title: Effects of thromboxane synthesis inhibitor triflusal on renal hemodynamics in microalbuminuric diabetic patients.
abstract: 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 F1 alpha (PGF1 alpha), and PGE2 in nine normotensive insulin-dependent diabetic patients with UAE between 30 and 103 micrograms/min. Plasma TXB2 and plasma renin activity (PRA) were also determined. After administration of triflusal, we observed a reduction in microalbuminuria (59 +/- 25 vs. 33 +/- 22 micrograms/min, P less than 0.01), an increase in RPF (648 +/- 119 vs. 722 +/- 134 ml.min-1 x 1.73 m-2, P less than 0.01), and a reduction in filtration fraction (0.24 +/- 0.04 vs. 0.20 +/- 0.03, P less than 0.01). Triflusal produced a significant reduction in both plasma TXB2 (130 +/- 39 vs. 52 +/- 32 pg/ml, P less than 0.02) and urine TXB2 (523 +/- 249 vs. 312 +/- 11 pg/min, P less than 0.02), without changes in PRA and UAE of 6-keto-PGF1 alpha 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.
authors: Endocrinology and Diabetes Unit, University of Barcelona, Spain.
authors: E
authors: E
authors: Esmatjes
authors: J I
authors: JI
authors: Conget
authors: J
authors: J
authors: Gaya
authors: M R
authors: MR
authors: Fernandez
authors: J P
authors: JP
authors: Ferrer
authors: F
authors: F
authors: Rivera
authors: E
authors: E
authors: Vilardell
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000652:urine; D000328:Adult; D000419:Albuminuria; D001786:Blood Glucose / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D015232:Dinoprostone / Q000652:urine; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects*; D006801:Humans; D008297:Male; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D012079:Renal Circulation / Q000187:drug effects*; D012083:Renin / Q000097:blood; D012459:Salicylates / Q000494:pharmacology*; D013929:Thromboxane B2 / Q000037:antagonists & inhibitors / Q000097:blood* / Q000652:urine
chemical_list: D001786:Blood Glucose; D010975:Platelet Aggregation Inhibitors; D012459:Salicylates; C016167:triflusal; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D012083:Renin; D015232:Dinoprostone