Therapeutics: DIN 2

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  1. How do ACEIs and ARBs cause Functional AKI?
    • Decrease glomerular capillary hydrostatic pressure
    • Thus, reduce glomerular filtration
  2. What is the clinical presentation of ACEI or ARB induced AKI?
    • Increase in SCr
    • Normal = 30% in 2-5 days
    • Stabilizes in 2-3 weeks
  3. What are the risk factors for ACEI and ARB induced AKI?
    • Renal artery stenosis (bilateral = ACEIs and ARBs are CI)
    • Decreased arterial renal blood flow (CHF, V depletion, Hepatic cirrhosis, ascites, nephritic syndrome)
  4. How can you prevent ACEI or ARB induced AKI?
    • Use low doses of Short acting agents
    • Titrate uo
    • Monitor BUN, SCr and K judiciously (2-3 day as outpatient and daily as inpatient)
    • Avoid dehydration (watch diuretics if started)
  5. What is a shorter acting ACEI?
  6. Renal PGs normally dilate __________ arteriole
  7. What is the MOA of NSAIDs in AKI?
    • In setting of renal ischemia & compensatory increase in PG activity
    • NSAIDs inhibit PG production┬« renal vasoconstriction & ischemia
  8. How does NSAID induced AKI present?
    • Occurs within days
    • Edema
    • Urine volume low
    • UNa low
    • Weight gain
    • Increased SCr, BUN, K and granular casts
  9. What are the Risk Factors for NSAID induced DIN?
    • Pre-existing renal insufficiency
    • High plasma renin (CHF, liver disease)
    • Systemic lupus
    • Multiple drug therapy, diuretic, atherosclerotic CVD
    • Avoid combining ACEI, ARB, & NSAID
  10. How do you Prevent NSAID DIN?
    • Use analgesics with less PG inhibition in high risk patients
    • APAP, ASA, possibly nabumetone
    • Caution if use NSAIDs with ACEI/ARB
  11. How is NSAID induced DIN managed?
    • Discontinue therapy and supportive care
    • Rarely need to use dialysis
  12. What is eth MOA for Cyclosporine or Tacrolimus in DIN?
    • Dose-related hemodynamic effect due to:
    • Increased activity in vasoconstrictors
    • (thromboxane A2, endothelin and sympathetic nervous system)
    • Diminished activity of vasodilators
    • (nitric oxide or prostacyclin)
  13. What is the clinical presentation of Cyclosporine and Tacrolimus induced DIN?
    • Acute renal toxicity occurs within days
    • Increased: SCr, HTN, K, Mg
    • Decreased: CrCl
    • Renal biopsy shows thickening of arterioles
  14. What diagnostic measure can help detect between acute CSA toxicity & renal allograft rejection?
    Renal biopsy showing thickening arterioles indicates CSA/Tacrolimus DIN
  15. What are the Risk Factors for CSA/Tacrolimus DIN?
    • Older age
    • High dose of CSA and tacrolimus
    • Renal graft rejection
    • Hypotension, infection
    • Concomitant nephrotoxic drugs, drugs that inhibit CSA metabolism (CYP drugs)
  16. How can you prevent CSA/Tacrolimus DIN?
    • Use lowest effective doses with other non-nephrotoxic immunosuppressants
    • Monitor kinetics
    • CCBs vasodilate vessels and prevent acute decreases in renal blood flow
  17. How do you manage CSA/Tacrolimus DIN?
    Dose reduction, treat contributing illness, stop interacting drugs
  18. What can cause Obstructive nephropathy?
    • Uric acid deposition
    • Myoglobin deposition
    • Crystal precipitation
    • Extrarenal obstruction
    • Nephrolithiasis (Kidney stones)
  19. How can you treat or prevent Obstructive nephropathy by uric acid?
    • Pretreat with hydration
    • Alkalize urine to pH7
    • Give allopurinol
  20. What drugs can cause precipitation of myoglobin leading to obstructive nephropathy?
    Statins = due to rhabdomyolysis
  21. Intratubular obstruction from crystal precipitation can be caused by what drugs?
    Methotrexate, foscarnet (form Ca-foscarnet salt crystals)
  22. How do you prevent/treat Intratubular obstruction from crystal precipitation?
    Prehydrating the pt, maintaining high urine volume and urinary alkalinization
  23. What drugs can cause extrarenal obstruction of ureters or bladder?
    • Anticholinergic drugs like TCAs, disopyramide
    • Cyclophosphamide or ifosfamide- hemorrhagic cystitis, give mesna
  24. What drugs can cause Nephrolithiasis (Kidney stones)?
    Indinavir, triamterene
  25. How does Glomerular or Tubulointersitial disease present?
    Proteinuria w/o decreased GFR
  26. What treatment may be needed for Glomerular or Tubulointersitial disease?
  27. Acute allergic interstitial nephritis requires what treatment?
    Prednisone 1mg/kg/day x 4 weeks
  28. Chronic interstitial nephritis presents in what way?
    Progressive lesion, impaired ability to concentrate urine, dehydration from diabetes insipidus
  29. When do you see Chronic interstitial nephritis?
    With lithium therapy
  30. How would you prevent/treat Chronic interstitial nephritis ?
    Maintain lithium concentrations as low as therapeutically possible, avoid dehydration
  31. What is Renal vasculitis?
    Inflammation of vessel wall, capillaries or glomeruli
  32. What can cause Renal vasculitis
    • Thrombotic microangiopathy
    • Cholesterol Emboli
  33. What drugs can cause Thrombotic microangiopathy, thus causing renal vasculitis?
    Hydralazine, PTU, allopurinol, gemcitabine, CSA, bevacizumab, adalimumab
  34. How does Thrombotic microangiopathy, thus caused renal vasculitis present?
    Hemolytic anemia, fragmented red cells, decreased platelets, intraluminal platelet thrombi in small vessels
  35. How is Thrombotic microangiopathy caused renal vasculitis treated?
    Steroids, antiplatelet agents, IVIG, plasmapheresis
  36. How is Cholesterol Emboli cuased renal vasculitis caused?
    • Warfarin or thrombolytic agents
    • Induction of hemorrhage within clots cause cholesterol crystals to lodge in renal arterioles and glomerular capillaries of kidney
  37. How do you treat Cholesterol Emboli cuased renal vasculitis?
    Usually supportive treatment
Card Set:
Therapeutics: DIN 2
2014-05-03 04:44:09
Therapeutics DIN
Therapeutics: DIN 2
Therapeutics: DIN 2
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