ISSN No. (Print): 0975-1718 ISSN No. (Online): 2249-3247 Neutrophil Gelatinase-Associated Lipocalin as an Early Marker of Acute Kidney Injury in Snake Bites Victims Subramanian Senthilkumaran* , **, Dharmar Manimaran*, Ponniah Thirumalaikolundusubramanian*** and Namasivayam Elangovan* * Department of Biotechnology, School of Biosciences, Periyar University, Salem, (Tamil Nadu), INDIA ** Department of Emergency & Critical Care, Sri Gokulam Hospital, Salem, (Tamil Nadu), INDIA *** Department of Internal Medicine, Chennai Medical College Hospital & Research Center, Irungalur, Trichy, (Tamil Nadu), INDIA (Corresponding author: Namasivayam Elangovan) (Received 14 September, 2017 Accepted 07 October, 2017) (Published by Research Trend, Website: www.researchtrend.net) ABSTRACT: The effects of viper envenomation in renal tissues leading to acute kidney injury (AKI) are well known. However, the usefulness of Neutrophil gelatinase-associated lipocalin (NGAL) as a biomarker to detect AKI in viper bite cases was not attempted much. Hence the present study was undertaken to find out the plasma NGAL levels among the hospitalized viperidae group snake bite victims, compare it with serum creatinine and assess the usefulness of NGAL. The plasma NGAL level was elevated within 6 to 8 hours of all the 131 cases of viper bites much before the elevation of serum creatinine levels, irrespective of the age and gender of the patient, and bite to hospital time. The sensitivity, specificity, positive predictability and negative predictability were 96.5, 70.5, 95.7 and 75% respectively which was significant statistically (p<0.001). Elevated plasma NGAL levels in viper bite cases acts as biomarker to detect AKI early, and also helps to plan for an appropriate intervention. So, it is suggested to include estimation of plasma NGAL in the point of care testing especially in emergency settings handling snake bite cases. However more studies are recommended to find out its serial levels in snake bites following different kind of snakes with different manifestations as observed in different age groups belonging to different gender in different population so as to arrive embarking conclusions / recommendations. Keywords: Neutrophil gelatinase-associated lipocalin - NGAL – serum creatinine – biomarker – Acute kidney injury – viper bite – diagnostic test I. INTRODUCTION Acute Kidney Injury (AKI) remains a significant cause of morbidity and mortality among victims of viperidae group snake and sea snake bites [1]. In India, Russell’s viper and Echiscarinatus are the important viper species that often cause acute tubular necrosis, at times acute cortical necrosis and rarely a combination of both [2]. The AKI which occurs after snake bite is usually reversible with supportive management and injection anti-snake venom, but if acute cortical necrosis develops, it may lead to an incomplete recovery. The gold standard for the diagnosis of impaired renal function is the rising serum creatinine levels from the basal level. Currently accepted definition of AKI is absolute increase in serum creatinine by ≥ 0.3 mg/dl [3]. As elevation of serum creatinine is delayed by day(s), it becomes a less reliable biomarker in the scenario of viper envenomation. Therefore, there is a need to find out better biomarkers to recognize AKI at the earliest and institute appropriate measures so as to reduce the morbidity and mortality associated with it. Neutrophil gelatinase-associated lipocalin (NGAL) was originally identified as a 25-kDa protein covalently bound to gelatinase of neutrophils. Although NGAL is expressed only at very low levels in several human tissues, it is markedly elevated in injured epithelial cells [4]. This is likely to be elevated whenever renal tubular or cortical cells are injured either by drugs or toxins. Moreover, this biomarker plays a central role in the control and regulation of cell survival, and proliferation. The expression of NGAL in proliferating and regenerating tubular epithelial cells indicates its role in the process of repair. NGAL, in the context of AKI, plays a role in the preservation of function and attenuation of apoptosis as well as reflects the proliferative response. This protective effect is dependent on the chelation of toxic iron from extracellular environment and the regulated delivery of siderophore and iron to intracellular sites [5]. International Journal of Theoretical & Applied Sciences, 9(2): 178-180(2017)