SERUM AND URINARY MICRORNAS AS BIOMARKERS FOR ACUTE KIDNEY INJURY FOLLOWING POISONING WITH POTASSIUM PERMANGANATE AND OXALIC ACID

FS HANIFFA SALAHUDEEN1,2, MV JOGLEKAR3, AA HARDIKAR3, D SETH4,5, NA BUCKLEY1,2
1Department of Pharmacology, Sydney Medical School, University of Sydney, Camperdown, Australia, 2South Asian Clinical Toxicology of Research Collaboration, Faculty of Medicine, University of Peradeniya, Peradeniya, Sri Lanka, 3Diabetes and Islet Biology Group, NHMRC Clinical Trials Centre, Faculty of Medicine, University of Sydney, Camperdown, Australia, 4Discipline of Clinical Medicine & Addiction Medicine, Faculty of Medicine, University of Sydney, Camperdown, Australia, 5Drug Health Services, Royal Prince Alfred Hospital and Centenary Institute of Cancer Medicine & Cell Biology, Camperdown, Australia

Aim: This study aims to identify a signature of urinary and circulating microRNAs as early biomarkers of acute kidney injury (AKI) in patients following poisoning with oxalic acid and potassium permanganate.
Background: Early detection of AKI is difficult due to lack of sensitive and specific biomarkers. MicroRNAs are stable biomarkers, which are released following cellular injury. Cellular microRNAs can end in bio fluids, where their expression can be detected to assess local (urine) or systemic (serum) effects.
Methods: Serum samples from age and gender-matched patients with acute self-poisoning following oxalic acid and potassium permanganate (NOAKI=6, AKIN2/3=13) and healthy controls (n=4) were profiled for microRNAs using TaqMan OpenArray quantitative real-time PCR (qPCR) platform.  Urinary microRNAs were assessed in a subset of these patients (NOAKI=2, AKIN3=3), and two healthy individuals.
Results: The expression of 44 microRNAs was significantly downregulated in serum and five of these were upregulated in urine of AKIN2/3 patients compared to healthy control and NOAKI. Seven microRNAs were significantly different between serum and urine. A set of three microRNAs (miR-30b, miR-30c & miR-223) distinguished patients with and without AKI. Several serum microRNAs (miR-15b, miR-16, miR-24, miR-26b, miR-146a, 29a-3p, miR-93, miR-126) that we identified have been reported in other types of AKI (ICU AKI and post-cardiac surgery AKI) in humans. The increased abundance of urinary microRNAs (including miR-204) correlated with urinary albumin, a routine kidney injury marker.
Conclusion: A microRNA signature indicative of AKI was identified in human urine and serum samples.  Differences in relative abundance of dysregulated microRNAs between urine and serum may provide insights into understanding their potential as early biomarkers of AKI. Validation studies are merited.


Biography:
Ms Shihana was Analytical Chemist and Research Associate at the South Asian Clinical Toxicology Research Collaboration in Sri Lanka. Shihana is currently based in Australia, completing her PhD on Investigating the role of MicroRNA in early detection of hepatotoxicity and nephrotoxicity following-poisoning at the University of Sydney. Her research interests include developing bedside test and assays for early treatment of poisoning.

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