## 1 Introduction  
Exposure to various toxins is the main cause of nephropathy in vivo [1]. One of these causes is medications, such as acetaminophen, also known as paracetamol (N-acetyl-p-aminophen) (APAP), which is sold under the brand names Tylenol and Panadol. This medication, along with other analgesics and antipyretics, can cause nephrotoxicity when taken in excess [2]. When taken in therapeutic doses, it has no negative effects, but prolonged usage and overdosing can have fatal consequences for the kidneys and liver [3]. Although the extrahepatic symptoms of acetaminophen poisoning are presently not very well documented in the literature, acetaminophen-induced liver necrosis has already been intensively investigated. Nearly 1-2% of patients who consume an excessive amount of acetaminophen develop renal dysfunction [4]. Although numerous underlying mechanisms have been identified, including the activity of N-deacetylase and prostaglandin synthetase enzymes, it has been hypothesized that the cytochrome P-450 mixed function oxidase isoenzymes present in the kidney are the pathophysiology of nephrotoxicity in acetaminophen intoxication [5]. Acetaminophen-induced nephropathy (renal damage) can happen in two distinct ways: primarily through acetaminophen's detrimental consequences on the kidneys or subsequently through the medication's liver damage. As acetaminophen is metabolized by the liver, a hazardous metabolite known as N-acetyl-p-benzoquinone imine is formed (NAPQI) [6]. NAPQI is routinely mitigated by glutathione (GSH), a common antioxidant found in hepatocytes. When the dosage of APAP is excessive, GSH is depleted, and NAPQI accumulates in the liver cells, causing hepatotoxicity. As the kidneys filter the blood and remove wastes, including all those generated by a diseased liver, liver damage can, in turn, lead to renal impairment [7]. In addition, deacetylation of APAP in the kidneys results in the production of the nephrotoxic metabolite para-aminophenol, which results in renal cortex necrosis. Conventional medications, such as N-acetyl cysteine (NAC), used for replenishing this toxicity, have a narrow therapeutic window of just 8 h [8]. Therefore, there is an urgent need for natural antioxidants that could minimize the overdose effects. The use of herbal remedies with antioxidant characteristics has been explored since oxidative stress is implicated in the progression of liver and kidney damage caused by APAP [9; 10]. In the Ayurveda healthcare system, the herbs _Urtica dioica_ (UD), _Capsella bursa-pastoris_ (CBP), and _Inula racemosa_ (IR) have been employed as well-known hepatotoxicity and nephprotective medicines. These three species include phytochemicals renowned for their ethnomedial properties, including polyphenols, quercetin, alkaloids and vitamins. UD is identified as stinging nettle or common nettle [11; 12]. It is well known for its medicinal benefits. Leaves of this plant are used as vegetables in soups and salads [13]. Phenolic compounds detected in nettle plants are chlorogenic acid, 2-O-caffeoyl malic acid, P-coumaroyl malic acid, rutin, caffeic acid, isoquercetin, kaempferol 3-Orutinoside, isornamentin hexoside and isornhametic-3-Orutinoside [14]. Some fatty acids are also present, especially cis-9,12-linoleic acid, palmitic, linolenic acids, phenolic compounds and some essential amino acids [15]. The prior investigation discovered that UD leaves are packed with antioxidants and possess a range of health benefits, such as anti-genotoxic, anticarcinogenic, and anti-inflammatory properties [16] and hepatotoxicity and cardiovascular properties [17]. Studies have demonstrated that nettle leaf extract has antihyperglycemic activity [18]. UD extract ameliorated acetaminophen-induced hepatotoxicityicity in rats, as explained by one examination by [PERSON] et al. (2020) [19]. UD is a potential neuroprotective, hepatotoxicityective and nephprotective chemopreventive and therapeutic agent against oxidative stress induced by potassium bromate in rodents [11; 20].