Nafamostat mesilate (NM), a potent protease inhibitor, has been known to induce hyperkalemia. We reported here two cases with hyperkalemia, induced by NM. The first case, a 51-year-old female, had received chronic hemodialysis therapy since May, 1989, because of primary amyloidosis. On September 19, 1989, she suffered from acute exacerbation of chronic pancreatitis, and 150mg a day NM was continuously administered. On the day following the start of NM administration, serum potassium rose to 7.0mEq/
l, and had increased to 7.2mEq/
l on the next day. As the symptoms of chronic pancreatitis had improved by September 21, NM administration was discontinued, and serum potassium had faller to within the normal range by the following day, and remained within normal range there after. The second case, a 76-year-old man, suffered from a dissecting aneurysm (Stanford A, early thrombosed type) on December 10, 1993. As pneumonia was revealed on December 19, 2g Silastatin sodium was prescribed. However, since renal failure progressed with antibiotics, continuous hemofiltration was started on December 22, with 30mg NM an hour as an anticoagulant.
Although adequate K removal was achieved by hemofiltration, and K supplementation was discontinued, serum potassium gradually increased to 5.6mEq/
l several hours after the start of NM administration. Thus, NM and continuous hemofiltration were discontinued on December 23, and serum K had decreased to within normal range by the next day. In both cases, NM appeared to induce hyperkalemia. However, the first case had anuria, and in the second 110mEq K was removed by hemofiltration. These findings lead us to conclude that NM and/or its derivatives induced hyperkalemia by affecting the extrarenal potassium regulatory system, rather than renal potassium excretion.
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