ISSN:
1432-1041
Keywords:
Key words Nafamostat mesilate
;
Haemodialysis; anticoagulant
;
hyperkalaemia
;
erythrocyte
;
potassium
;
6-amidino-2-naphthol
;
p-guanidinobenzoic acid
Source:
Springer Online Journal Archives 1860-2000
Topics:
Chemistry and Pharmacology
,
Medicine
Notes:
Abstract Objective: Nafamostat mesilate, a potent protease inhibitor, is widely used for the treatment of pancreatitis, disseminated intravascular coagulation and as an anticoagulant in haemodialysis. However, hyperkalaemia associated with nafamostat mesilate has been reported. It is thought to be due to decreased urinary potassium excretion, of the drug suppression of aldosterone secretion, and a direct inhibitory action on the apical Na+ conductance in collecting ducts. We have seen two cases of nafamostat mesilate associated-hyperkalaemia, which indicated that extrarenal potassium imbalance might play a role in inducing hyperkalaemia. Methods: To examine the effect of nafamostat mesilate on potassium transport in erythrocytes in vitro, 86RbCl uptake was measured in red blood cells from eight healthy volunteers. Results: Nafamostat mesilate and a metabolite, 6-amidino-2-naphthol, at concentrations of 10−4 and 10−3 M, respectively, significantly, suppressed potassium influx whilst another metabolite, p-guanidinobenzoic acid, had no effect. The inhibitory action of nafamostat mesilate was not affected by various inhibitors. Conclusion: Nafamostat mesilate and its metabolite, 6-amidino-2-naphthol, suppressed potassium influx in erythrocytes by inhibition of a Na-K ATPase dependent pathway, which was not inhibited by amiloride, barium, nor by frusemide (furosemide).
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s002280050176
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