Triflusal (2-acetoxy-4-trifluormethylbenzoic acid) is a platelet-antiaggregant drug that selectively inhibits thromboxane synthesis with little effect on prostacyclin production. In this study, we evaluated the effect of 5- day administration of 900 mg/day triflusal on glomerular filtration rate (GFR), renal plasma flow (RPF), urinary albumin excretion (UAE), thromboxane B2 (TXB2), 6-ketoprostaglandin F1α (PGF1α), and PGE2 in nine normotensive insulin-dependent diabetic patients with UAE between 30 and 103 fxg/min. Plasma TXB, and plasma renin activity (PRA) were also determined. After administration of triflusal, we observed a reduction in microalbuminuria (59 ± 25 vs. 33 ± 22 μg/min, P < 0.01), an increase in RPF (648 ± 119 vs. 722 ± 134 ml· min−1 · 1.73 m−2, P < 0.01), and a reduction in filtration fraction (0.24 ± 0.04 vs. 0.20 ± 0.03, P < 0.01). Triflusal produced a significant reduction in both plasma TXB2 (130 ± 39 vs. 52 ± 32 pg/ml, P < 0.02) and urine TXB2 (523 ± 249 vs. 312 ± 11 pg/min, P < 0.02), without changes in PRA and UAE of 6-keto-PGF1α and PGE2. Metabolic control and arterial blood pressure did not change during the study. These results suggest that platelet-antiaggregant therapy can reduce microalbuminuria in diabetic patients. This effect could be mediated by a reduction in the transglomerular hydraulic pressure through a vasodilation of efferent arterioles secondary to renal thromboxane synthesis inhibition.

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Copyright © 1990 by the American Diabetes Association
1990