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Acute Kidney Injury - Hospitalist Approach (KDIGO)

Acute Kidney Injury - Hospitalist Approach (KDIGO): Acute Kidney Injury Identified → KDIGO AKI Staging → Determine Etiology → Pre-renal AKI (Most common...

Interactive Decision Tree

Mini Map

Algorithm Steps

  1. Start

    Acute Kidney Injury Identified

    Rising creatinine or decreased UOP

    1. Action

      KDIGO AKI Staging

      Classify severity

      • STAGE 1:
      • - Cr 1.5-1.9x baseline, OR
      • - Cr increase ≥0.3 mg/dL, OR
      • - UOP <0.5 mL/kg/hr x 6-12h
      • STAGE 2:
      • - Cr 2.0-2.9x baseline, OR
      • - UOP <0.5 mL/kg/hr x ≥12h
      • STAGE 3:
      • - Cr ≥3x baseline, OR
      • - Cr ≥4.0 mg/dL, OR
      • - UOP <0.3 mL/kg/hr x ≥24h, OR
      • - Anuria x ≥12h, OR
      • - Initiation of RRT
      1. Decision

        Determine Etiology

        Pre-renal vs Intrinsic vs Post-renal

        1. Action

          Pre-renal AKI (Most common)

          Decreased renal perfusion

          • CAUSES:
          • - Hypovolemia (bleeding, dehydration)
          • - Hypotension (sepsis, cardiac)
          • - Decreased effective circulating volume
          • (CHF, cirrhosis, nephrotic)
          • - Renal artery stenosis
          • - ACEi/ARB in CKD
          • LABS:
          • - FENa <1%
          • - BUN/Cr ratio >20:1
          • - Urine Na <20 mEq/L
          • - Bland sediment
          1. Action

            Workup

            Diagnostic tests

            • BASIC:
            • - BMP, Mg, Phos, CBC
            • - UA with microscopy (sediment)
            • - Urine electrolytes (Na, Cr)
            • - Renal ultrasound (if not recent)
            • CALCULATE:
            • - FENa = (UNa × PCr)/(PNa × UCr) × 100
            • IF INTRINSIC SUSPECTED:
            • - Consider nephrology consult
            • - Complement (C3/C4)
            • - ANA, ANCA, anti-GBM
            • - Serum/urine protein electrophoresis
            1. Action

              Management Principles

              General approach

              • 1. TREAT UNDERLYING CAUSE
              • 2. OPTIMIZE VOLUME STATUS:
              • - Fluids if hypovolemic
              • - Diuretics if overloaded
              • 3. STOP NEPHROTOXINS:
              • - NSAIDs, aminoglycosides
              • - Hold ACEi/ARB temporarily
              • 4. ADJUST DRUG DOSES for GFR
              • 5. AVOID CONTRAST if possible
              • 6. MONITOR I/Os, daily weights
              • 7. NUTRITION: Avoid excessive protein
              1. Warning

                Dialysis Indications (AEIOU)

                When to call nephrology urgently

                • A - Acidosis (pH <7.1, refractory)
                • E - Electrolytes (K+ >6.5, refractory)
                • I - Intoxication (lithium, methanol, etc)
                • O - Overload (pulmonary edema, refractory)
                • U - Uremia (encephalopathy, pericarditis)
                • ALSO CONSIDER:
                • - Rapidly rising Cr without clear cause
                • - Oliguria/anuria >24h despite resuscitation
                1. Outcome

                  Outcomes

                  Monitoring and prognosis

                  • Monitor Cr daily until stable
                  • Recovery: Days to weeks depending on cause
                  • Prerenal: Usually recovers quickly if treated
                  • ATN: May take 1-3 weeks to recover
                  • Increased CKD risk after AKI episode
                  • Follow-up with nephrology if severe
        2. Action

          Intrinsic AKI

          Damage to kidney itself

          • ATN (most common intrinsic):
          • - Ischemic (prolonged prerenal)
          • - Nephrotoxic (contrast, aminoglycosides)
          • - Muddy brown casts
          • - FENa >2%
          • AIN (Interstitial nephritis):
          • - Drug-induced (NSAIDs, PPIs, abx)
          • - WBC casts, eosinophils
          • GLOMERULONEPHRITIS:
          • - RBC casts, proteinuria
          • - Systemic symptoms
        3. Action

          Post-renal AKI

          Obstruction

          • CAUSES:
          • - BPH (most common in men)
          • - Malignancy
          • - Nephrolithiasis (bilateral/solitary)
          • - Retroperitoneal fibrosis
          • DIAGNOSIS:
          • - Renal US: Hydronephrosis
          • - Bladder scan: Retention
          • TREATMENT:
          • - Foley catheter (lower)
          • - Nephrostomy tube (upper)

Guideline Source

KDIGO Clinical Practice Guideline for Acute Kidney Injury

Clinical Safety Information

Clinical Decision Support — Not a Substitute for Clinical Judgment

Individual patient factors may require deviation from these recommendations.

Known Limitations

  • Creatinine lags behind injury
  • Baseline Cr may be unknown
  • Volume status assessment challenging
  • FENa less reliable with diuretics

Applicable Regions

USEU
Version 1Next review: 2027-01-11

Frequently Asked Questions

What is the Acute Kidney Injury - Hospitalist Approach (KDIGO)?

The Acute Kidney Injury - Hospitalist Approach (KDIGO) is a emergency clinical algorithm for Internal Medicine. It provides a structured decision tree to guide clinical decision-making, based on KDIGO Clinical Practice Guideline for Acute Kidney Injury.

What guideline is the Acute Kidney Injury - Hospitalist Approach (KDIGO) based on?

This algorithm is based on KDIGO Clinical Practice Guideline for Acute Kidney Injury (DOI: 10.1038/kisup.2012.1).

What are the limitations of the Acute Kidney Injury - Hospitalist Approach (KDIGO)?

Known limitations include: Creatinine lags behind injury; Baseline Cr may be unknown; Volume status assessment challenging; FENa less reliable with diuretics. Individual patient factors may require deviation from these recommendations.

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