Drug-Induced Nephrotoxicity of Aminoglycosides and the Role of Medicinal Plants as Nephroprotective Agents

Nephrotoxicity occurs when the body is exposed to a medication or poison that harms the kidneys. A 50% rise in serum creatinine or a 50% drop in creatinine clearance, along with an increase in Blood Urea Nitrogen (BUN), is considered nephrotoxicity. Drugs cause about 20% of nephrotoxicity, but as the average life span rises, the incidence of nephrotoxicity in the elderly increases to 66%. Blood tests that quantify BUN, serum creatinine concentration, Glomerular Filtration Rate (GFR), and creatinine clearance are used to assess nephrotoxicity. Aminoglycosides, amphotericin B, cisplatin, contrast dye, and cyclosporine are among the medications that are nephrotoxic by nature. Due to preferential endocytosis and buildup of aminoglycosides via the multi-ligand receptor megalin, aminoglycosides produce nephrotoxicity, which mostly damages the proximal tubule epithelial cells. This sets off a number of cellular cascades that eventually result in cell death. Of all the aminoglycosides, AK has the widest range and the least amount of resistance. It attaches itself to a 16S ribosomal Ribonucleic acid (RNA) location on the 30S ribosome, preventing the synthesis of proteins and causing harm to bacterial cells. Various nephroprotective plants are Aegle marmelos, Bauhinia purpurea, Cassia auriculata, Descurainia Sophia, Euphorbia paralias, Glycyrrhiza glabra, Trema guineensis, Orthosiphon stamineus, Pistacia atlantica, Vernonia cinerea, Costus afer, etc. The bioactive molecules of nephroprotective medicinal plants have anti-inflammatory, cytoprotective, and antioxidant properties that might help prevent kidney damage, without side effects, because the herbal remedies are free of adverse effects and can help mitigate the unwanted effects of synthetic drugs during rare diseases.