Is Thromboxane a Potent Antinatriuretic Factor and Is It Involved in the Development of Acute Renal Failure?

Abstract

Glycerol-treated rats exhibited significantly increased urinary thromboxane B₂ (TXB)₂, prostaglandin E₂ (PGE₂) and 6-ketoprostaglandin F_1α (6kPGF_1α) excretion and urine volume (UV). These increases were associated with significant decreases in creatinine clearance (C_Cr), urinary sodium concentration (U_Na), urinary sodium excretion (U_NaV), and fractional excretion of sodium (FE_Na%), which is consistent with the development of the prerenal (reversible) phase of acute renal failure (ARF). When glycerol-treated rats were pretreated with a selective inhibitor of thromboxane A₂ (TXA₂) synthesis (imidazole), urinary PGE₂ and 6kPGF_1α excretion and UV remained unchanged, whereas C_Cr, U_Na, U_NaV decreases were partially prevented. Additionally, FE_Na% was increased, indicating inhibition of sodium reabsorption. The findings indicate that inhibition of TXA₂ synthesis increases U_NaV and partially improves C_Cr in glycerol-treated rats. Further histologic observation and functional follow-up over longer periods of time are needed to clarify the role of TXA₂ in the development of ARF.