A Potential Biomarker for Acute Kidney Injury in Preterm Infants from Metabolic ProfilingLindsey E. Romick-Rosendale1, Kurt R. Schibler2, and Michael A. Kennedy1*
- *Corresponding Author:
- Michael A. Kennedy
Department of Chemistry and Biochemistry
Miami University, Oxford, Ohio 45056, USA
E-mail: [email protected]
Received date: December 09, 2011; Accepted date: January 28, 2012; Published date: February 02, 2012
Citation: Romick-Rosendale LE, Schibler KR, Kennedy MA (2012) A Potential Biomarker for Acute Kidney Injury in Preterm Infants from Metabolic Profiling. J Mol Biomark Diagn S3:001. doi:10.4172/2155-9929.S3-001
Copyright: © 2012 Romick-Rosendale LE, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Currently used biomarkers for acute kidney injury (AKI), namely Ngal, SCr, and BUN, are inadequate for timely detection of AKI in preterm infants.
Methods: Nuclear magnetic resonance (NMR) spectroscopy-based metabolic profiling was conducted on urines from 20 preterm infants to determine if novel metabolic biomarkers could be identified for early detection of AKI. Urines were collected from every patient each day for the first 14 days of life. NMR spectra were measured for all urines and metabolic profiling analysis conducted.
Results: One metabolite, carnitine, increased significantly in urines of three extremely low birth weight (ELBW) infants starting on day five of life. The three affected infants either received prolonged antibiotic treatment, extended treatment with indomethacin, or both. One ELBW patient who received both treatments and reached the highest urinary carnitine level died on day 10 of life due to localized gut perforation complicated by suspected AKI.
Conclusions: It was concluded that carnitine increased in the three neonates in part due to antibiotic- and/ or indomethacin-induced AKI. It is hypothesized that combined antibiotic and indomethacin treatment promoted AKI resulting in reduced proximal renal tubule reabsorption of carnitine and that β-lactam antibiotics blocked renal carnitine uptake by human organic cation transporter, hOCTN2.