A Case of Liddle's-like Syndrome With Diabetic Nephropathy Diagnosed from Hypokalemia

DOI
  • Tawa Kakino
    Department of Internal Medicine (I), Osaka Medical College, Takatsuki
  • Nakamura Hidetoshi
    Department of Internal Medicine (I), Osaka Medical College, Takatsuki
  • Fujisawa Reiko
    Department of Internal Medicine (I), Osaka Medical College, Takatsuki
  • Nakagawa Terumasa
    Department of Nephrology, Kumamoto University Graduate School of Medical Sciences
  • Inbe Hisashi
    Department of Internal Medicine (I), Osaka Medical College, Takatsuki
  • Kakizoe Yutaka
    Department of Nephrology, Kumamoto University Graduate School of Medical Sciences
  • Sano Hiroyuki
    Department of Internal Medicine (I), Osaka Medical College, Takatsuki
  • Kanatsuna Norio
    Department of Internal Medicine (I), Osaka Medical College, Takatsuki
  • Onisi Mineki
    Department of Internal Medicine (I), Osaka Medical College, Takatsuki
  • Terasaki Jungo
    Department of Internal Medicine (I), Osaka Medical College, Takatsuki
  • Mori Tatsuhiko
    Department of Internal Medicine (III), Osaka Medical College, Takatsuki
  • Mukoyama Masashi
    Department of Nephrology, Kumamoto University Graduate School of Medical Sciences
  • Imagawa Akihisa
    Department of Internal Medicine (I), Osaka Medical College, Takatsuki

Bibliographic Information

Other Title
  • 低カリウム血症を契機に診断に至った，糖尿病腎症にLiddle症候群類似病態をきたした1例

Description

<p>A 38-year-old man was admitted to our hospital to undergo treatment for diabetes, nephrotic syndrome, hypokalemia and hypertension. He had been diagnosed with type 2 diabetes 11 years previously, and his glucose control had been poor. Four years previously, he was normotensive and showed trace levels of urinary albumin excretion and a normal serum potassium concentration. On admission, he showed metabolic alkalosis, low plasma renin activity, and low a plasma aldosterone concentration with hypertension. Because we suspected Liddle syndrome, triamterene was administered, and his hypertension and hypokalemia both improved. Our patient had no family history of hypertension, and no mutation of ENaC (amyloid-sensitive epithelial sodium channel) gene exon 13, but showed increased urinary excretion of serine protease. These findings suggested that the increased serine protease level had a similar effect to the high activation of ENaC. This case showed a similar presentation to Liddle syndrome due to nephrotic syndrome caused by diabetic nephropathy.</p>

Journal

Keywords

Details 詳細情報について

  • CRID
    1390845713084756736
  • NII Article ID
    130007684567
  • DOI
    10.11213/tonyobyo.62.383
  • ISSN
    1881588X
    0021437X
  • Text Lang
    ja
  • Data Source
    • JaLC
    • CiNii Articles
  • Abstract License Flag
    Disallowed

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