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How do ACEIs and ARBs cause Functional AKI?
- Decrease glomerular capillary hydrostatic pressure
- Thus, reduce glomerular filtration
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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
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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)
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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)
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What is a shorter acting ACEI?
Captopril
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Renal PGs normally dilate __________ arteriole
Afferent
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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
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How does NSAID induced AKI present?
- Occurs within days
- Edema
- Urine volume low
- UNa low
- Weight gain
- Increased SCr, BUN, K and granular casts
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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
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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
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How is NSAID induced DIN managed?
- Discontinue therapy and supportive care
- Rarely need to use dialysis
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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)
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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
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What diagnostic measure can help detect between acute CSA toxicity & renal allograft rejection?
Renal biopsy showing thickening arterioles indicates CSA/Tacrolimus DIN
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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)
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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
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How do you manage CSA/Tacrolimus DIN?
Dose reduction, treat contributing illness, stop interacting drugs
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What can cause Obstructive nephropathy?
- Uric acid deposition
- Myoglobin deposition
- Crystal precipitation
- Extrarenal obstruction
- Nephrolithiasis (Kidney stones)
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How can you treat or prevent Obstructive nephropathy by uric acid?
- Pretreat with hydration
- Alkalize urine to pH7
- Give allopurinol
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What drugs can cause precipitation of myoglobin leading to obstructive nephropathy?
Statins = due to rhabdomyolysis
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Intratubular obstruction from crystal precipitation can be caused by what drugs?
Methotrexate, foscarnet (form Ca-foscarnet salt crystals)
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How do you prevent/treat Intratubular obstruction from crystal precipitation?
Prehydrating the pt, maintaining high urine volume and urinary alkalinization
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What drugs can cause extrarenal obstruction of ureters or bladder?
- Anticholinergic drugs like TCAs, disopyramide
- Cyclophosphamide or ifosfamide- hemorrhagic cystitis, give mesna
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What drugs can cause Nephrolithiasis (Kidney stones)?
Indinavir, triamterene
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How does Glomerular or Tubulointersitial disease present?
Proteinuria w/o decreased GFR
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What treatment may be needed for Glomerular or Tubulointersitial disease?
Immunosuppressive
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Acute allergic interstitial nephritis requires what treatment?
Prednisone 1mg/kg/day x 4 weeks
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Chronic interstitial nephritis presents in what way?
Progressive lesion, impaired ability to concentrate urine, dehydration from diabetes insipidus
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When do you see Chronic interstitial nephritis?
With lithium therapy
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How would you prevent/treat Chronic interstitial nephritis ?
Maintain lithium concentrations as low as therapeutically possible, avoid dehydration
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What is Renal vasculitis?
Inflammation of vessel wall, capillaries or glomeruli
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What can cause Renal vasculitis
- Thrombotic microangiopathy
- Cholesterol Emboli
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What drugs can cause Thrombotic microangiopathy, thus causing renal vasculitis?
Hydralazine, PTU, allopurinol, gemcitabine, CSA, bevacizumab, adalimumab
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How does Thrombotic microangiopathy, thus caused renal vasculitis present?
Hemolytic anemia, fragmented red cells, decreased platelets, intraluminal platelet thrombi in small vessels
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How is Thrombotic microangiopathy caused renal vasculitis treated?
Steroids, antiplatelet agents, IVIG, plasmapheresis
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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
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How do you treat Cholesterol Emboli cuased renal vasculitis?
Usually supportive treatment
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