多発性嚢胞腎‐ここ10年の進展と2002年の話題‐

DOI

書誌事項

タイトル別名
  • POLYCYSTIC KIDNEY DISEASE: CLINICAL ADVANCES IN THE PAST 10 YEARS AND TOPICS IN 2002
  • ―ここ10年の進展と2002年の話題―

抄録

The year 2002 was an epoch-making year for the pathogenesis and treatment of polycystic kidney disease (PKD). The last genetic puzzle concerning major PKD gene, the gene PKHD1 causing autosomal recessive PKD had remained elusive for many years. However, cloning of the gene PKHD1 was achieved at the beginning of the year. In the end of the year, it was elucidated that most of the different kinds of PKD gene products concentrated in the cilia of the renal tubular epithelial cells. In the field of therapy, an angiotensin II receptor blocker, candesartan, was reported to better preserve renal function of autosomal dominant PKD patients with hypertension than calcium antagonist did. On the other hand, the candidate medicine for PKD, pioglitazone, which was already being used as a drug for diabetes mellitus was proposed as an effective drug. For the mass effect of PKD and polycystic liver disease transcatheter renal and hepatic arterial embolization treatment was established.<br>In this review, the author explains clinical development against PKD in the past 10 years in Japan as well as major topics of PKD in 2002.

収録刊行物

  • 医療

    医療 57 (9), 551-557, 2003

    一般社団法人 国立医療学会

キーワード

詳細情報 詳細情報について

  • CRID
    1390001206313968640
  • NII論文ID
    130004316209
  • DOI
    10.11261/iryo1946.57.551
  • ISSN
    18848729
    00211699
  • 本文言語コード
    ja
  • データソース種別
    • JaLC
    • CiNii Articles
  • 抄録ライセンスフラグ
    使用不可

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