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Abstract
Furosemide frequently is advocated as a prophylaxis against renal failure in septic
and injured patients; this effect is thought to be secondary to an increase in renal
blood flow. This postulate was tested within 72 hours of admission in 22 previously
healthy patients with acute pancreatitis (two), massive trauma (ten), or severe sepsis
(ten). Renal clearances of inulin (GFR), para-amino hippurate (ERPF), sodium (CNA), osmoles (Cogsm), and free water (CH2o) were measured in milliliters per minute before and after the intravenous infusion
of furosemide (0.5 mg. per kilogram of body weight). Renal vein PAH levels (EPAH)
in eight patients were used to calculate true renal plasma flow (TRPF), true renal
blood f ow (TRBF), and renal vascular resistance (RVR). Furosernide caused a significant
increase in urine volume, CNa, and Cogsm; there were no significant changes in GFR, ERPF, RVR, TRBF, and EPAH. These findings also were observed when the patients were subgrouped according to
elevated, normal, or low renal plasma flow and elevated renal vascular resistance.
No significant changes were seen in EPAH, thus making a redistribution of renal blood flow unlikely. These studies indicate
that furosemide has only a diuretic effect and no hemodynamic effect in the kidney;
it has the potential of seriously reducing the circulatory volume and causing renal
failure in critical patients.
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Article info
Publication history
Accepted:
November 7,
1975
Footnotes
☆Supported by the Detroit General Hospital Research Corporation.
Identification
Copyright
© 1976 Published by Elsevier Inc.