Kidney Toxicity (Table) Flashcards
Mechanisms of chemically induced AKI:
Diuretics, ACE, ARBS, Antihypertensives
Pre-renal
Mechanisms of chemically induced AKI:
NSAIDS, Radiocontrast Agents, Cyclosporine, Tacrolimus, Amphotericin B
Vasoconstriction
Mechanisms of chemically induced AKI:
Sulfonamides, Methotrexate, Acyclovir, Triamterene, Ethylene glycol, Protease inhibitors
Crystalluria
Mechanisms of chemically induced AKI:
Aminoglycosides, Cisplastin, vancomycin, Pentamidine, Radiocontrast agents, Heavy metals, haloalkane and haloalkene
Tubular Toxicity
Mechanisms of chemically induced AKI:
Cyclosporine, Mitomycin C, Tacrolimus, Cocaine, Conjugated estrogens, Quinin
Endothelial Injury
Mechanisms of chemically induced AKI:
Gold, Pencillamine, NSAIDS
Glomerulopathy
Mechanisms of chemically induced AKI:
Antibiotics, NSAIDs, Diuretics
Interstitial Nephritis
Glomerular Injury:
Impair glomerular ultrafiltration
without significant loss of structural
integrity and decrease GFR
Cyclosporine,
Amphotericin B, and
Gentamicin
● ↓ GFR by renal vasoconstriction
● ↓ Glomerular capillary ultrafiltration
coefficient (Kf)
Amphotericin B
Interacts with anionic sites on the
endothelial cells → ↓ GFR and Kf
Gentamicin
T/F: Gentamicin drug has
a narrow therapeutic index
True
Renal vasoconstriction and vascular
damage, injurious to the glomerular
endothelial cell
Cyclosporine
Drugs that causes glomerular injury
Cyclosporine,
Amphotericin B, and
Gentamicin
drugs that causes LOOP OF HENLE/DISTAL TUBULE/
COLLECTING DUCT INJURY
Amphotericin B, Methoxyflurane, Cisplastin
The initial target of abusive consumption of analgesics is the
Medullary interstitial cells > Degenerative changes in the
medullary capillaries > Loops of Henle > Collecting ducts
The acute nephrotoxicity induced
by HgCl2 is characterized by
proximal tubular necrosis and AKI
within 24 to 48 hours after
administration
Mercury
Can cause brain defects and affect
kidneys
Mercury
seafood
exposed in industrial waste
Mercury
produces proximal
tubule dysfunction (S1 and S2
segments) and injury that may
progress to chronic interstitial
nephritis
Cadmium
primary cellular target of
chloroform is the ______ with no primary damage to the
glomerulus or the distal tubule
proximal tubule
Proteinuria, glucosuria, ↑ BUN levels
Chloroform
is the
penultimate nephrotoxicant of Tetrafluoroethylene
Cysteine S-conjugate
The products of the reaction are
ammonia, pyruvate, and a reactive
thiol that is capable of binding
covalently to cellular
macromolecules, causing cellular
damage
Tetrafluoroethylene
________________ of bromobenzene
and other halogenated benzenes is
critical for their nephrotoxicity
Biotransformation
Metabolizes bromobenzene and
conjugates it to glutathione, and
releases it as a form that can cause
nephrotoxicity
Hepatic
cytochrome
P450
1000-fold more potent than
bromobenzene
Diglutathione
conjugate of the
hydroquinone
are products of molds
and fungi, and a number of
mycotoxins produce nephrotoxicity
Mycotoxins
↓ urine osmolality, GFR and RBF,
glycosuria, ↑urinary enzyme
excretion
Citrinin
nephrotoxicity
Found on corn and corn products
Fumonisins
B1 and B2
nephrotoxicity in rats and rabbits
Fumonisins
B1 and B2
↑ urine volume, ↓ osmolality, ↑ low
and high MW proteins
Fumonisins
B1 and B2
Aristolachia and I genera
Aristolochic
acids and aristolactams
can lead totubular dysfunction,
proteinuria, interstitial fibrosis
Aristolochic
acids and aristolactams
Proximal tubular necrosis with
increases in BUN and plasma
creatinine, ↓ GFR, and clearance of
para-aminohippurate
Acetaminophen
reversible on withdrawal of the drug
NSAIDs
NSAIDs: _________ RBF and GFR by _______
↓ RBF and GFR by oliguria
Chronic consumption of NSAIDS
> 3 years
Characterized by non oliguric renal
failure with ↓ GFR, ↑ serum
creatinine, and proteinuria
Aminoglycosides
