Additional mechanisms of nafamostat mesilate-associated hyperkalaemia

Abstract

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).

Pretreatment with nafamostat mesilate, a kallikrein inhibitor, to decrease withdrawal response associated with rocuronium

“…This is also in agreement with other studies [5,12]. Nafamostat mesilate may also be associated with hyperkalemia due to decreased urinary potassium excretion, suppression of aldosterone secretion, and direct inhibition of apical sodium conductance in the collecting ducts [15]. There were no significant changes in the serum potassium concentration at the doses used in this study, which is also in agreement with other studies [5].…”

THE CLINICAL APPLICATION OF CRRT—CURRENT STATUS: Anticoagulation for Continuous Renal Replacement Therapy

“…However, studies have demonstrated that levels of thrombin–antithrombin III complex and prothrombin activation fragment 1 + 2 increase, while protein C activity decreases, leading to circuit clotting (67,68). Several side effects (anaphylaxis, agranulocytosis, hyperkalemia) have been reported with use of nafamostat (69–71).…”

Nafamostat mesilate, a noncalcium compound, as an anticoagulant, induces calcium‐dependent haemolysis when infused with packed erythrocytes

“…As shown in Table 6, extracellular calcium may enter the erythrocytes through the reaction with citrate and NM. NM is an inhibitor of the Na + /K + ‐ATPase pump, resulting in hyperkalaemia (Muto et al , 1994; Ookawara et al , 1996). Although there are no reports on haemolysis due to Na + /K + ‐ATPase pump inhibition, inhibitors such as digitalis may elevate intracellular calcium (Giunta et al , 2007; Clausen, 1998).…”