Impaired potassium handling after acute oral potassium loading in outpatients on standard dose of trimethoprim/sulfamethoxazole(TMP/SMX).
- Author:
Kyung Hwan MIN
1
;
Sang Woong HAN
;
Chun Sik CHOI
;
Tae Young KIM
;
Kwang Ho ROH
;
Young Jo YOU
;
Seong Kyu YANG
;
Jun Ho YOO
;
Suk Joong OH
;
Jung Don MUN
;
Ho Jung KIM
Author Information
1. Dept. of Internal Medicine, Hanyang University KURI Hospital, Kuri, Korea.
- Publication Type:Original Article
- Keywords:
TMP/SMX;
KCl;
hyperkalemia;
diabetes mellitus
- MeSH:
Creatinine;
Diabetes Mellitus;
Homeostasis;
Humans;
Hyperkalemia;
Hypoaldosteronism;
Outpatients*;
Plasma;
Potassium*;
Prospective Studies;
Renin;
Sodium Channels
- From:Korean Journal of Medicine
1999;57(1):75-83
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: 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.
