Why the study?
Does aspirin affect renal function and the prostaglandin-kallikrein systems in patients with recent myocardial infarction?
Does aspirin affect renal function and the prostaglandin-kallikrein systems in patients with recent myocardial infarction?
Aspirin suppresses PGE2 excretion but does not alter urinary kallikrein activity or renal function early after myocardial infarction, contrasting with the effects of sulfinpyrazone.
Aspirin does not impair renal function or kallikrein activity early post-MI despite PGE2 suppression; extends distinction from sulfinpyrazone on these pathways.
Using a double-blind procedure, 29 patients with a recent myocardial infarction were randomly allocated to a placebo group (n = 14) and to a group receiving aspirin, 300 mg three times a day (n = 15) over 7 days. No change in renal function was observed in either treatment group. Compared with the placebo group, the 24-h urinary excretion of prostaglandin E2 (PGE2) was significantly suppressed in the aspirin group, but the urinary kallikrein activity was unchanged. These results contrast with our previous study of similar patients, in which sulfinpyrazone decreased renal function, as well as the urinary PGE2 and kallikrein excretions. These divergent effects of aspirin and sulfinpyrazone on urinary kallikrein activity could explain the different trends in renal function observed early after myocardial infarction.
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Lijnen et al. (1984) studied this question.
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