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Acute kidney injury

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AKI Fundamentals - The Kidney Crisis

  • Definition: Abrupt kidney dysfunction causing ↑ creatinine & ↓ urine output.
    • ↑ SCr by ≥0.3 mg/dL within 48h
    • ↑ SCr to ≥1.5x baseline
    • Urine output <0.5 mL/kg/h for >6 hours
  • Types:
    • Prerenal: Hypoperfusion (e.g., dehydration). BUN/Cr >20, $FeNa$ <1%.
    • Intrinsic: Direct kidney damage (e.g., ATN, AIN).
    • Postrenal: Urinary tract obstruction (e.g., BPH, stones).

Acute Kidney Injury: Causes, Classification, & Complications

⭐ Fractional excretion of sodium ($FeNa$) is a key test to differentiate prerenal AKI from ATN, but its utility is limited in patients on diuretics.

Prerenal AKI - The Dry Spell

  • Pathophysiology: ↓ Renal perfusion triggers physiologic Na⁺/H₂O retention. It is typically reversible with restored blood flow.
  • Etiologies:
    • True volume loss (e.g., hemorrhage, dehydration).
    • ↓ Effective circulating volume (e.g., heart failure, cirrhosis).
    • Renal artery stenosis.
    • Drugs: NSAIDs, ACE inhibitors, ARBs.
  • Key Labs:
    • BUN/Cr Ratio > 20:1
    • Urine Osmolality > 500 mOsm/kg
    • FENa < 1%
    • Urine Na⁺ < 20 mEq/L

⭐ The hallmark is a BUN/Cr ratio > 20:1, reflecting increased passive urea reabsorption in the proximal tubule due to enhanced sodium and water reabsorption.

Intrinsic AKI - Muddy Waters

  • Direct damage to kidney structures (tubules, interstitium, glomeruli). Characterized by FENa > 2% and Urine Osm < 350 mOsm/kg.

Acute Tubular Necrosis (ATN)

  • Most common cause.
    • Ischemic: Prolonged hypotension/hypoxia (e.g., shock, sepsis).
    • Nephrotoxic: Aminoglycosides, contrast dye, myoglobin, ethylene glycol.
  • Urinalysis: Muddy brown granular casts are pathognomonic.

Acute Interstitial Nephritis (AIN)

  • Inflammatory infiltrate in the interstitium, often drug-induced.
    • Classic Triad: Fever, rash, arthralgias.
    • Urinalysis: WBC casts, sterile pyuria, and eosinophiluria.

⭐ Muddy brown casts in ATN are composed of necrotic tubular epithelial cells and Tamm-Horsfall protein.

Urinary casts and associated kidney conditions

Postrenal AKI - The Block Party

  • Pathophysiology: Urinary tract obstruction → ↑ intratubular pressure → ↓ GFR.
  • Etiologies: Benign Prostatic Hyperplasia (BPH) is the most common cause. Others include nephrolithiasis, tumors (prostate, cervical), and neurogenic bladder.
  • Diagnosis:
    • Bladder ultrasound is the initial test to look for hydronephrosis.
    • Catheterization can be both diagnostic and therapeutic.
  • Labs: Early phase shows BUN:Cr > 15:1.

⭐ Unilateral obstruction does not cause AKI unless the patient has only one functioning kidney.

Acute Kidney Injury (AKI) Quick Facts Infographic

AKI Management - Dialysis Decisions

Indications for urgent dialysis (📌 AEIOU):

  • Acidosis: Severe, refractory metabolic acidosis (pH < 7.1)
  • Electrolytes: Severe, refractory hyperkalemia (K⁺ > 6.5 mEq/L)
  • Intoxication: Specific poisons (e.g., salicylates, lithium, methanol, ethylene glycol)
  • Overload: Refractory fluid overload causing pulmonary edema
  • Uremia: Symptomatic (encephalopathy, seizures, or pericarditis)

⭐ Uremic pericarditis is an absolute indication for immediate dialysis.

High‑Yield Points - ⚡ Biggest Takeaways

  • Prerenal AKI, the most common type, shows a BUN/Cr ratio > 20:1 and FeNa < 1%, often from hypovolemia.
  • Acute Tubular Necrosis (ATN), the top intrinsic cause, presents with muddy brown granular casts and an FeNa > 2%.
  • Postrenal AKI results from obstruction; diagnose with a renal ultrasound looking for hydronephrosis.
  • Cardiorenal and hepatorenal syndromes are critical diagnoses in advanced heart failure and cirrhosis, respectively.
  • Always review medications for nephrotoxins like NSAIDs and contrast dye, especially in high-risk settings.

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