Renal - Review Questions Flashcards
analgesic nephropathy
chronic consumption of combinations of NSAIDs and/or APAP (more than 3 years)
papillary necrosis with chronic interstitial nephritis.
Klaassen, Curtis D.. Casarett & Doull’s Toxicology: The Basic Science of Poisons, 9th Edition (p. 786). McGraw-Hill Education. Kindle Edition.
aminoglycosides
S1 and S2 segments
phospholipidosis due to inhibition of lysosomal hydrolases
radioconstrast agents
third most common cause of AKI
altered renal perfusion due to high viscosity and direct effects on endothelial cells
NGAL
distal nephron damage
Halogenated hydrocarbons (e.g. chloroform)
cytochrome P450 metabolism -> reactive intermediate that covalently binds to nucelophilic groups on macromolecules
haloalkenes (tetrafluorethylene)
proximal tubular necrosis (S3 segment)
KIM-1
proximal tubular damage
charge and glomerular filtration
Filtration of anionic molecules tends to be restricted compared to that of neutral or cationic molecules of the same size; this is primarily due to the charge-selective properties of the GBM
Klaassen, Curtis D.; Watkins, John B.. Casarett & Doull’s Essentials of Toxicology, Third Edition (Lange) . McGraw-Hill Education. Kindle Edition.
cyclosporine
acute vasculopathy
chronic glomerular sclerosis and tubular atrophy (vasoconstriction)
The decrease in RBF and GFR is related to marked vasoconstriction induced by cyclosporine, and it is probably produced by a number of factors:
including an imbalance in vasoconstrictor and vasodilatory prostaglandin production,
increased production of the vasoconstrictor thromboxane and endothelin,
and activation of the renin-angiotensin system.
Klaassen, Curtis D.. Casarett & Doull’s Toxicology: The Basic Science of Poisons, 9th Edition (p. 788). McGraw-Hill Education. Kindle Edition.
Depleted uranium
renal tubular necrosis
Proximal tubule
S1 (pars convoluta): vascular lysosomal system
S2: the end of the convoluted segment and the initial portion of the straight segment.
S3 (pars recta): catabolism, glutathione transport, GGT activity
indomethacin
papillary necrosis
Acetaminophen
acute proximal tubular necrosis
biotransformation at recommended doses generally via conjugation to sulfate or glucuronic acid and excreted in urine (Phase I not needed)
High doses saturate conjugation capacity -> CYP2E1 biotransformation -> NAPQI
Von-Hippel Lindau (VHL) germline mutations
target hypoxia inducible factor (HIF) proteins for degradation
loss of VHL results in increased HIF1 expression -> neovascularization
loss of both alleles required for tumorigenesis -> retinal and brain hemangioblastomas, renal clear cell carcinomas, pheochromocytomas, pancreatic neuroendocrine tumors, endolymphatic sac tumors
mutations can be induced by trichloroethylene (TCE)