Pavuluri Lakshmi Aishwarya, Bitla Aparna R, Vishnubotla Siva Kumar, Rapur Ram
Department of Nephrology, Sri Venkateswara Institute of Medical Sciences, Tirupati, India.
Department of Biochemistry, Sri Venkateswara Institute of Medical Sciences, Tirupati, India.
Indian J Nephrol. 2025 May-Jun;35(3):349-354. doi: 10.25259/ijn_545_23. Epub 2024 Jul 22.
Snakebite-induced acute kidney injury (SAKI) is a life-threatening complication. Despite its impact on public health, the understanding of the underlying cellular and molecular mechanisms remains limited. There is a lack of studies investigating the role of oxidative stress, oxidative deoxyribonucleic acid (DNA) damage, inflammation, and endothelial dysfunction in SAKI. This study aims to address this knowledge gap.
Biomarkers of oxidative stress, including oxidative DNA damage, inflammation, and endothelial dysfunction were assessed in 30 patients with SAKI and 30 healthy controls. Malondialdehyde (MDA), protein carbonyl content (PCC), advanced glycation end products (AGEs), 8-hydroxy-2'-deoxyguanosine (8-OHdG), ferric reducing ability of plasma (FRAP), high-sensitivity C-reactive protein (hs-CRP), and nitric oxide (NO) were used as biomarkers.
We found significantly elevated levels of MDA (2.1590±0.68221 µmol/L vs 0.8769±0.2958 µmol/L, p = <0.001), PCC (0.0905±0.040 nmol/L vs 0.0501±0.024 nmol/L, p = <0.001) and 8-OHdG (47.0757±37.09105 ng/mL vs 18.8450±9.31479 ng/mL, p = <0.001) in SAKI patients compared to controls, indicating increased oxidative damage to lipids, proteins, and DNA respectively. Although AGEs showed higher levels in SAKI patients, the difference was not significant. FRAP levels were significantly reduced [0.214 (0.051-0.489) mmol/L vs 0.470 (0.136-0.564) mmol/L, p = 0.024], indicating compromised antioxidant capacity. Significantly elevated levels of hs-CRP [40.18 (16.96-77.56) mg/L vs 1.44 (0.5-4.45) mg/L, p = <0.001] and NO [25.59 (22.75-28.43) µmol/L vs 14.218 (11.37-16.35) µmol/L, p = <0.001] confirmed the presence of inflammation and endothelial dysfunction in these patients.
Our study demonstrated oxidative stress, including oxidative DNA damage, inflammation, and endothelial dysfunction, in SAKI patients. Understanding these intricate mechanisms could lead to the development of novel diagnostic tools and therapeutic strategies.
蛇咬伤所致急性肾损伤（SAKI）是一种危及生命的并发症。尽管其对公众健康有影响，但对其潜在细胞和分子机制的了解仍然有限。缺乏关于氧化应激、氧化性脱氧核糖核酸（DNA）损伤、炎症和内皮功能障碍在SAKI中的作用的研究。本研究旨在填补这一知识空白。
在30例SAKI患者和30例健康对照中评估氧化应激生物标志物，包括氧化性DNA损伤、炎症和内皮功能障碍。丙二醛（MDA）、蛋白质羰基含量（PCC）、晚期糖基化终产物（AGEs）、8-羟基-2'-脱氧鸟苷（8-OHdG）、血浆铁还原能力（FRAP）、高敏C反应蛋白（hs-CRP）和一氧化氮（NO）用作生物标志物。
我们发现SAKI患者的MDA水平显著升高（2.1590±0.68221µmol/L对0.8769±0.
