Renal Handling of Beta-2-Microglobulin in Neonates Treated with Gentamicin

Abstract

Increased levels of urinary β<sub>2</sub>-microglobulin (β<sub>2</sub>M) have been used as a marker of proximal tubular dysfunction in human neonates. To assess the value of β<sub>2</sub>M in the detection of early stages of tubular damage caused by gentamicin, renal handling of β<sub>2</sub>M was studied sequentially in 18 gentamicin-treated neonates with idiopathic respiratory distress syndrome (mean birth weight 1,781 g, mean gestational age 33.7 weeks) during the first 7 days of life. These data were compared with those obtained from 10 control infants matched for gestational and postnatal ages. In addition, follow-up studies of renal function were conducted in 14 of 18 study infants 1 week after termination of therapy, on day 14 postpartum. The ( ± SD) fractional tubular excretion of β<sub>2</sub>M (FEβ<sub>2</sub>M) tended to decrease significantly in the control infants from 10.3 ± 1% on day 1 to 6.5 ± 0.8% on day 7 postpartum (p < 0.05). In infants treated with gentamicin, the mean FEβ<sub>2</sub>M rose from 10.5 ± 2% on day 1 to 17.1 ± 1%on day 7 (p < 0.01), followed by a decrease to 8.2 ± 0.5% over the next 7 days (p < 0.001). Compared with the control infants, values for the infants receiving gentamicin were significantly higher on postpartum days 3,5, and 7 (p < 0.001). No significant differences in serum creatinine, creatinine clearance, or fractional tubular excretion of sodium were observed between the two groups during the study period. These results suggest that administration of gentamicin with a penicillin antibiotic to preterm infants with idiopathic respiratory distress syndrome is associated with increased FEβ<sub>2</sub>M and that the FEβ<sub>2</sub>M may serve as a useful indicator of tubular dysfunction in infants treated with gentamicin.