Furosemide did not appear to reduce the risk of
requiring renal replacement therapy (relative risk (RR)
1.02, 95% CI 0.90–1.16, p = 0.73) and hospital mortality
(RR 1.12, 95%CI 0.93–1.34, p = 0.23) when used as a
preventive or therapeutic drug in patients at risk of or
with established AKI, respectively (Figs 2 and 3). Using
all-cause mortality as an end-point, the funnel plot does
not suggest the presence of publication bias (Fig. 4).
These results confirmed the findings of our previous
meta-analysis [17].
First, it is important to emphasise that furosemide can
increase urine output without improving the creatinine
clearance and renal function. A transient increase in urine
output after furosemide may create a false sense of
security, as if the drug has ‘fixed the problem' or changed
the course of AKI. This has the potential to delay the
diagnostic and therapeutic process targeting the underlying
causes of AKI, such as hypovolaemia, urinary
outflow tract obstruction and sepsis. As such, the administration
of furosemide should only be considered after
close attention to the underlying causes of oliguria and the
haemodynamic status of the patient. Adequate hydration is
important in determining the diuretic and renovascular
protective response to furosemide [30, 37].
http://ether.stanford.edu/urology/Furosemide.pdf
