Trimethoprim / Sulfamethoxazole ( TMP / SMX ) 을 복용 중인 외래 환자에서 발생하는 경구 칼륨 투여 후 칼륨 대사 장애

• Published in: The Korean journal of medicine Vol. 57; no. 1; pp. 75 - 83
• Main Authors: 최춘식, Chun Sik Choi, 유영조, Young Jo Yoo, 김태영, Tae Young Kim, 민경환, Kyung Hwan Min, 한상웅, Sang Woong Han, 노광호, Kwang Ho Roh, 양성규, Seong Kyu Yang, 유준호, Jun Ho Yoo, 오석중, Suk Joong Oh, 문중돈, Jung Don Mun, 김호중, Ho Jung Kim
• Format: Journal Article
• Language: Korean
• Published: 대한내과학회 01.07.1999
• Subjects: diabetes mellitus; hyperkalemia; KCl; TMP / SMX
• ISSN: 1738-9364

TMP/SMX has been shown to cause hyperkalemia in a few outpatients on standard-dose. This prospective study was aimed at investigating other associated factors inducing clinically important hyperkalemia in outpatients on standard-dose of TMP/SMX. Methods : Age-matched diabetic(n=22) and non-diabetic (n=20) patients with UTI on standard dose of TMP/SMX for 5 days were given acute oral intake of 40 mEq of potassium chloride(KCl). Results : Before the intake of TMP/SMX, basal levels of serum potassium(K), serum BUN and creatinine, plasma renin activity(PRA), aldosterone(PA), and transtubular potassium gradient(TTKG) were comparable between diabetic and non-diabetic subjects. Also after TMP/SMX was taken, all parameters didnt reveal any overt changes except a slightly increased serum K but not significantly (from 4.20±0.15 to 4.14±0.21mEq/L in non-diabetics; from 4.13±0.18 to 4.25±0.13mEq/L in diabetics). Following acute oral KCl load, however, the peak increases of serum K changes were significantly higher in diabetics compared to non-diabetics(0.34 0.06 vs 0.62 0.09mEq/L, p<0.01). Furthermore, 8 out of 22 diabetics but none of non-diabetics after acute KCl load developed hyperkalemia(> 5.0 mEq/L). After KCl load, PRA did not show any significant changes, whereas PA was increased simultaneously with the increments of serum K in both diabetic subgroups hyperkalemic(n=8) and normokalemic (n=14) diabetics. But increment was blunted in hyperkalemic diabetic subgroup. TTKG was increased prominently in normokalemic diabetic subgroup(9.20 from 4.50), while it was slightly increased in hyperkalemic diabetic subgroup(4.63 from 3.79mEq/L). There was statistical difference between two subgroups(p < 0.05). In conclusion, Besides the known effect of blocking sodium channels in distal K secreting cells by TMP/SMX, insulinopenia(DM). Hypoaldosteronism with its decreased tubular bioactivity, and increased exogenous K intake in concert could cause clinically overt hyperkalemia on standard-dose of TMP/SMX. When standard- dose of TMP/SMX is administered to patients with deranged K homeostasis, especially to diabetics with hypoaldosteronism, blood K level should be monitored meticulously to avoid hyperkalemia.