Abstract
Objective We evaluated whether urinary excretion of tubular injury markers could be useful
for early detection of gentamicin (GM)-induced renal damage in neonates.
Study Design We conducted a prospective, observational trial in neonates admitted to the neonatal
intensive care unit (26 GM treated, 20 control). Kidney injury molecule-1 (KIM-1),
neutrophil gelatinase–associated lipocalin (NGAL), N-acetyl-β-D-glucosaminidase (NAG), and π- and α-glutathione-S-transferase (GSTP1–1
and GSTA1–1) were measured every 2 hours during admission and compared with serum
creatinine (sCr) and urine output.
Results Nine neonates developed AKI during the course of the study. The peak in excretion
of urinary biomarkers preceded the peak in sCr (p < 0.0001). GM administration resulted in a more pronounced increase of sCr compared
with control (13 [12–28] vs. 10 µmol/L [8.5–17]; p < 0.05). The urinary excretion of NAG (178 [104–698] vs. 32 ng/mol Cr [9–82]; p < 0.001) and NGAL (569 [168–1,681] vs. 222 ng/mol Cr [90–497]; p < 0.05) was higher in the GM group compared with control and preceded the peak of
sCr and urine output decrease.
Conclusion GM administration to neonates is associated with renal damage reflected by a more
pronounced increase in sCr preceded by urinary excretion of biomarkers. Urinary biomarkers
may be useful for earlier identification of renal injury in neonates.
Keywords
urinary biomarkers - gentamicin - acute kidney injury - neonates