Renal Cell Function and Phospholipidosis

Study Notes

NSAIDs can cause phospholipidosis, a condition that results in necrosis, especially at higher doses.
NSAIDs reversibly inhibit the production of renal prostaglandins via inhibition of COX-1 and COX-2, leading to decreased vasodilation of afferent and efferent arterioles.
This results in reduced renal plasma flow and acute kidney injury (AKI).
To avoid AKI, patients with long-standing kidney disease should avoid using NSAIDs, and alternative analgesics can be prescribed.

MTX-induced renal dysfunction is believed to be mediated by the precipitation of MTX and its metabolites in the renal tubules, resulting in crystal formation, especially at acidic pH urine.
Hydration, urine alkalinization with sodium bicarbonate, and avoiding drugs that prevent MTX excretion can help prevent MTX-induced renal dysfunction.

The pathophysiology of CIN is based on three distinct mechanisms: medullary ischaemia, formation of reactive oxygen species, and direct tubular cell toxicity.
Periprocedural hydration, use of low-osmolality contrast, limiting the amount of contrast agent, and prophylactic administration of acetylcysteine and fenoldopam can help prevent CIN.

Sulphonamides cause AKI by forming insoluble crystals in renal tubules and ureters, resulting in obstruction to urine output.
Hydration and alkalinization of urine during therapy, and withdrawing the drug on manifestation of renal symptoms can help prevent AKI.

TDF-induced nephrotoxicity is due to its cellular accumulation within the mitochondrial-rich cells of the proximal tubules, resulting in tubular injury.
Renal function assessment and monitoring at baseline and during TDF treatment are the main approaches to prevention.
Withdrawal of TDF and prescribing Tenofovir alafenamide instead of Tenofovir disoproxil fumarate can help prevent nephrotoxicity.