High anion gap metabolic acidosis associated with aminocaproic acid.
OBJECTIVE
To report a case of high anion gap metabolic acidosis related to infusion of aminocaproic acid (ACA) that temporarily corrected during hemodialysis and resolved upon ACA discontinuation.


METHODS
A 65-year-old white woman with staphylococcal sepsis complicated by acute renal failure was treated with ACA to control a hemorrhagic coagulopathy. After receiving an initial 5-g bolus of ACA, she received a continuous intravenous infusion of 500 mg/h for just over 5 days, then 250 mg/h for a final 12 hours. Immediately after beginning ACA therapy, she developed a severe anion gap metabolic acidosis that briefly improved after hemodialysis. The condition resolved completely only after the discontinuation of ACA and therapy with a systemic alkalinizer.


CONCLUSIONS
ACA is not among the previously identified causes of high anion gap metabolic acidosis. The temporal profile relating anion gap to ACA initiation, hemodialysis treatment, and ACA discontinuation supports causality in this case. The magnitude of increase in the anion gap appears to have been proportional to the dose of ACA.


CONCLUSIONS
In patients with renal impairment, ACA administration may produce a dose-related, high anion gap metabolic acidosis that might be reversible during hemodialysis. Insufficient data are available, but when ACA must be used in such patients, a more conservative dosing of ACA should be coupled with close monitoring.
Budris
W A
WA
Department of Pharmacy, Northwestern Memorial Hospital, Chicago, IL 60611, USA.
Roxe
D M
DM
Duvel
J M
JM
D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000139:chemically induced*; D058186:Acute Kidney Injury / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D000368:Aged; D000614:Aminocaproates / Q000009:adverse effects* / Q000627:therapeutic use; D005260:Female; D006801:Humans; D006435:Renal Dialysis
D000614:Aminocaproates