Failure of loop diuretics to improve the long term outcome of ischaemic damage in rat kidneys.

The effects of furosemide administered at the onset of postischaemic renal failure were investigated in Sprague-Dawley rats one month after exposing the left kidney to 45 min of renal ischemia. In the experimental group, 13 mg furosemide was given intravenously both before and a few minutes after induction of the ischaemia and then, by an osmotic pump, in a daily dose of 2-3 mg for the following 7 days. The animals of the control group were treated similarly but with saline alone. After one month, the glomerular filtration rate (GFR) in the damaged left kidneys of the furosemide-treated rats was 0.5+/-0.08 ml/min, which was not significantly different from that in the untreated control rats, of 0.8+/-0.14 ml/min. As expected, the right intact kidneys responded with an increase in GFR to about 2 ml/min. Further effects that were similar in the damaged kidneys of the furosemide-treated and untreated animals were a decrease in potassium secretion and in the urine concentration ability; the urine osmolality in the diseased left kidneys was thus 1000-1500 mOsm/kg, as against over 2000 mOsm/kg in the right, intact kidneys. The function of the individual nephrons in terms of such variables as single nephron filtration rate, fractional fluid reabsorption and tubular and vascular hydrostatic pressures remained unaltered, however. Hence, the severe reduction in whole kidney GFR appeared to be due to a loss of nephrons rather than to an equal decrease in each individual nephron. It is also clear that furosemide did not improve the long-term outcome of acute postischaemic renal failure.