Mechanism of Nephrotoxicity of Selected Drugs PDF

MECHANISM OF NEPHROTOXICITY OF SOME DRUGS Pharmacologic Drugs Therapeutic Class Mechanism of Nephrotoxicity Recommendations/remedy...

MECHANISM OF NEPHROTOXICITY OF SOME DRUGS Pharmacologic Drugs Therapeutic Class Mechanism of Nephrotoxicity Recommendations/remedy Group These cause vasoconstriction of the afferent and efferent glomerular Calcineurin 1. Tacrolimus/Sirolimus/Cyclosporine Immunosuppressants arterioles and reductions in renal Inhibitors blood flow and glomerular filtration rate leading to renal tubular injury These cause kidney injury by selectively targeting the 1. Discontinue phospholipids in proximal tubule administration epithelial cells. They accumulate 2. Gentamicin/Streptomycin Antibiotics Aminoglycosides 2. Allow patients renal within these cells to cause function to restore phospholipidosis – a condition that normally or initiate RRT results in necrosis especially at higher doses of the drug. NSAIDs reversibly inhibit the production of renal prostaglandins via inhibition of COX-1 and COX-2. Cyclooxygenase 1. Avoid use in patients These rest in decreased vasodilation Non-Steroidal Anti- (COX) non- with long standing of afferent and efferent arterioles 3. Indomethacin/Ibuprofen/Diclofenac inflammatory Drugs selective kidney disease resulting in reduced renal plasma (NSAIDs) enzyme 2. Alternate analgesics can flow and consequently acute kidney inhibitor be prescribed. injury (AKI). NSAIDs disrupt the compensatory vasodilation response of renal  prostaglandins to vasoconstrictor hormones released by the body. The aetiology of MTX-induced renal dysfunction is believed to be 1. Hydration mediated by the precipitation of 2. Urine alkalinization with MTX and its metabolites in the renal Sodium bicarbonate 4. Methotrexate (MTX) Immunosuppressants Antimetabolite tubules resulting - formation of 3. Avoiding drugs that crystals especially at acidic pH urine. prevent MTX excretion such as penicillins, It could also be due to its direct toxic NSAIDs, effect on the renal tubules 1. periprocedural hydration, 2. use of a low-osmolality contrast The pathophysiology of contrast- 3. limiting the amount of induced nephropathy (CIN) is based contrast agent. on three distinct mechanisms: 4. Prophylactic Radiocontrast Media/Contrast Diagnostic Imaging  medullary ischaemia 5. administration of agents/Contrast dyes Compounds  formation of reactive oxygen acetylcysteine and species/direct oxidative tissue fenoldopam. The former damage may prevent the direct  direct tubular cell toxicity oxidative tissue damage, whereas the latter is a selective intrarenal vasodilator.  1. Hydration and Sulphonamides cause AKI by alkalinization of urine forming insoluble crystals during therapy 6. Sulphadoxine/Sulphadiazine Antibiotics Sulphonamides (Crystalluria) in renal tubules and 2. Withdraw the drug on ureters resulting in obstruction to manifestation of the urine output. renal symtoms 1. Renal function assessment and monitoring at baseline Nucleotide TDF – induced nephrotoxicity is due and during TDF Reverse to its cellular accumulation within treatment are the main 7. Tenofovir (TDF)/Indinavir Antiretroviral Transcriptase the mitochondrial rich cells of the approach to prevention Inhibitors proximal tubules resulting in 2. Withdrawal of TDF (NRTIs) tubular injury. 3. Prescribe the Tenofovir alafenamide instead of the Tenofovir disoproxil fumarate