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. CASE SUMMARY: A 65-year-old white woman with staphylococcal sepsis complicated by acute renal failure...

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Bibliographic Details
Published in:The Annals of pharmacotherapy 1999-03, Vol.33 (3), p.308-311
Main Authors: Budris, WA, Roxe, DM, Duvel, JM
Format: Article
Language:English
Subjects:
Acid-Base Equilibrium
Acidosis - chemically induced
Acute Kidney Injury - etiology
Acute Kidney Injury - physiopathology
Acute Kidney Injury - therapy
Aged
Aminocaproates - adverse effects
Aminocaproates - therapeutic use
Biological and medical sciences
Drug toxicity and drugs side effects treatment
Female
Humans
Medical sciences
Miscellaneous (drug allergy, mutagens, teratogens...)
Pharmacology. Drug treatments
Renal Dialysis
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Summary: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. CASE SUMMARY: 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. DISCUSSION: 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.
ISSN:1060-0280
1542-6270
DOI:10.1345/aph.18029