AKI
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formula for fractional excretion of sodium | [urine Na/urine Cr]/[serum Na/serum creatinine]x100
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definition of anuric vs oliguric vs non-oliguric urine output | anuric is anything less than 50 ml in 24 hours. oliguric is between 50 and 500 ml in 24 hours. non-oliguric is greater than 500 ml in 24 hours.
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what is pseudonephrotoxicity | drug induced inhibition of creatinine secretion, examples trimethoprim and cimetidine. increases in BUN due to drugs such as steroids and tetracyclines. drugs that interfere with creatinine assay such as cefoxitin/cephalosporins
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three classifications of AKI | interstitial/intrinsic (AIN/ATN), prerenal and postrenal
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examples of causes of prerenal AKI | volume depletion, CHF, renal artery stenosis, high calcium, NSAIDS/ACEi/ARBs, cyclosporine
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examples of causes of postrenal AKI | kidney stones, BPH, cancers
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examples of causes of intrinsic AKI or acute tubular necrosis or acute interstitial nephritis | nephrotoxins, vasculitis, glomerulonephritis, long standing renal hypoperfusion
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urinalysis indications of prerenal AKI | BUN:Scr >20:1, urinalysis shows concentrated urine, urine sodium <20, FeNa<1%,
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urinalysis indications of intrinsic AKI | BUN:Scr <15:1, urine not concentrated, muddy casts, FeNa>2%, urine sodium >40. WBCs/RBCs positive, protein positive,
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urinalysis indications of postrenal AKI | BUN Scr <15:1, urine not concentrated, FeNa>2%, urine sodium >40. protein negative, blood positive,
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causes of acute tubular necrosis | aminoglycosides, iodinated contrast, cisplatin/carboplatin, amphotericin B
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causes of acute allergic interstitial nephritis, timing of presentation and treatment | beta lactams and NSAIDS - for beta lactams usually presents 1-2 weeks into treatment. for NSAIDs presents after 6 months. treat with withdrawal of the offending drug and give steroids
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causes of chronic interstitial nephritis, timing of presentation | lithium (>10 years of treatment), cyclosporin and tacrolimus (6-12 months of therapy for both.
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how do you prevent ATN due to radiocontrast | give fluids for volume expansion with NS or bicarb 6-12 hours prior to procedure. maintain a urine output of >150 ml/hr.
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treatments for prerenal AKI | correct the primary hemodynamics with NS, pressure management and blood products
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treatments for intrinsic AKI | remove causative agent, manage fluids and electrolytes, loops to deal with hypervolemia.
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treatments for post renal AKI | relieve obstructions
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indications for renal replacement therapy in AKI | BUN>100, volume overload not responding to diuretics, uremia or encephalopathy, life threatening electrolyte imbalances such as K or Mg, refractory metabolic acidosis
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