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ACUTE KIDNEY INJURY

Initial Assessment

  1. Assessing risk and preventing acute kidney injury (AKI) (see page 191)

  2. Definition and staging (KDIGO 2012)

    1. AKI is defined as any of the following:

      1. Increase in serum Cr by ≥0.3 mg/dL within 48 hours; or

      2. Increase in serum Cr to ≥1.5× baseline within 7 days; or

      3. Urine volume <0.5 mL/kg/h for 6 hours

    2. AKI is staged for severity

      1. Stage 1: Cr 1.5–1.9× baseline or ≥0.3 mg/dL increase; UOP <0.5 mL/kg/h for 6–12 hours

      2. Stage 2: Cr 2.0–2.9× baseline; UOP <0.5 mL/kg/h for ≥12 hours

      3. Stage 3: Cr 3.0× baseline or Cr ≥4.0 mg/dL or dialysis; UOP <0.3 mL/kg/h for ≥24 hours or anuria for ≥12 hours

  3. Identify the cause of AKI (NCGC 2013)

    1. Obtain urinalysis

      1. Dipstick UA for blood, protein, leukocytes, nitrites and glucose in all patients with AKI; document results and ensure appropriate action if abnormal

      2. Consider acute nephritis and consult nephrology when a patient with AKI with no obvious cause has a urine dipstick showing protein or blood in the absence of UTI, menses, or trauma due to catheterization

    2. Obtain US if the cause of AKI is unknown

      1. When pyonephrosis is suspected, get an immediate US (within 6 hours)

      2. With no identified cause of AKI, get an urgent US (within 24 hours)

Acute Medical Management

  1. Relieve obstruction (NCGC 2013)

    1. When nephrostomy or stenting is used, undertake within 12 hours of diagnosis

    2. Immediate referral to urology for:

      1. Pyonephrosis

      2. Obstructed solitary kidney

      3. Bilateral hydronephrosis or bilateral ureteral obstruction

      4. Complications of AKI caused by urological obstruction

  2. Pharmacological management (NCGC 2013, KDIGO 2012)

    1. Loop diuretics

      1. Do not routinely use to treat AKI

      2. Consider for treating fluid overload or edema while awaiting dialysis or while renal function is recovering if not on dialysis

    2. Fluids: Unless in shock, use isotonic crystalloids rather than colloids as initial management for volume expansion

    3. If vasomotor shock and AKI: Use vasopressors with fluids

    4. Do not use the following to treat AKI:

      1. Dopamine

      2. Fenoldopam

      3. ANP (atrial natriuretic peptide)

      4. Recombinant human insulin-like growth hormone

    5. Anticoagulation in patients with AKI on dialysis

      1. Use anticoagulation during dialysis in AKI if the patient does not have an increased risk of bleeding or impaired coagulation and is not already receiving systemic anticoagulation

        1. Use unfractionated or low-molecular-weight (LMW) heparin for intermittent dialysis

        2. Use regional citrate anticoagulation for continuous dialysis; for patients on continuous dialysis with contraindications to citrate, use unfractionated or LMW heparin

      2. For patients with increased risk of bleeding who are not on systemic anticoagulation:

        1. Use regional citrate during continuous dialysis in patients without contraindication for citrate

        2. Avoid regional heparin during continuous dialysis

      3. For patients with HIT (heparin-induced thrombocytopenia):

        1. Use direct thrombin inhibitors (i.e., argatroban) or factor Xa inhibitors (i.e., fondaparinux) rather than other or no anticoagulation during dialysis

        2. In a patient with HIT and AKI on dialysis who does NOT have severe liver failure, use argatroban preferentially

Interventions

  1. Refer to nephrology (NCGC 2013)

    1. Refer patients with AKI immediately if they meet criteria for dialysis

    2. Do not refer when there is a clear cause for AKI and the condition ...

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