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   <subfield code="a">Renal amyloidosis caused by apolipoprotein A-II without a genetic mutation in the coding sequence</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Ryuji Morizane, Toshiaki Monkawa, Konosuke Konishi, Akinori Hashiguchi, Mitsuharu Ueda, Yukio Ando, Hirobumi Tokuyama, Koichi Hayashi, Matsuhiko Hayashi, Hiroshi Itoh]</subfield>
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   <subfield code="a">Although the majority of renal amyloidosis is caused by either acquired monoclonal immunoglobulin light-chain amyloidosis or reactive systemic amyloid A, some cases are caused by hereditary amyloidosis. Apolipoprotein A-II (apoAII) amyloidosis is a rare form of hereditary amyloidosis and cannot be diagnosed by a routine examination. Thus, the prevalence and etiology of apoAII amyloidosis are uncertain. In humans, a genetic mutation in the stop codon of apoAII is considered to be a cause of amyloid fibril formation. We report on a 68-year-old man who presented with proteinuria by apoAII amyloidosis without family history. His proteinuria gradually increased to 6g/day within 1year. A renal biopsy showed amyloid deposition in the glomeruli, however, acquired monoclonal immunoglobulin light-chain amyloidosis and reactive systemic amyloid A were ruled out. Immunohistochemistry revealed apoAII deposition in the glomeruli, but DNA sequencing did not identify any genetic mutation in the coding sequence of apoAII. Here, we report a case of apoAII amyloidosis without a genetic mutation in the coding sequence and discuss the etiology of apoAII amyloidosis.</subfield>
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   <subfield code="a">Japanese Society of Nephrology, 2011</subfield>
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   <subfield code="a">Amyloidosis</subfield>
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   <subfield code="a">Apolipoprotein A-II</subfield>
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   <subfield code="a">Nephrosis</subfield>
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   <subfield code="a">Morizane</subfield>
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   <subfield code="u">Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, 160-8582, Tokyo, Japan</subfield>
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   <subfield code="a">Monkawa</subfield>
   <subfield code="D">Toshiaki</subfield>
   <subfield code="u">Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, 160-8582, Tokyo, Japan</subfield>
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   <subfield code="D">Konosuke</subfield>
   <subfield code="u">Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, 160-8582, Tokyo, Japan</subfield>
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   <subfield code="a">Hashiguchi</subfield>
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   <subfield code="u">Department of Pathology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, 160-8582, Tokyo, Japan</subfield>
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   <subfield code="a">Ueda</subfield>
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   <subfield code="u">Department of Diagnostic Medicine, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, 860-0811, Kumamoto, Japan</subfield>
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   <subfield code="u">Department of Diagnostic Medicine, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, 860-0811, Kumamoto, Japan</subfield>
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   <subfield code="a">Hayashi</subfield>
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   <subfield code="u">Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, 160-8582, Tokyo, Japan</subfield>
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   <subfield code="a">Hayashi</subfield>
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   <subfield code="a">Itoh</subfield>
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   <subfield code="u">Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, 160-8582, Tokyo, Japan</subfield>
   <subfield code="4">aut</subfield>
  </datafield>
  <datafield tag="773" ind1="0" ind2=" ">
   <subfield code="t">Clinical and Experimental Nephrology</subfield>
   <subfield code="d">Springer Japan</subfield>
   <subfield code="g">15/5(2011-10-01), 774-779</subfield>
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   <subfield code="q">15:5&lt;774</subfield>
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   <subfield code="B">NATIONALLICENCE</subfield>
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