation in a child across the barrier of persisting angiotensin II type I receptor antibodies"],"prefix":"10.1007","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8667-5492","authenticated-orcid":false,"given":"Annika","family":"Gold","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexander","family":"Fichtner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniela","family":"Choukair","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Claus Peter","family":"Schmitt","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2521-8201","authenticated-orcid":false,"given":"Caner","family":"S\u00fcsal","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Duska","family":"Dragun","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6598-6910","authenticated-orcid":false,"given":"Burkhard","family":"T\u00f6nshoff","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2020,12,23]]},"reference":[{"key":"4879_CR1","doi-asserted-by":"publisher","first-page":"2520","DOI":"10.1111\/j.1600-6143.2009.02799.x","volume":"9","author":"G Einecke","year":"2009","unstructured":"Einecke G, Sis B, Reeve J, Mengel M, Campbell PM, Hidalgo LG, Kaplan B, Halloran PF (2009) Antibody-mediated microcirculation injury is the major cause of late kidney transplant failure. 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