Furosemide does not prevent indomethacin-induced renal side effects in preterm infants

Abstract

Objective: To determine whether furosemide could prevent renal side effects of indomethacin (INN, indometacin) used for the pharmacologic closure of the patent ductus arteriosus (PDA) in preterm infants.

Methods: Thirty-six preterm infants with birth weights < 1750 gm affected by hemodynamically significant PDA were randomly assigned to one of two study groups. Group 1 consisted of 18 infants treated with three doses of indomethacin (0.20 mg/kg every 12 hours); each dose was followed by a dose of furosemide (1 mg/kg). Group 2 consisted of 18 infants treated only with the same doses of indomethacin. Body weight, urine output, glomerular filtration rate (GFR), fractional excretion of sodium (FENa+) and potassium (FEK+), and osmolal and free water clearance were evaluated in both groups before, during, and after treatment.

Results: The body weight trend, serum sodium, chloride and potassium concentrations, plasmatic and urinary osmolality were similar during the treatment in both the groups. A significant reduction of urine output (p < 0.01) was detected in group 2 but not in group 1. A significant increase of blood urea nitrogen and serum creatinine was detected at the end of treatment in group 1 compared with group 2. During the treatment, a significantly higher GFR (p < 0.05) was found in group 2 than in group 1. FENa+ and FEK+ were significantly higher (p < 0.05 and p < 0.001, respectively) in group 1 than in group 2 during and after the treatment. The osmolol clearance and free water clearance were significantly higher during and after treatment (p < 0.01 and p < 0.001, respectively) in group 1 than in group 2.

Conclusions: Our findings show that furosemide cannot prevent the indomethacin-induced renal failure, but it does not have any negative influence on its therapeutic effectiveness.