BACKGROUND: Paraquat (PQ)-induced acute kidney injury (AKI) might show the role for reactive oxygen species (ROS) in AKI. The purpose of this study was to investigate the characteristics of early urinary biomarkers in patients with acute PQ poisoning. We prospectively investigated changes in urinary kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) in acute PQ intoxication. METHODS: From May 2008 to September 2008, 20 patients were included. Urine KIM-1, NGAL, and 8-hydroxy-2-deoxyguanosine (8-OH-dG) were measured at 6, 12, 24, 48, 72, and 120 h after ingestion. The serum creatinine was measured also at the same intervals. RESULTS: AKI was diagnosed in 11 out of 20 patients. There was a significant difference in the creatinine at 12 h between patients with AKI and those without AKI (0.50 +/- 0.15 vs. 1.04 +/- 0.53 mg/dL, p = 0.01). Urinary NGAL was higher in patients with AKI compared to patients without AKI at 24 h (2.84 vs. 0.96 ng/mL). Urinary KIM-1 was not different in comparisons between patients with AKI and those without AKI. Regardless of the AKI, the NGAL and KIM-1 were increased at between 24 and 48 h. CONCLUSION: PQ is a very potent stimulant of NGAL-1 and KIM-1. Therefore, the NGAL might reflect reactive oxygen species-induced kidney injury.
BACKGROUND:Paraquat (PQ)-induced acute kidney injury (AKI) might show the role for reactive oxygen species (ROS) in AKI. The purpose of this study was to investigate the characteristics of early urinary biomarkers in patients with acute PQpoisoning. We prospectively investigated changes in urinary kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) in acute PQ intoxication. METHODS: From May 2008 to September 2008, 20 patients were included. Urine KIM-1, NGAL, and 8-hydroxy-2-deoxyguanosine (8-OH-dG) were measured at 6, 12, 24, 48, 72, and 120 h after ingestion. The serum creatinine was measured also at the same intervals. RESULTS: AKI was diagnosed in 11 out of 20 patients. There was a significant difference in the creatinine at 12 h between patients with AKI and those without AKI (0.50 +/- 0.15 vs. 1.04 +/- 0.53 mg/dL, p = 0.01). Urinary NGAL was higher in patients with AKI compared to patients without AKI at 24 h (2.84 vs. 0.96 ng/mL). Urinary KIM-1 was not different in comparisons between patients with AKI and those without AKI. Regardless of the AKI, the NGAL and KIM-1 were increased at between 24 and 48 h. CONCLUSION:PQ is a very potent stimulant of NGAL-1 and KIM-1. Therefore, the NGAL might reflect reactive oxygen species-induced kidney injury.
Authors: Klintean Wunnapuk; Fahim Mohammed; Indika Gawarammana; Xin Liu; Roger K Verbeeck; Nicholas A Buckley; Michael S Roberts; Flora T Musuamba Journal: Br J Clin Pharmacol Date: 2014-10 Impact factor: 4.335
Authors: Darren M Roberts; Martin F Wilks; Michael S Roberts; Ramasamyiyer Swaminathan; Fahim Mohamed; Andrew H Dawson; Nick A Buckley Journal: Toxicol Lett Date: 2011-02-01 Impact factor: 4.372