Part 2 Drug Induced Kidney Disease Flashcards
Mechanisms of Renal susceptibility
Large drug exposure Renal hemodynamics Drug accumulation Metabolism to toxic species Increased energy requirements Concentration of drug Precipitation of drug Compensatory mechanism
Reduced glomerular capillary hydrostatic pressure
ACEi and Ang II receptor blockers effect the RAS system
NSAIDs inhibit
COX which reduces PG synthesis from arachidonic acid
PGs
Cause vasodilation
Decreased RBF: protect form ischemia and hypoxia by antagonizing vasoconstrictors
NSAIDs + Renal ischemia
Increase vasoconstriction, ischemia, and loss of glomerular filtration
Calcineurin inhibitors are
Cyclosporine and tacrolimus
Calcineurin inhibitors
Effect immunosuppressive agents for solid organ transplant
Dose limiting toxicity with Calcineurin inhibitors
Nephrotoxicity involving acute hemodynamically mediated kidney injury
Calcineurin inhibitors Nephrotoxicity Pathogenesis
Increased in potent vasoconstrictors (TXA, endothelin, Ang II) and decrease vasodilators (NO, prostacyclin, PGE2)
Define Systemic polyarteritis nodosa
Vasculitis with involvement of small and medium sized renal arteries
After methamphetamine abuse
Thrombus formation
Has been described with oral contraceptives, cyclosporin, mitomycin C, cisplatin and quinine
Anticoagulatns and thrombolytics AE
Embolize cholesterol particles from aortic athersclerotic plaques to small arteries
Glomerular Disease
Involves damage to the glomerular capillary filtration surface
Proteinuria > 3.5 g/d with or without renal insufficiency
Minimal change Glomerular Disease
NSAID induced nephropathy
T-lymphocytes release lympokines
NSAID induced nephropathy
Associated with T-lymphocytic interstitial infiltrate suggesting disordered cell-mediated immunity
T-lymphocytes release lympokines
that increase glomerular capillary permeability to proteins
Focal Segmental Glomerulosclerosis
Characterized by patchy areas of sclerosis with interstitial inflammation