Screening models of nephrotoxicity and their molecular mechanism

Kidney is among the most vital organs in the anatomy of human body which filters 200 litres of fluid every 24 hours and has many more function which include regulating acid-base balance, maintaining electrolytes balance, eliminating waste and toxins products from the human body. Nephrotoxicity refers as the deterioration in the kidney function due to toxic effect of drugs and chemical and is characterized by alterations in glomerular hemodyanmics, renal tubular failure and thrombotic microangiopathy. Drug-induced nephrotoxicity is becoming more well identified as a principal reasons of kidney illness, such as acute kidney injury (AKI) and chronic kidney disease (CKD) (CKD). Nephrotoxicity covers a broad range, displaying damage to various nephron segments as a result of distinct pharmacological actions. There are various agents which exerts nephrotoxic effects through pathogenic mechanisms like non-steroidal agents (Indomerhacin, Paracetamol, Mefenamic acid), anticancer agents (Carmustine, Cisplatin, Methotrexate), antibiotics (Gentamicin, Tobramycin, Amikacin), antiviral (Acyclovir, Tenofovir, Cidofovir), antifungal (Amphotericin B, Vancomycin, Nystatin)and immunosuppresant drugs(Cyclosporine, Tacrolimus). Alteration in glomerular hemodynamics, tubular cell toxicity, inflammation, crystal nephropathy, rhabdomyolysis, and thrombotic microangiopathy are all possibilities for drug-induced nephrotoxicity. In this review, we have explained different experimental models for nephrotoxicity that might assist in developing novel drugs to cure nephrotoxicity.