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Tuesday, September 18, 2018

Topic Discussion: Common Nephrotoxic drugs and their mode of enteries


Common Renal toxic drugs and their mode of entering the tubule and mechanism of toxicity

Drug Name
Mode of entry
Mechanism
Clinical Presentation(s)
Tenofivir(TDF)
Secreted via the basolateral side via OAT and then enters lumen via MRP2 in the urine.
Mitochondrial dysfunction
ATI
Proximal tubulopathy
Diabetes Insipidus(rare)
Gentamicin(Aminoglycosides)
They are all filtered and they are attracted to negative phospholipids and bind to megalin cubulin receptor and enter the cell.
Lysosomes binding and then cause mitochondrial damage and tubular injury—myelin bodies
ATI
Bartter’s syndrome( via activating of the CaSR in the TAHL)
Fanconi syndrome(rare)
Polymixin
All filtered, punch holes enter cells via organic cationic transporter(OCT) on apical surface
Apoptosis and necrosis
ATI
Vancomycin
Unclear how it enters
Complement activation
Activation of reactive oxygen species
Mitochondrial injury
Vancomycin cast formations
ATI
Worse when combined with Piperacillin / Tazobactam
Amphotericin B
Unclear how it enters
Principal cell defect via holes in the apical membrane
Distal hypokalemic RTA
ATI
Hypomagnesemia
Nephrogenic DI
Heta-Starch, Dextran, Sucrose, Mannitol
Filtered and enter proximal cell – pinocytosis and build up and swell up cells. Cannot be metabolized
Osmotic nephrosis
ATI
Atazanavir
Minimal renal excretion, poorly soluble in urinary ph- leading to crystallization
Crystal formation
Crystal Nephropathy
Cisplatin
Enters via OCT on the basolateral side, enters and activates apoptosis
Oxidative stress

ATI
Hypomagnesemia
Proximal tubulopathy
Salt wasting nephropathy
Nephrogenic DI

Ifosfamide
Enters proximal tubular cell via OCT on the basolateral side and then metabolized to its metabolized that causes the damage
Increased oxidative stress and mitochondrial injury
ATI
Fanconi syndrome

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