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AKI (Clinical Presentation/evaluation (Abrupt rise in pt's baseline…

- - - - Balanced solutions do not cause hyperchloremic metabolic acidosis as often as isotonic saline
    - - Avoid HES
      - Albumin can be a good option with concomitant cirrhosis or SBP
- - - - Occlusion of the larger renal vessels is not common
      - Atheroemboli - most common during vascular procedures
      - Thromboemboli - may arise from dislodgement of a thrombus in the left ventricle in pts with severe heart failure
      - Smaller vessels may be obstructed, but unlikely to cause AKI
        
        neutrophils invade the vessel wall and cause damage including thrombus formation or collagen deposition
    - - Uncommon cause of AKI
        
        AKI may develop when circulating immune complexes deposit in the glomeruli and cause an inflammatory response
    - - usually acute tubular necrosis
        
        4 stages (initiation, extension, maintenance, recovery)
        Initiation - tubular epithelial cell injury
        Extension - continued hypoxia and inflammation
        Maintenance - GFR reaches lowest point & repair tries to occur
        Recovery - new tubule cells are regenerated
      - Most intrinsic AKI are due to ATN-- which can result from renal ischemia or nephrotoxin exposure
        
        ischemic conditions caused by severe hypotension or exposure to vasoconstrictive drugs preferentially affect the tubules more than any other portion of the kidney
    - - AIN - idiosyncratic delayed hypersensitivity immune rxn that is most commonly caused by drugs
        
        characterized by tubular and interstitial inflammation
  - - - Intravascular volume depletion
        
        hemorrhage
        excessive GI losses
        dehydration
        extensive burns
        diuretic therapy
      - reduced circulating blood volume
        
        decreased cardiac output
        systemic vasodilation
    - - commonly associated w/ bilateral renal artery occlusion or unilateral occlusion in a patient with a single functioning kidney
    - - Stimulation of sympathetic nervous and RAAS systems
        
        these responses work together to maintain blood pressure by vasoconstriction and thirst stimulation
        
        GFR may be maintained by afferent arteriole dilation and efferent arteriole constriction
- - - - Sc increase > 0.3 mg/dL or 1.5-1.9x from baseline; urine output < 0.5 mgL/kg/hr for 6-12 hours
    - - Scr increase 2-2.9x from baseline; urine output <0.5 mL/kg/hr for >12 hours
    - - Scr increase 3x from baseline, or Scr >4 mg/dL. or need for RRT, or eGFRc < 35 mL/min/1.73 m^2 in patients < 18 years; anuria for >12 hours