MECHANISM OF DRUG INDUCED RENAL FAILURE: A REVIEWHTML Full Text
MECHANISM OF DRUG INDUCED RENAL FAILURE: A REVIEW
Department of Biological Sciences, Midnapore City College, Kuturia, Bhadutala, Midnapore - 721129, West Bengal, India.
ABSTRACT: Acute renal failure (ARF) is characterized by a rapid, potentially reversible decline in renal function, including a rapid fall in glomerular filtration rate (GFR) and retention of nitrogenous waste products over a period of hours or days. The mortality rate of patients with ARF has remained 25–70% despite the use of various pharmacologic agents. Due to the multiple causes of renal failure, many animal models have been developed to advance our understanding of human nephropathy. Among the experimental models, rodents have been extensively used to enable a mechanistic understanding of kidney disease induction and progression, as well as to identify potential targets for therapy. Numerous experimental models have confirmed the nephrotoxicity induced by gentamicin, cisplatin, acetaminophen, glycerol, CCl4, adenine, potassium dichromate, and others. Nephrotoxicity induced in these experimental models showed pathophysiological, ultrastructural and functional renal impairments in the form of tubular desquamation and necrosis and elevated blood urea and serum creatinine. The aim of this study was to know the mechanism of actions of different nephrotoxic agents for inducing renal failure in an animal model. That will help in the prevention and treatment of drug-induced nephrotoxicity.
Acetaminophen, Acute renal failure, Necrosis, Nephropathy, Nephrotoxic
INTRODUCTION: The kidney is a highly complex organ consisting of well-defined components that function in a highly coordinated manner to allow the smooth regulation of a myriad of interdependent processes. Novel and imaginative approaches have led to the development of experimental techniques and models that now serve to direct the biochemical, cellular, and molecular approaches used to elucidate the mechanisms of disease at cellular and subcellular levels.
Acute kidney injury (AKI) is responsible for approximately 2 million deaths annually worldwide 1, 2. AKI ultimately leads to end-stage renal disease and kidney failure. AKI is increasingly common in critically ill patients, and those patients with the most severe form of AKI, requiring renal replacement therapy, have a mortality rate of 50–80% 3.
Over the past 10 years, there has been substantial progress in the field of AKI. Drug-induced renal failure also becomes very common nowadays. Different studies were done using a different type of drugs or agents for causing uremia and renal failure. The mechanisms of actions for causing renal failure by drugs are different according to the causative agents. Studies throughout the world are going to establish an effective alternative method towards prevention and treatment of renal failure. For that purpose, researchers are establishing different experimental models for induce renal failure and treating them accordingly. Research involving animals is a critical step in understanding physiology, pathophysiology and the development of therapies in both humans and animals. Animal experiments have provided us with fundamental concepts of kidney biology, ranging from hyper-tension and diabetes to renal manifestations of systemic disease, primarily affecting the kidney, such as glomerulonephritis and tubular necrosis. Rodent models remain the most popular species to approximate human disease. There has been a progressive increase in research studies using mouse and rat models of renal disease.
Agents that cause acute renal failure are extensively used experimentally throughout the world. So this review work will facilitate the knowledge to the common people about the toxic effects of commonly used different drugs or agent and their mechanism of actions for causing renal damage. In a case of undiagnosed renal disease, there may be possibility of drug-induced renal failure. This study will help to know the toxic effects of many nephrotoxic agents and for the prompt removal of the drug and supportive management can reverse the renal dysfunction to a large extent.
1. Acetaminophen Induced Renal Failure: Among the various forms of AKI, drug-induced AKI is a common concern in clinic4. Kidneys are primarily involved in filtering and concentrating on various substances and chemical agents. Acetaminophen (APAP), an analgesic and anti-pyretic agent, is better known as paracetamol. APAP is used in adults and children worldwide with a safety profile in therapeutic doses 5. However, excess dose of APAP can cause severe hepatotoxicity, nephrotoxicity and even death in experimental animals and humans 6, 7. Recent studies suggested that both oxidative stress and inflammation contributed to APAP-induced renal injury 8.
1.1 Mitochondrial Dysfunction Related AKI: Mitochondria are the most complex intracellular organelles which are responsible for the important physiological functions.
Renal tubular cells are densely packed with mitochondria. Mitochondrial dysfunction is likely to be a key mechanism for the pathogenesis of AKI9. APAP-induced nephrotoxicity is frequently associated with an elevation in the blood urea nitrogen, serum creatinine, and acute tubular injury 10. In addition to these traditional serums biochemical markers of renal injury, kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) are considered as the more sensitive and reliable early biomarkers. The elevation of KIM-1 and NGAL is obvious; the proof of renal tubule damage and the increments in serum creatinine (SCr) and blood urea nitrogen (BUN) levels are found to be later. Mitochondrial damage leads to the excessive production of ROS, which could directly cause cellular injury.
1.2 Oxidative Stress-Related AKI: The primary toxicity of acetaminophen is the result of drug metabolism in both the liver and extrahepatic tissues. With therapeutic dosing in adults, approximately 63% of acetaminophen is metabolized via glucuronidation and 34% by sulfation. These reactions occur primarily in the liver and result in water-soluble metabolites that are excreted via the kidney. At therapeutic doses, 5% percent of APAP is oxidized by the microsomal P-450 enzyme system to a reactive intermediate, N-acetyl-p-benzoquinone imine (NAPQI). In therapeutic dosing, this electrophilic metabolite is then reduced by glutathione and subsequently excreted as mercapturic acid, a relatively non-toxic compound. In the condition of excess APAP, stores of sulfate and glutathione are depleted. This shunts more of the acetaminophen to the CYP-450 mixed-function oxidase system, generating more NAPQI reactive intermediates. When large doses of a drug are ingested, there is more severe glutathione depletion, as well as a massive production of metabolites, leaving large amounts of reactive species unbound. These electrophilic intermediates then form adducts with sulfhydryl and glutathione moieties on cellular proteins 11. This process disrupts homeostasis, with subsequent activation of caspases and lysosomal enzymes that initiate apoptosis, or programmed cell death. This has been demonstrated in both liver and kidney tissue in animal models. The resultant cell death leads to tissue necrosis and ultimately, organ dysfunction 12.
FIG. 1: ACETAMINOPHEN METABOLISM AND KIDNEY INJURY
2. Gentamicin Induced AKI: Consequences of drug toxicity include both glomerular and tubular injuries leading to acute or chronic functional abnormalities in kidneys. The frequency of drug-induced nephrotoxicity is approximately 14-26% in adult populations 13. Gentamicin (GM) is a cheap important, and widely used antibiotic of the aminoglycoside group for the treatment of gram-negative bacterial infection. Gentamicin induced acute renal failure has proved to be an excellent useful animal model for exploring the pathogenesis of drug-induced acute renal failure 14.
2.1 ROS Production and Cell Injury: Normally, gentamicin is almost entirely eliminated by the kidney, but a small toxic portion is selectively reabsorbed and accumulates in lysosomes of proximal renal tubular cells and cause apoptosis at clinically relevant doses 15. Gentamicin binds the cell wall phospholipids, blocking, thus the chain reaction of phosphatidylinositol, which impairs the cell integrity 16. An excess amount of gentamicin can stimulate free radical formation. Therefore, it is claimed with great certainty that gentamicin induces oxidative stress. Kidney cells can produce free radicals in endothelial cells, glomerular mesangial cells, and in tubular epithelial cells 17. Epithelial cells of proximal tubules are very sensitive to the effects of oxygen free radicals, as 50% of cells die after being exposed to the effect of H2O2 18. These free radicals impair the tubular function, destroy the glomerular basement membrane, degrade the collagen and other components of matrix 19. ROS is also responsible for cellular damage and necrosis via several complex mechanisms, including peroxidation of membrane lipids, protein carbonylation, and DNA damage. Gentamicin has long been known to cause acute renal failure in patients, in addition to histological and functional signs of proximal tubule toxicity.
2.2 Role of Pro and Anti-apoptotic Protein: In cytoplasm, gentamycin acts on mitochondria both directly and indirectly, and activates intrinsic apoptosis pathway, breaks the respiratory chain, decrease ATP synthesis and leads to oxidative stress by creating superoxide anion and hydroxyl radical 20 resulting in cell death. The indirect mitochondrial effect is mediated by increased levels of Bcl-2 associated protein X (Bax) through inhibition of its degradation in proteasomes 15. Lysosomal content is made of highly active proteases called cathepsins capable of inducing cell death. Large quantities of gentamycin inhibit protein synthesis, disrupts translation accuracy, and post-translation modification of proteins. This results in endoplasmic reticulum stress and activation of apoptosis by caspase 12 and calpain. Apoptosis of mesangial cells induced by gentamycin is also characterized by an early increase in pro-apoptotic protein Bax and late increase in anti-apoptotic Bcl-2 protein 21.
3. CCl4 Induced Renal Failure: Carbon tetrachloride (CCl4) is one of the xenobiotics that have been reported to induce acute and chronic tissue injuries and is a well-established hepatotoxin. It was used extensively to study hepatotoxicity in animal models by initiating lipid peroxidation and thereby causing injuries to kidney, heart, testis and brain by excessive production of free radicals. The liver is particularly susceptible to oxidative stress due to the direct release of CCl4 metabolites and cytokines, which propagate the inflammatory response. CCl4 shows a high affinity to the kidney cortex that contains cytochrome P-450 predominantly 22. Due to CCl4 hepatorenal injury, the transport function of hepatocytes and nephrotic cells gets disturbed, resulting in the leakage of the plasma membrane, thereby causing an increased enzyme level in the serum 23. CCl4 metabolism begins with the formation of CCl3• by cytochrome p-450 system. In the presence of oxygen, CCl3• reacts with oxygen to form CCl3OO•, a highly reactive species. CCl3OO• attacks and destroys polyunsaturated fatty acids, thereby initiating the chain reaction of lipid peroxidation (LPO) 24. It has been reported that LPO is one of the major causes of CCl4-induced nephrotoxicity mediated by the production of free radical derivatives of CCl4 25. In order to cope with the excess of free radicals produced upon oxidative stress, organisms have developed enzymatic and non-enzymatic antioxidant systems to scavenge or detoxify reactive oxygen species (ROS), block their production or sequester transition metals which are the source of free radicals 26 thereby causing a low level of the anti-oxidative defense system, and hepatorenal cellular necrosis occurs.
FIG. 2: CISPLATIN INDUCED RENAL FAILURE
4. Cisplatin Induced Nephrotoxicity:
4.1 Cisplatin Induced Cell Apoptosis and Necrosis: Cisplatin (cis-diaminedichloroplatinium) is one of the major standard antineoplastic drugs, which still has a central role in cancer chemo-therapy. However, its significant antitumor activity is often limited due to the development of renal toxicity 27. The accumulation of high concen-trations of cisplatin in the kidneys caused nephrotoxicity. The development of renal tubule injury is caused by the oxidative stress induced by cisplatin. The reactive oxygen species (ROS) and reactive nitrogen species (RNS) production alter the structure and function of cellular membranes. Cisplatin damages the DNA resulting in apoptosis induction. In response to cisplatin, several signaling pathways, which can be activated by lipid peroxidation and oxidative stress, modulate cell survival or apoptosis 28. The mitogen-activated protein kinase (MAPK) pathways regulate differentiation, proliferation, apoptosis, and are activated by chemical and physical stresses 29. The three major MAPK pathways terminate in ERK, p38 and JNK/SAPK enzymes. Cisplatin is known to activate these three pathways in various cell lines, including renal epithelial cells. p38 MAPK was involved in inflammation, cell cycle regulation, and differentiation 30. Also, research suggests that p38 MAPK is able to control the p53-mediated response to cisplatin. Through this pathway, cisplatin-induced nephrotoxicity results in apoptosis and necrosis, vascular damages, and inflammation of the tubules 31.
4.2 Cisplatin Induced Lipid Peroxidation: Cisplatin-induced nephrotoxicity occurs by increasing MDA levels and reducing activities of enzymatic antioxidants, including SOD and catalase 32. NADPH oxidase is a membrane-bound enzyme complex which donates an electron from NADPH to molecular oxygen (O2) to produce O2•. Thereafter, O2•-is converted into H2O2 by SOD. H2O2 is also converted to •OH by the Fenton reaction. Cisplatinplay a key role in ROS production by enhancement of NADPH oxidase gene expression, causing increased lipid per-oxidation, ultimately may cause membrane damage and cell death.
5. Glycerol Induced Acute Kidney Injury: The most commonly used model for studying ARF is obtained in the rat by intramuscular injection of glycerol, which produces a myoglobinuric state similar to clinical Rhabdomyolysis (RM) and is characterized by rapid increases in BUN and serum creatinine which are associated with a marked reduction in glomerular filtration rate within 3 h after glycerol administration 33. Creatine kinase level is the most sensitive damage index for muscle cell damage and marks the occurrence of RM. Rhabdomyolysis is defined as a massive break-down of skeletal muscle in which a potentially large amount of damaging intracellular content enters into blood 34. RM is measured by estimation of creatine kinase the development of RM is associated with causes such as crush syndrome, exhaustive exercise, medications, infections, and toxins 35. AKI is one of the most severe complications of RM, with approximately 15% of patients with RM developing AKI6, and 5–15% of AKI cases are attributed to RM. Myoglobin-induced renal toxicity plays a key role in RM-associated AKI by increasing oxidative stress, inflammation, endothelial dysfunction, vasocon-striction, and apoptosis 36.
In glycerol-induced AKI, myoglobin heme induces oxidative stress and lipid peroxidation of the proximal tubular cells, triggering the release of a series of mediators, including cytokines and chemokines, leading to leukocyte activation and subsequent tubular necrosis in the renal cortical area 37.
6. Adenine Induced Chronic Kidney Disease: Orally administered adenine metabolizes to 2, 8-dihydroxyadenine, which forms crystal in the proximal tubular epithelia leading to inflammation and subsequent tubulointerstitial fibrosis 38, as well as anemia. Fifty mg/kg oral administration of adenine for 28 days caused a significant reduction in hematocrit and plasma EPO levels. It has been reported that long–term consumption of adenine suppresses the excretion of nitrogenous compounds through occlusion of renal tubules, and produces metabolic abnormalities resembling CRF in humans.
In mammalian metabolism, when adenine is present in excess, it becomes a significant substrate for xanthine dehydrogenase. This enzyme can oxidize adenine to 2, 8-dihydroxyadenine (DHA) 39. Because adenine and DHA have low solubility, they precipitate in renal tubules 40. It is not known whether mice transform adenine to a renal damaging metabolite more efficiently than rats, or whether there are other genetic, biochemical, or histological explanations for this species difference. Biochemical indicators of cell death include caspase-3, which is a crucial mediator of programmed cell death (apoptosis). Caspase-3 activation by cleavage has been considered as an apoptotic index, and this is essential for the formation of apoptotic bodies and commitment to loss of cell viability. Adenine - treated mice and rats showed detectable caspase-3 cleavage, which may be considered a possible mechanism involved in the adenine-induced kidney damage 41.
7. Potassium Dichromate Induced Nephro-toxicity: Potassium dichromate is a hexavalent form of Cr and it has been used in the induction of renal oxidative stress. K2Cr2O7 is a potent oxidizing agent displaying a marked affinity, once reduced to trivalent chromium (Cr+3) by numerous cell metabolites, to form several complexes with diverse biological ligands, nucleic including acids.
7.1 K2Cr2O7 Induces Oxidative Stress: It was reported that acute exposure induces anatomical lesions at the proximal tubular cells and lipid peroxidation in the human kidney. Chromium reduced intermediates were thought to reacted with hydrogen peroxide to form hydroxyl radicals 42, with subsequent alterations in proteins, DNA, and phospholipids leading to disturbing cellular functions and its integrity 43. So that, rats were intoxicated with K2Cr2O7 with subsequent increase in the serum creatinine, urea, uric acid, proteins and sodium levels and severe alteration in the histo-pathological examination in comparison with normal control group, through the elevation of reactive oxygen species (ROS) that induces tissues damage such as liver, pancreas, cerebellum and kidney 44. ROS generated by this process can bring on injury to cellular proteins, lipids, and DNA leading to oxidative stress also ROS generation enhances activation of key signaling molecules that regulate cell death, survival, differentiation, and proliferation 45. The incredible increase in MDA and NO and decrease of GSH, SOD and CAT are excellent indicators for oxidative stress through the activation of inducible nitric oxide synthase (iNOS), leading in over production of NO and generation of toxic peroxynitrite that reflected on reducing body weight and kidney enlargement 46.
7.2 K2Cr2O7 Induces Inflammation: Another elucidation of nephrotoxicity induced by K2Cr2O7 is by the activation of the inflammatory process as shown by elevated pro-inflammatory cytokine renal TNF-α level. This was proved before that hexavalent chromium could upshot ROS generation, induce the Akt, NF-kB, and MAPK pathways beside elevation of cytokines, including TNF-α and IL-1α levels 47.
CONCLUSION: Large numbers of drugs are available today. Judicious use of such drugs is required to prevent untoward side effects, especially on such a vital organ like the kidney. Identifying high-risk patients and quick recognition of drug-induced injury-related syndrome with the prompt cessation of the offending drug are the keys to managing such a case before the injury causes permanent damage to the renal tissue. Physicians should be up to date with the wide range of medications harmful to the kidney and be aware of the lesions they bring about. The incidence of drug-induced nephrotoxicity is rising in the worldwide population. It is the time to focus on the therapeutic uses on the drugs with proper doses that will prevent the harmful effect on the overdoses of medicines.
ACKNOWLEDGEMENT: The author sincerely thank to the Director, Midnapore City College, for his constant support for preparing this manuscript.
CONFLICTS OF INTEREST: The authors have declared that no conflict of interest exists.
- Ali T, Khan I, Simpson W, Prescott G, Townend J, Smith W and Macleod A: Incidence and outcomes in acute kidney injury: a comprehensive population-based study. J Am Soc Nephrol 2007; 18: 1292-98.
- Murugan R and Kellum JA: Acute kidney injury: what’s the prognosis?. Nature Reviews Nephrology 2011; 7: 209-17.
- Uchino S, Kellum JA, Bellomo R, Doig GS, Morimatsu H, Morgera S, Schetz M, Tan I, Bouman C, Macedo E, Gibney N, Tolwani A and Ronco C: Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA 2005; 294: 813-8.
- Perazella MA: Renal vulnerability to drug toxicity. Clinical Journal of American Society of Nephrology 2009; 4: 1275-83.
- Stollings JL, Wheeler AP and Rice TW: Incidence and characterization of acute kidney injury after acetaminophen overdose. Journal of Critical Care 2016; 35: 191-4.
- Sheehan WJ, Mauger DT, Paul IM, Moy JN, Boehmer SJ, Szefler SJ, Fitzpatrick AM, Jackson DJ, Bacharier LB, Bacharier MD, Covar R, Holguin F, Robert F, JrLemanske RF, Martinez FD, Pongracic JA, Beigelman A, Baxi SN, Benson MSNM, Blake K, Chmiel JF, Daines CL, Daines MO, Gaffin JM, Gentile DA, Gower WA, Israel E, Kumar HV, Lang JE, Lazarus SC, Lima JJ, Ngoc Ly, Marbin J, Morgan WJ, Myers RE, Olin T, Peters SP, Raissy HH, Robison RG, Ross K, Sorkness CA, Thyne SM, Wechsler ME and Phipatanakul W: Acetaminophen versus ibuprofen in young children with mild persistent asthma. The New England Journal of Medicine 2016; 375: 619-30.
- Lazerow SK, Abdi MS and Lewis JH. Drug-induced liver disease 2004. Current Opinion in Gastroenterology 2005; 2: 283-92.
- Ahmad ST, Arjumand W, Nafees S, Seth A, Ali N, Rashid S and Sultana S: Hesperidin alleviates acetaminophen induced toxicity in Wistar rats by abrogation of oxidative stress, apoptosis and inflammation. Toxicology Letters 2012; 208: 149-61.
- Hall AM and Schuh CD: Mitochondria as therapeutic targets in acute kidney injury. Current Opinion in Nephrology and Hypertension 2016; 25: 355-62.
- Das J, Ghosh J, Manna P and Sil PC: Taurine protects acetaminophen-induced oxidative damage in mice kidney through APAP urinary excretion and CYP2E1 inactivation. Toxicology 2010; 269: 24-34.
- Roy S, Pradhan S, Das K, Mandal A, Mandal S, Patra A, Samanta A, Sinha B and Nandi DK: Acetaminophen induced kidney failure in rats: a dose response study. Journal of Biological Sciences 2015; 15: 187-93.
- Lorz C, Justo P, Sans AB, Egido J and Ortíz A: Role of Bcl-xL in paracetamol-induced tubular epithelial cell death. Kidney International2005; 67: 592-601.
- Hoste EA, Bagshaw SM, Bellomo R, Cely CM, Colman R, Cruz DN, Edipidis K, Forni LG, Gomersall CD, Govil D, Honoré PM, Joannes-Boyau O, Joannidis M, Korhonen AM, Lavrentieva A, Mehta RL, Palevsky P, Roessler E, Ronco C, Uchino S, Vazquez JA, Vidal Andrade E, Webb S and Kellum JA: Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Medicine 2015; 41: 1411-23.
- Murakami H, Yayama K, Chao J and Chao L: Atrial natriuretic peptide gene delivery attenuates gentamycin-induced nephrotoxicity in rats. Nephrology Dialysis Trans-plantation 1999; 14: 1376-84.
- Servais H, Jossin Y, Van Bambeke F, Tulkens PM and Mingeot-Leclercq MP: Gentamicin causes apoptosis at low concentrations in renal LLC-PK1 cells subjected to electroporation. Antimicrobial Agents and Chemotherapy 2006; 50: 1213-21.
- Walker RJ and Duggin GG: Drug nephrotoxicity. Annual Review of Pharmacology and Toxicology 1988; 28: 331-45.
- Baliga R, Ueda N, Walker PD and Shah SV: Oxidant mechanisms in toxic acute renal failure. Drug Metabolism Reviews 1999; 31: 971-97.
- Baud L, Hagege J, Sraer J, Rondeau E, Perez J and Ardaillou R: Reactive oxygen production by cultured rat glomerular mesangial cells during phagocytosis is associated with stimulation of lipoxygenase activity. Journal of Experimental Medicine 1983; 158: 1836-52.
- Andrighetto S, Leventhal J, Zaza G and Craved P: Complement and complement targeting therapies in glomerular diseases. International Journal of Molecular Sciences 2019; 20: 6336
- Cuzzocrea S, Mazzon E, Dugo L, Serraino I, Di Paola R, Britti D, De Sarro A, Pierpaoli S, Caputi A, Masini E and Salvemini D: A role for superoxide in gentamicin-mediated nephropathy in rats. European Journal of Pharmacology 2002; 450: 67-76.
- Martinez-Salgado C, Eleno N, Morales AI, Pérez-Barriocanal F, Arévalo M and López-Novoa JM: Gentamicin treatment induces simultaneous mesangial proliferation apoptosis in rats. Kidney International 2004; 65: 2161-71.
- Jaramillo-ju´arez F, Rodriguez-V´azquez ML, Rinc´on- S´anchez AR, ConsolaciónMartínez M, Ortiz GG, Llamas J, Anibal Posadas F and Reyes JL: Acute renal failure induced by carbon tetrachloride in rats with hepatic cirrhosis. Annals of Hepatology 2008; 7: 331-8.
- Safhi MM: Nephroprotective Effect of zingerone against CCl4-induced renal toxicity in swiss albino mice: molecular mechanism. Oxidative Medicine and Cellular Longevity 2018; 1-7.
- Yoshioka H, Usuda H, Fukuishi N, Nonogaki T and Onosaka S: Carbon tetrachloride-induced nephrotoxicity in mice is prevented by pre-treatment with zinc sulfate. Biological and Pharmaceutical Bulletin 2016; 39: 1042-46.
- Weber LW, Boll M and Stampfl A: Hepatotoxicity and mechanism of action of haloalkanes: carbon tetrachloride as a toxicological model. Critical Reviews in Toxicology 2003; 33: 105-36.
- Makni M, Chtourou Y, Garoui EM, Boudawara T and Fetoui H: Carbon tetrachloride-induced nephrotoxicity and DNA damage in rats: protective role of vanillin. Human & Experimental Toxicology 2012; 31: 844-52.
- Chaudiere J and Ferrari-Iliou R: Intracellular antioxidants: from chemical to biochemical mechanism. Food and Chemical Toxicology 1999; 37: 949-62.
- Yao X, Panichpisal K, Kurtzman N and Nugent K: Cisplatin nephrotoxicity: a review. The American Journal of the Medical Sciences 2007; 334: 115–24.
- Abdel-Daim MM, El-Sayed YS, Eldaim MA and Ibrahim A: Nephroprotective efficacy of ceftriaxone against cisplatin-induced subchronic renal fibrosis in rats. Naunyn Schmiedeberg's Archives of Pharmacology 2017; 390: 301-9.
- Ma X, Dang C, Kang H, Dai Z, Lin S, Guan H, Liu X, Wang X and Hui W: Saikosaponin-D reduces cisplatin-induced nephrotoxicity by repressing ROS-mediated activation of MAPK and NF-kappaB signalling pathways. International Immunopharmacology 2015; 28: 399-08.
- Koul HK, Pal M and Koul S: Role of p38 MAP Kinase signal transduction in solid tumors. Genes Cancer 2013; 4: 342–59.
- Kumar P, Sulakhiya K, Barua CC and Mundhe N: TNF-alpha, IL-6 and IL-10 expressions, responsible for disparity in action of curcumin against cisplatininduced nephrotoxicity in rats. Molecular and Cellular Bio-chemistry 2017; 431: 113-22.
- Rashed LA, Hashem RM and Soliman HM: Oxytocin inhibits NADPH oxidase and P38 MAPK in cisplatin-induced nephrotoxicity. Biomedicine & Pharmacotherapy 2011; 65: 474-80.
- Parekh R, Care DA and Tainter CR: Rhabdomyolysis: advances in diagnosis and treatment. Emergency medicine practice 2012; 14: 1-15.
- Mai MH and EI-Gowelli HM: Montelukast abrogates rhabdomyolysis-induced acute renal failure via rectifying detrimental changes in antioxidant profile and systemic cytokines and apoptotic factors production. European Journal of pharmacology 2012; 683: 294-300.
- Wu GL, Chen YS, Huang XD and Zhang LX: Exhaustive swimming exercise related kidney injury in rats-protective effects of acetylbritannilactone. International journal of Sports Medinine 2012; 33: 1-7.
- Panizo N, Rubio-Navarro A, Amaro-Villalobos JM, Egido J and Moreno JA: Molecular mechanisms and novel therapeutic approaches to rhabdomyolysis-induced acute kidney injury. Kidney and Blood Pressure Reseaech 2015; 40: 520-32.
- Zager RA and Burkhart KM: Differential effects of glutathione and cysteine on Fe2+, Fe3+, H2O2 and myoglobin-induced proximal tubular cell attack. Kidney International 1998; 53: 1661-72.
- Ali BH, Al-Salam S, Al Za'abi M, Waly MI, Ramkumar A, Beegam S, Al-Lawati I, Adham SA and Nemmar A: New model for adenine-induced chronic renal failure in mice, and the effect of gum acacia treatment thereon: Comparison with rats. Journal of Pharmacological and Toxicological Methods 2013; 68: 384-93.
- Rahman A, Yamazaki D, Sufiun A, Kitada K, Hitomi H, Nakano D and Nishiyama D: A novel approach to adenine-induced chronic kidney disease associated anaemia in rodents. PLOS One 2018; 13: e0192531.
- Shuvy M, Nyska A, Beeri R, Abedata S, Gal-Moscovicic A, Rajamannand NM and Lotana C: Histopathology and apoptosis in an animal model of reversible renal injury. Experimental and Toxicologic Pathology 2011; 63(4): 303-6.
- Elshazly MO, Abd El-Rahman SS, Morgan AM and Ali ME: The remedial efficacy of spirulina platensis versus chromium-induced nephrotoxicity in male sprague-dawley rats. PLOS One 2015; 10: e0126780.
- Bucher JR: NTP toxicity studies of sodium dichromate dihydrate (CAS No. 7789-12-0) administered in drinking water to male and female F344/N rats and B6C3F1 mice and male BALB/c and am3-C57BL/6 mice. Toxicity Report Series 2007; 72: 1-G4.
- Dayem AA, Hossain MK, Lee SB, Kim K, Saha SK, Yang G, Choi HY and Cho S: The role of reactive oxygen species (ROS) in the biological activities of metallic nanoparticles. International Journal of Molecular Sciences 2017; 18: 120.
- Mehany HA, Abo-youssef AM, Ahmed LA, Arafa ES and Abd El-Latif HA: Protective effect of vitamin E and atorvastatin against potassium dichromate-induced nephrotoxicity in rats. Beni-Suef University Journal of Basic and Applied Sciences 2013; 2: 96-102.
- Molina-Jijon E, Zarco-Marquez G, Medina-Campos ON, Zataraín-Barrón ZL, Hernández-Pando R, Pinzón E, Zavaleta RM, Tapia E and Pedraza-Chaverri J: Deferoxamine pre-treatment prevents Cr (VI)-induced nephrotoxicity and oxidant stress: role of Cr (VI) chelation. Toxicology 2012; 291: 93-101.
- Zhao J, Zheng DY, Yang JM, Wang M, Zhang XT, Sun L and Yun XG: Maternal serum uric acid concentration is associated with the expression of tumour necrosis factor-alpha and intercellular adhesion molecule-1 in patients with preeclampsia. Journal of Human hypertension 2016; 30: 456-62.
How to cite this article:
Roy S: Mechanism of drug induced renal failure: a review. Int J Pharm Sci & Res 2020; 11(8): 3587-94. doi: 10.13040/IJPSR.0975-8232. 11(8).3587-94.
All © 2013 are reserved by the International Journal of Pharmaceutical Sciences and Research. This Journal licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License.
Department of Biological Sciences, Midnapore City College, Kuturia, Bhadutala, Midnapore, West Bengal, India.
04 December 2019
06 March 2020
19 April 2020
01 August 2020