333.1 🎓 醫孞生版

333.1.0.1 📌 䞀頁重點

333.1.0.1.1 KDIGO 2012 Criteria

AKI (any 1 of): 1. ↑ SCr ≥ 0.3 mg/dL within 48 hours 2. ↑ SCr ≥ 1.5× baseline (within prior 7 days) 3. UO < 0.5 mL/kg/h × 6 hours

333.1.0.1.1.1 KDIGO Staging

Stage 1 (Mild): - SCr ↑ 0.3 mg/dL OR 1.5-1.9× baseline - UO < 0.5 mL/kg/h × 6-12 h

Stage 2 (Moderate): - SCr 2.0-2.9× baseline - UO < 0.5 mL/kg/h × > 12 h

Stage 3 (Severe): - SCr ≥ 3× baseline OR - SCr ≥ 4.0 mg/dL OR - Initiation of RRT OR - UO < 0.3 mL/kg/h × 24 h OR - Anuria × 12 h

333.1.0.1.2 Etiology — Three Categories

333.1.1 Pre-Renal (~ 50-60%)

Mechanism: Reduced renal perfusion → reduced GFR (kidney intrinsically intact)

Causes: - Hypovolemia: hemorrhage, GI loss, burns, diuretics, sepsis (3rd spacing) - Low cardiac output: HF, cardiogenic shock - Liver disease: hepatorenal syndrome - Drugs: - NSAIDs: ↓ afferent arteriole - ACE/ARB: ↓ efferent arteriole - Diuretics - Renal artery stenosis (bilateral or solitary) - Sepsis (initially pre-renal, later ATN)

Laboratory Features: - BUN/Cr ratio > 20:1 - FENa < 1% - Urine Na < 20 mEq/L - Urine osmolality > 500 mOsm/kg - FEUrea < 35% (more useful if on diuretics) - Sediment: bland (hyaline casts) - Reversible with volume / treatment of cause

333.1.2 Intrinsic Renal Disease (~ 20-30%)

Tubular (ATN) — Most Common Intrinsic: - Ischemic ATN: prolonged pre-renal injury → tubular cell death - Nephrotoxic ATN: - Aminoglycosides (gentamicin, tobramycin, amikacin) - Vancomycin - Contrast media (post-contrast AKI) - Cisplatin, carboplatin, ifosfamide - Tenofovir, adefovir - Amphotericin B - Calcineurin inhibitors (acutely) - Lithium - Acetaminophen overdose - Pigment ATN: rhabdomyolysis (myoglobin), hemolysis (Hb) - Crystal ATN: TLS (uric acid), acyclovir, methotrexate

Glomerular (GN): - Acute GN syndromes - See Ch338-339

Interstitial (AIN): - Drugs (penicillin, NSAIDs, PPI, ICI) - Infection - Autoimmune (Sjögren, IgG4) - Sarcoidosis

Vascular: - Microangiopathy (TTP, HUS, malignant HTN, scleroderma renal crisis) - Atheroembolism (cholesterol embolism) - Cortical necrosis

Laboratory Features for ATN: - BUN/Cr ratio < 20 - FENa > 2% - Urine Na > 40 mEq/L - Urine osmolality 300-350 mOsm/kg (isothenuric) - Sediment: muddy brown granular casts + tubular epithelial cells

Laboratory Features for AIN: - WBC casts - Urine eosinophils (Hansel stain) — historical, low sensitivity - Sterile pyuria - Often allergic features (rash, fever, eosinophilia in some)

333.1.3 Post-Renal (~ 10-15%)

Mechanism: Obstruction → backflow → reduced GFR

Levels: - Upper tract (ureter): stones, tumors, retroperitoneal fibrosis, malignancy - Lower tract (bladder, prostate, urethra): BPH, prostate cancer, urethral stricture, neurogenic bladder, retention

Key: Bilateral obstruction (or unilateral with single kidney) needed for AKI

Laboratory Features: - Variable - Imaging: hydronephrosis on US (gold standard)

333.1.3.0.1 Diagnosis Workflow
333.1.3.0.1.1 History
  • Volume status: thirst, weight changes, edema
  • Symptoms: oliguria, anuria, polyuria
  • Drug history: NSAIDs, ACE/ARB, antibiotics, contrast, herbals
  • Comorbidities: HF, cirrhosis, sepsis, malignancy
  • Recent surgery: ICU stay
  • Trauma: rhabdomyolysis
333.1.3.0.1.2 Examination
  • Vital signs (BP, HR, orthostatic)
  • Volume assessment (JVD, edema, mucous membranes)
  • Cardiopulmonary
  • Abdomen (bladder, masses)
  • Skin (rash for AIN, sclerodactyly, livedo for atheroembolism)
  • Neurologic (uremia signs)
333.1.3.0.1.3 Laboratory
  • BMP (Cr, BUN, electrolytes)
  • CBC + differential
  • LFTs
  • Urinalysis with microscopy
  • Urine electrolytes + creatinine
  • FENa (or FEUrea if on diuretics)
  • CK (rhabdomyolysis)
  • LDH, haptoglobin (hemolysis)
  • Immunology if GN/vasculitis suspected (ANA, dsDNA, ANCA, anti-GBM, C3/C4, hepatitis, HIV)
  • Free light chains (myeloma)
333.1.3.0.1.4 Imaging
  • Renal US (first-line):
    • Size, echogenicity
    • Hydronephrosis (obstruction)
    • Stones
  • CT: stones, masses, retroperitoneal disease
  • MRI: vascular, masses
  • Dopplers: renal artery stenosis or thrombosis
333.1.3.0.1.5 Biomarkers (Newer)

Conventional: - Serum creatinine (delayed by ~ 24-48h) - BUN - Urine output

Functional vs Damage Markers: - Creatinine: functional (delayed) - Damage markers (early detection): - NGAL (neutrophil gelatinase-associated lipocalin) - KIM-1 (kidney injury molecule) - IGFBP7 × TIMP-2 (Nephrocheck) — FDA approved for AKI risk - L-FABP (liver-type fatty acid binding protein) - Cystatin C (functional marker, less muscle-dependent)

Clinical Use: emerging, not all in routine practice yet

333.1.3.0.1.6 Renal Biopsy
  • Indications: unclear cause, suspected GN/vasculitis, ATN not improving, unusual presentations
  • Complications: bleeding (1-2%), pneumothorax, AVF
  • Tissue: light microscopy + immunofluorescence + electron microscopy
333.1.3.0.2 Specific AKI Causes
333.1.3.0.2.1 Contrast-Associated Acute Kidney Injury (CA-AKI / CIN)
  • Within 24-48 hours of iodinated contrast
  • CKD highest risk
  • Other risks: DM, HF, age, volume depletion, repeated doses
  • Prevention: hydration (isotonic saline IV), minimize contrast volume
  • Recent literature: incidence overestimated; modern contrast lower risk
  • Statins, NAC: limited evidence
333.1.3.0.2.2 Hepatorenal Syndrome (HRS)
  • Cirrhosis + AKI without other cause
  • HRS-AKI (Type 1): rapid; precipitated by SBP, GI bleed, infection
  • HRS-NAKI: subacute (Type 2 historical)
  • Pathophysiology: splanchnic vasodilation → reduced effective volume → renal vasoconstriction
  • Treatment:
    • Terlipressin (vasopressin analog, FDA 2022) + albumin
    • Norepinephrine + albumin (ICU)
    • Liver transplantation (definitive)
  • Avoid: nephrotoxins, diuretics in active HRS
333.1.3.0.2.3 Sepsis-AKI
  • Most common cause in ICU
  • Multifactorial (hypotension, cytokines, microcirculatory)
  • Treat sepsis + supportive
  • Often involves ATN
333.1.3.0.2.4 Rhabdomyolysis-Induced AKI
  • CK > 5000 (severe, AKI risk)
  • Muscle injury, trauma, statin myopathy, crush, exercise, ischemia, alcohol, drugs
  • Myoglobin → tubular obstruction + direct toxicity + heme oxidant
  • Treatment: aggressive IV fluids; alkalinization debated; mannitol debated
  • Urine output > 200-300 mL/h target
333.1.3.0.2.5 Tumor Lysis Syndrome (TLS)
  • Rapid tumor cell death
  • Hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia
  • AKI from uric acid crystals + Ca-PO4 precipitation
  • Prevention: allopurinol or rasburicase + hydration
  • Hematologic malignancies (AML, ALL, lymphoma) high risk
333.1.3.0.2.6 Cardiorenal Syndrome (CRS)
  • Cardiac dysfunction → renal injury (Type 1, 2)
  • Renal dysfunction → cardiac (Type 3, 4)
  • Combined (Type 5)
  • Diuretic resistance, decongestion strategies
333.1.3.0.2.7 COVID-19 AKI
  • 20-30% of hospitalized COVID
  • Multifactorial (hemodynamic, viral, hypercoagulability)
  • Often resolves; some develop CKD

333.1.3.1 🩺 床邊速查

  • KDIGO criteria: Cr ↑ ≥ 0.3 in 48 h, OR Cr ≥ 1.5× baseline in 7 d, OR UO < 0.5 mL/kg/h × 6 h
  • Pre-renal: BUN/Cr > 20, FENa < 1%, U Na < 20, U Osm > 500
  • ATN: BUN/Cr < 20, FENa > 2%, U Na > 40, isothenuric, muddy brown casts
  • Imaging first: renal ultrasound to rule out hydronephrosis
  • HRS: terlipressin + albumin (FDA 2022)
  • Rhabdo: CK > 5000, aggressive IVF
  • TLS: allopurinol/rasburicase + hydration