Am J Perinatol 2016; 33(02): 180-187
DOI: 10.1055/s-0035-1563714
Original Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Tubular Injury Biomarkers to Detect Gentamicin-Induced Acute Kidney Injury in the Neonatal Intensive Care Unit

Diana Jansen
1   Department of Intensive Care Medicine, Radboud university medical center, Nijmegen, The Netherlands
,
Esther Peters
1   Department of Intensive Care Medicine, Radboud university medical center, Nijmegen, The Netherlands
2   Department of Pharmacology and Toxicology, Radboud university medical center, Nijmegen, The Netherlands
,
Suzanne Heemskerk
1   Department of Intensive Care Medicine, Radboud university medical center, Nijmegen, The Netherlands
2   Department of Pharmacology and Toxicology, Radboud university medical center, Nijmegen, The Netherlands
,
Linda Koster-Kamphuis
3   Department of Pediatric Nephrology, Radboud university medical center, Nijmegen, The Netherlands
,
Martijn P.W.J.M. Bouw
1   Department of Intensive Care Medicine, Radboud university medical center, Nijmegen, The Netherlands
,
Hennie M.J. Roelofs
4   Department of Gastroenterology, Radboud university medical center, Nijmegen, The Netherlands
,
Wim van Oeveren
5   Haemoscan, Groningen, The Netherlands
,
Arno F.J. van Heijst
6   Department of Neonatology, Radboud university medical center, Nijmegen, The Netherlands
,
Peter Pickkers
1   Department of Intensive Care Medicine, Radboud university medical center, Nijmegen, The Netherlands
› Author Affiliations
Further Information

Publication History

17 July 2015

21 July 2015

Publication Date:
07 September 2015 (online)

Zoom Image

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.

Supplementary Material