{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,31]],"date-time":"2026-03-31T02:29:16Z","timestamp":1774924156572,"version":"3.50.1"},"reference-count":17,"publisher":"Wiley","issue":"S2","license":[{"start":{"date-parts":[[2018,7,2]],"date-time":"2018-07-02T00:00:00Z","timestamp":1530489600000},"content-version":"vor","delay-in-days":1,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Nephrology"],"published-print":{"date-parts":[[2018,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Apolipoprotein A\u2010I amyloidosis is a rare, autosomal dominant disorder of <jats:italic>APOA\u20101<\/jats:italic> gene characterized by the deposition of apolipoprotein A\u2010I in various organs and can be classified into either hereditary or nonhereditary form in the absence of a family history. Renal disease caused by Apolipoprotein A\u2010I amyloidosis commonly manifested as slowly progressive renal function impairment without heavy proteinuria. Apolipoprotein A\u2010I\u2010related amyloidosis of kidney is of pathogenetic interest because the renal failure is due to peritubular and interstitial amyloid deposits without glomerular deposits. Tubulointerstitial lesion of amyloid deposits was diagnosed in half of carriers of <jats:italic>APOA1<\/jats:italic> gene mutation, only 13% of patients progressed to renal failure requiring hemodialysis or kidney transplantation. Recurrence of apolipoprotein A\u2010I\u2010related amyloidosis after kidney transplantation is very rare. We report a case of a 63\u2010year\u2010old Japanese female without a family history of kidney and\/or liver disease who showed slowly progressive renal graft dysfunction without overt proteinuria. Graft biopsy revealed characteristic Congo red stain positive amyloid deposits localized in the renal interstitial area. No glomerular, vascular and tubular amyloid deposits were noted. Laser microdissection\u2010liquid chromatography tandem mass spectrometry\u2010based proteomic analysis elucidated the type of amyloidosis as apolipoprotein A\u2010I amyloidosis. Genetic analysis of DNA sequence study revealed two novel <jats:italic>APOA1<\/jats:italic> gene mutations of Leu202Arg and Lys262Asn. This is a first and very rare case report of the recurrence of non\u2010familial hereditary apolipoprotein A\u2010I amyloidosis in Japanese transplant recipient.<\/jats:p>","DOI":"10.1111\/nep.13278","type":"journal-article","created":{"date-parts":[[2018,7,3]],"date-time":"2018-07-03T05:00:51Z","timestamp":1530594051000},"page":"17-21","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Two novel <i>APOA1<\/i> gene mutations in a Japanese renal transplant recipient with recurrent apolipoprotein A\u2010I related amyloidosis"],"prefix":"10.1111","volume":"23","author":[{"given":"Keiji","family":"Horike","sequence":"first","affiliation":[{"name":"Department of Kidney Center Masuko Memorial Hospital  Nagoya Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Asami","family":"Takeda","sequence":"additional","affiliation":[{"name":"Department of Kidney Center Nagoya Daini Red Cross Hospital  Nagoya Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Makoto","family":"Tsujita","sequence":"additional","affiliation":[{"name":"Department of Kidney Center Nagoya Daini Red Cross Hospital  Nagoya Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Norihiko","family":"Goto","sequence":"additional","affiliation":[{"name":"Department of Kidney Center Nagoya Daini Red Cross Hospital  Nagoya Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoshihiko","family":"Watarai","sequence":"additional","affiliation":[{"name":"Department of Kidney Center Nagoya Daini Red Cross Hospital  Nagoya Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kazuharu","family":"Uchida","sequence":"additional","affiliation":[{"name":"Department of Kidney Center Masuko Memorial Hospital  Nagoya Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Akio","family":"Katayama","sequence":"additional","affiliation":[{"name":"Department of Kidney Center Masuko Memorial Hospital  Nagoya Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Morikuni","family":"Nishihira","sequence":"additional","affiliation":[{"name":"Department of Kidney Center Masuko Memorial Hospital  Nagoya Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Akira","family":"Shimizu","sequence":"additional","affiliation":[{"name":"Department of Pathology Nippon Medical College  Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kandai","family":"Nozu","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Kobe University  Kobe Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kunio","family":"Morozumi","sequence":"additional","affiliation":[{"name":"Department of Kidney Center Masuko Memorial Hospital  Nagoya Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2018,7,2]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa013354"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1097\/PAS.0b013e3181abdfa7"},{"key":"e_1_2_5_4_1","first-page":"149","article-title":"Familial nephropathic systemic amyloidosis caused by apolipoprotein AI variant Arg26","volume":"87","author":"Vigushin DM","year":"1994","journal-title":"Q. 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