Define AKI

  • Isolated oliguria: low urine output, stable creatinine
    • Often pre-renal, kidney is hypoperfused and compensates by reducing urine output
  • Non-oliguric: elevated creatinine with normal urine output

KDIGO criteria

  • Stage I AKI
    • Cr 1.5-1.9 times baseline.
    • Cr increase >0.3 mg/dL.
    • Urine output <0.5 ml/kg/hr for 6-12 hours.
  • Stage II AKI
    • Cr 2-2.9 times baseline.
    • Urine output <0.5 ml/kg/hr for 12-24 hours.
  • Stage III AKI 
    • Cr >3 times baseline.
    • Cr >4 mg/dL.
    • Initiation of dialysis.
    • Urine output <0.3 ml/kg/hr for >24 hours.
    • Anuria >12 hours.

Evaluate the cause

  • Labs: electrolytes (including Ca/Mg/Phos), CK, UA
  • Renal & bladder ultrasound to exclude hydronephrosis

Causes of AKI

  • Pre-renal:  disorders of perfusion
    • Shock of any etiology (e.g., hypovolemic shock, cardiogenic shock).
    • Hepatorenal syndrome.
    • Congestive nephropathy (systemic congestion impairs venous outflow).
    • Abdominal compartment syndrome.
    • Hypertensive emergency.
    • Thrombotic thrombocytopenic purpura & hemolytic uremic syndrome.
  • Intrinsic renal failure
    • Nephrotoxic medications
      • Antibiotics: Vancomycin, aminoglycosides, amphotericin, sulfonamides
      • Antivirals: -acyclovirs
      • ACEI/ARBs
      • NSAIDs
      • Antihypertensives if hypotensive
      • Many chemo drugs
    • Cellular lysis (rhabdomyolysis, hemolysis, tumor lysis syndrome).
    • Acute glomerulonephritis.
    • Acute tubulointerstitial nephritis (ATIN).
    • Acute tubular necrosis (ATN).
  • Post-renal:  Urologic obstruction
    • Prostate obstruction.
    • Occluded or malpositioned Foley catheter.
    • Nephrolithiasis.


  • Recent evidence shows it is actually not helpful in differentiating pre-renal vs. intrinsic renal failure. Nevertheless, here it is in case you are stubborn (FeNa>2%= intrinsic renal failure, FeNa<1%= pre-renal failure)
FENa Calculator

If a patient is taking diuretics, the FeUrea is more accurate as they are iatrogenically spilling sodium into their urine


Approach to the oliguric patient (<0.5cc/kg/hr)

  1. Exclude obstruction with bedside ultrasound
  2. Hemodynamic eval- VS trends, BP  meds, cardiac history, bolume status, HYPERtension (can cause intrinsic dx)
  3. Volume challenge?- If hypovolemic
  4. Vasopressor challenge?- if MAP <65
  5. Inotrope challenge?- If very poor cardiac output
  6. Furosemide stress test- 1-1.5mg/kg furosemide, >200mL urine output within 2h indicates good response (if poor response, suggest renal failure and potential need for dialysis)


Hemodynamics are key

  • MAP: Want MAP>65mm for most patients, but MAP>80mm in chronic hypertensives
  • Maintain euvolemia: generally avoid fluids, if they are non-oliguric then they aren't hypoperfusing. Give fluids only if undeniable evidence they are hypovolemic
  • Avoid volume overload: leads to intra-capsular edema in the kidney that worsens perfusion (like compartment syndrome) + venous backflow congestion
    • Diurese if needed
  • Phosphate Binder: Initiate if phosphate >6mg/dL with calcium acetate (667mgx2 TID) or sevalamer (800mg PO TID)
  • Dialysis indications: acidosis refractory to IV bicarb, electrolyte abnormalities (hyperkalemia), fluid overload refractory to diuretics, uremic symptoms (delirium, asterixis, pericardial effusion)

Best fluids?

  • Hypovolemia and uremic acidosis: isotonic bicarbonate (D5W w/ 150mEq/L sodium bicarb)
    • Shoot for pH>7.2, bicarb level ~17
  • Hypovolemia and normal serum bicarbonate: Lactated Ringers

Dialysis disequilibrium syndrome

  • Rapid reduction in BUN levels--> osmotic shifts--> cerebral edema
  • Management: Dialysate with higher sodium concentrations, hypertonic saline to reverse cerebral edema