Mechanisms in Acute Oliguric Renal Failure Induced by Tetracydine Infusion

Abstract

Tetracycline hydrochloride (TC), 30–70 mg/kg infused intravenously in dogs in the course of a few minutes, reduced clearance of inulin (C_in) and p-aminohippuric acid (C_PAH) on an average to less than 5% of control. In spite of increased intrarenal pressure (approximately 50 mm Hg), electro-magnetically recorded renal blood flow was preserved, indicating that the reduction of C_in and C_PAH resulted from tubular obstruction, not renai vasoconstriction. The metabolic rate of the cortex and outer medulla fell to 69% of control after TC, as measured by the heat accumulation rate. Further reduction to basal metabolic level (30% of control) was reversibly produced by elevating ureteral pressure, suggesting that the high metabolic rate was caused by continued active reabsorption of sodium chloride at about half the control rate. Thus C. greatly underestimated glomerular filtration rate in the TC-damaged kidney. From these results and the observation of TC-containing casts in the medullary tubules, we conclude that TC caused tubular obstruction and that leakage of inulin and PAH from the tubules occurred mainly distally to the major sodium-reabsorbing tubular segments.

Key Words:

• Intrarenal pressure
• kidney metabolic rate
• renal failure
• tetracycline
• tubular obstruction