A case of hyperkalemic renal tubular acidosis during total parenteral nutrition

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  • 高カロリー輸液に併発した高Ｋ血症性尿細管性アシドーシスの１例
  • ショウレイ ホウコク コウカロリーユエキ ニ ヘイハツ シタ コウK ケツショウセイ ニョウ サイカンセイ アシドーシス ノ 1レイ

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Abstract

A 90-year-old female with chronic renal failure and sequela associated with cerebral infarction was admitted to our hospital. After about 8 years (May 21, 1998), she complained of general fatigue and anorexia. She was unable to eat orally due to gradual loss of appetite. Thereafter, she developed with severe dehydration. Subsequently, total parenteral nutrition (TPN) was initiated on May 27, 1998. Five days later, she developed acute pneumonia and mixed acidosis accompanied by hyperkalemia. After 12 days, she showed hyperchloremic metabolic acidosis, laboratory findings demonstrated normal plasma anion gap (AG), normal aldosterone levels, lower transtubular potassium gradient (1.36), urinary AG level of 22.4mEq/L, and reduced serum creatinine levels (decreased from 1.8mg/dL on May 26, 1998 to 0.9mg/dL on June 8, 1998). Drug therapy and peritoneal dialysis led to improvement of hyperkalemia and hyperchloremic metabolic acidosis; however, she died 18 days later due to aggravation of acute pneumonia.<br>Based on these conditions, she was diagnosed as having hyperkalemic renal tubular acidosis (hyperkalemic RTA). We speculate that acute metabolic acidosis was caused by TPN, which reduced aldosterone responsiveness in the collecting tubule cells of the kidney, leading hyperkalemic RTA.

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