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- 저자 : 문중돈(Jung Don Mun) (검색결과 2 건)
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장이간 이뇨제 남용중인 특발성 또는 자가획득 부종간의 병태생리의 차이
민경환(Kyung Hwan Min),김호중(Ho Jung Kim),유준호(Jun Ho Ryu),한상웅(Sang Woong Han),강석우(Seok Woo Kang),문중돈(Jung Don Mun) 대한신장학회 2000 Kidney Research and Clinical Practice Vol.19 No.1
N/A Patients suffering from idiopathic or self-induced edema are uniformly characterized by chronic use of furosemide, which leads to vicious cycle of edema. Among chronic furosemide users who don't have any other specific edema forming diseases, 9 patients from the outpatient clinic(OC) and 6 patients examined at the emergency room(ER) used it mainly for weight reduction and for cyclical edema, respectively. All of the ER group patients were presented with severe hypokalemia(2.04±0.2mEq/L; range 1.3 to 2.7 mEq/L) and alkalosis(748±0.01; range 7.44 to 7.51) but none from the OC group showed such results. Other baseline parameters including Plasma renin activity(PRA) and aldosterone level on recumbency, and FEn₂were similar in both groups. In contrast, daily working hours(6.1±0.5 vs 10±0.6hr, p<0.01), average body weight gain between AM and PM(0.4±0.1 vs 0.9±0.lkg, p<0.01), peak weight gain interval(9±0.8 vs 5±0.1day, p<0.05), PRA(7.6±1.5 vs 23.5±7.2ng/ml/h, p<0.05) and aldosterone level(22.1±4.2 vs 64.8±10.4 ng/dl, p<0.01) on ambulation, and FEk. on normokalemia(ll±2A vs 36±7.7%, p<0.01) were statistically different between the two groups. In comparison to the OC group, both the amout of urine(617±39 vs 358±26ml, p<0.01) and the percent change of PRA(-14±4 vs -3±2%, p<0.05) and al-dosterone level(-17±5 vs -4±3%, p<0.05) after saline loading(lL over 1hr, IV) following ambulation were smaller in the Elt group. Moat of the ER group patients(5/6) required aldosterone antagonist (spironolactone) added to K(+) supplement, but all of the OC group patients were managed to maintain an edema-free status with conservative treatment. In conclusion, patients with idiopathic edema seem to have more fluid transudation out of intravascular space during orthostasis with a prominent degree of deranged renin-aldosterone axis and K(+) metabolism than those with self-induced edema.
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Trimethoprim / Sulfamethoxazole ( TMP / SMX ) 을 복용 중인 외래 환자에서 발생하는 경구 칼륨 투여 후 칼륨 대사 장애
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 Ki 대한내과학회 1999 대한내과학회지 Vol.57 No.1
N/A 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.
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