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<p>Severe hypokalemia with respiratory distress is rarely caused by intestinal potassium (K) excretion from the intestinal tract because most of the ingested K is excreted in the urine and the kidney primarily maintains K balance. However, we recently experienced a rare case in which severe hypokalemia may have been caused by K excretion from a portion of the intestinal tract used as a neobladder. This case was characterized by the massive dilatation of the sigmoid neobladder estimated to hold 2–3 L of urine, due to urinary retention. The patient developed respiratory distress and required K dosages in excess of 300&#xa0;mEq per day. Recent studies have demonstrated that the physical stimulus of membrane stretch increases the probability of opening the BK channel, a type of K channel expressed on the luminal side of the colon’s wall. Therefore, we presumed that, in our case, much potassium was excreted through the urine in the sigmoid neobladder due to colonic wall extension. Additionally, immunostaining of the sigmoid colon tissue of his bladder demonstrated a higher level of expression of BK channel protein than the patient with normal renal function. We speculated that BK channel upregulation also contributed to severe hypokalemia.</p>

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Severe hypokalemia through urinary retention: a case report of a patient with sigmoid neobladder replacement

  • 期刊论文

  • 发表日期：

    2025年6月3日

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  • Midori Kobayashi,
  • Katsuyuki Nagatoya,
  • Masafumi Wada,
  • Maho Tokuchi,
  • Soichiro Misegawa,
  • Rina Saito,
  • Hiroki Nomi,
  • Ryota Haga,
  • Daisuke Mori,
  • Atsushi Yamauchi

摘要

Severe hypokalemia with respiratory distress is rarely caused by intestinal potassium (K) excretion from the intestinal tract because most of the ingested K is excreted in the urine and the kidney primarily maintains K balance. However, we recently experienced a rare case in which severe hypokalemia may have been caused by K excretion from a portion of the intestinal tract used as a neobladder. This case was characterized by the massive dilatation of the sigmoid neobladder estimated to hold 2–3 L of urine, due to urinary retention. The patient developed respiratory distress and required K dosages in excess of 300 mEq per day. Recent studies have demonstrated that the physical stimulus of membrane stretch increases the probability of opening the BK channel, a type of K channel expressed on the luminal side of the colon’s wall. Therefore, we presumed that, in our case, much potassium was excreted through the urine in the sigmoid neobladder due to colonic wall extension. Additionally, immunostaining of the sigmoid colon tissue of his bladder demonstrated a higher level of expression of BK channel protein than the patient with normal renal function. We speculated that BK channel upregulation also contributed to severe hypokalemia.