Renal: Drug-Induced Renal Disease

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Author:
jcbarbery
ID:
214953
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Renal: Drug-Induced Renal Disease
Updated:
2013-04-21 22:29:16
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renal kidney drug pharmacotherapy
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Overview of DIRD
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  1. Reduced Renal Blood Flow (dehydration, CHF, ascites, renal artery stenosis, hypotension, hemorrhage, etc.)

    Nephrotoxic agents (vanc, diuretics, cisplatin, lithium, methotrexate, allopurinol, PPIs)

    Pre-existing renal disease
  2. ACEi/ARB
    Pre-renal vasodilation of efferent arteriole

    Presents as 30%+ inc. in SCr w/in 1-2 wks

    • Minimize reduction of blood volume
    • Use lowest dose of ACEi/ARB
    • Monitor SCr + K
  3. NSAID/COX-2 MOI
    Pre-renal vasoconstriction of afferent arteriole
  4. NSAID/COX-2 Presentation
    • Inc. SCr, BUN, K & BP
    • Dec. UO
    • Edema
    • Weight gain
    • Granular casts
  5. NSAID/COX-2 RF
    RFs: Age > 60 & SLE
  6. NSAID/COX-2 Prevention
    Use alt. analgesia in high risk ptsAvoid potent NSAIDs (indomethacin)Avoid agents that reduce renal blood flow
  7. Cyclosporine & Tacrolimus MOI
    Pre-renal

    • ACUTE (< 6 months)
    • Inc. prod. of vasoconstrictors
    • Dec. prod. of vasodilators
    • -> net dec. in filtration pressure

    • CHRONIC (> 6 months)
    • Inc. formation of extracellular matrices & endothelial cell damage
  8. Cyclosporine & Tacrolimus Presentation
    • ACUTE (<6 months)
    • Inc. SCr, HTN, hyperkalemia, Na retention
    • Oliguria
    • Injury dose dependent & reversible

    • CHRONIC (>6months)
    • Gradual SCr inc.
    • Injuries usu. dose dependent and irreversible
    • Biopsy: arteriolar hyalinosis
    • Biopsy:¬†glomerular sclerosis
    • Biopsy: tubulointerstitial fibrosis
  9. Cyclosporine & Tacrolimus RFs
    • Age > 65
    • High doses
    • 3A4 inhibitors
  10. Cyclosporine & Tacrolimus Prevention
    • Cyclosporine trough of 100-200 ng/mL
    • Tacrolimus trough of 5-15 ng/mL
    • Maintain hydration & renal blood flow
  11. Acute Tubular Necrosis (Definition)
    • Toxicity to renal tubular cells from direct drug
    • exposure or ischemia from pre-renal injuries. Most common with aminoglycosides.
  12. ATN MOI
    Cationic charges facilitate drug uptake -> generation of reactive O2 spp. -> cell necrosis

    Degree of toxicity determined by # of cationic groups -> neomycin > tobra, gent, amikacin > strepto
  13. ATN Presentation
    • S/Sx w/in 5-10d
    • Gradual SCr & BUN inc.
    • Nonoliguria
  14. ATN RFs
    • Cumulative doses
    • High troughs
  15. ATN Prevention
    • Use alt. Abx
    • Hydration
    • QD dosing (lower troughs)

    • Amikacin trough <10 mcg/mL
    • Gent/Tobra trough <2-3 mcg/mL (1mcg if QD)
  16. Contrast media-induced Nephrotoxicity MOI
    Accum. in tubules -> free radicals

    Dec. perfusion -> release of vasoconstrictors, osmotic diuresis & inc. blood viscosity
  17. CIN Presentation
    • S/Sx in 24-72h
    • SCr peak in 3-5d
    • Nonoliguria
    • U/A -> hyaline or granular casts
  18. CIN RFs
    • GFR < 60
    • High dose contrast media
    • High osmolarity contrast media
  19. CIN Prevention
    Alt. imaging method

    NS pre & post procedure w/bicarb (inc. pH = dec. free radicals)

    Low volume, low osmolarity contrasts

    NAC Tx (contraversial)
  20. Ampho B MOI
    Binds to tubular cell membranes

    Inc. cell permeability to loss of Na & K

    Inc. O2 requirements

    Dec. renal blood flow d/t vasoconstrictor release
  21. Ampho B Presentation
    • 1-2 wks after initiation
    • Inc. SCr& BUN
    • Inc. excretion og Mg, K & Na
    • Nonoliguria
    • Distal renal tubular acidosis
  22. Ampho B RFs
    • Cumulative dose
    • Short infusion time
    • Volume depletion
  23. Ampho B Prevention
    • Alt. antifungal
    • Limit dose
    • Inc. infusion time
    • Hydration
    • Lipid-based formulations
  24. Acute Allergic Interstitial Nephritis
    Immune-mediated damage to renal tubule cells or the interstitium

    Implicated Agents: *Beta-lactams*, *NSAIDs*, AGs, vanc, sulfonamides, TCNs, rifampin, Ampho B, diuretics, COX-2s, PPIs, allopurinol, APAP, ASA...
  25. Beta-lactam & NSAID AAIN MOI
    Antibodies to drug-hapten complexes or T-cell toxicitiy

    Interstitial infiltration on leukocytes
  26. Beta-lactam AAIN Presentation
    S/Sx ~14d after initiation

    • Fever
    • Maculopapular rash
    • Eosinophilia
    • Arthralgia
    • Oliguria
  27. NSAID AAIN Presentation
    S/Sx ~6 months after initiation

    Less likely to have hypersensitivity symptoms

    Proteinuria > 3.5 g/day in 70% of pts
  28. AAIN RFs
    Idiosyncratic (none known)
  29. AAIN Prevention
    None recommended d/t idiosyncratic nature
  30. Crystal Nephropathy Contributing Factors
    • Urine pH
    • Drug solubility/conc.
    • Renal blood flow
  31. Acyclovir MOI
    High urine conc. & relative insolubility -> precipitation
  32. Acyclovir Presentation
    24-48hrs post initiation

    • Crystaluria
    • Pyuria
    • Hematuria
  33. Acyclovir RFs
    • Aggressive high-dose Tx
    • Low volume states
  34. Acyclovir Prevention
    • Dose reductions (based on renal fxn)
    • Hydration
  35. DIRD general Tx Strategies
    • D/C offending agent
    • Dose reduction
    • Supportive care (electrolytes and fluids)
    • RRT in severe cases

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