Acute Tubular Necrosis for PA
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Acute Tubular Necrosis for the Physician Assistant Licensing Exam
- Definition:
- Acute tubular necrosis (ATN) is a form of acute kidney injury (AKI) characterized by damage to the renal tubular epithelial cells. It commonly results from ischemia or exposure to nephrotoxic substances.
- Etiology:
- Ischemic ATN:
- Caused by reduced renal perfusion from hypotension or hypovolemia. Common triggers include:
- Shock: Hypovolemic, septic, or cardiogenic shock.
- Surgery: Prolonged surgeries with hypotension.
- Nephrotoxic ATN:
- Caused by direct tubular damage from:
- Medications: Aminoglycosides, NSAIDs, radiocontrast agents, cisplatin.
- Endogenous Toxins: Myoglobin (rhabdomyolysis), hemoglobin (hemolysis), uric acid (tumor lysis syndrome).
- Exogenous Toxins: Heavy metals (e.g., lead, mercury).
- Pathophysiology:
- Tubular Cell Injury:
- Hypoxia or toxins damage tubular epithelial cells, causing sloughing into the tubular lumen and reducing the glomerular filtration rate (GFR).
- Intrarenal Vasoconstriction:
- Vasoconstriction reduces renal blood flow, worsening tubular ischemia.
- Backleak of Filtrate:
- Damaged tubules allow filtrate to leak into the interstitium, further impairing renal function.
- Clinical Features:
- Oliguria or Non-oliguria:
- Oliguria (<400 mL/day) is typical, though non-oliguric ATN can occur with nephrotoxic injury.
- Volume Overload:
- Symptoms include edema, hypertension, and pulmonary congestion.
- Electrolyte Imbalances:
- Hyperkalemia, metabolic acidosis, and hyperphosphatemia due to impaired renal function.
- Diagnosis:
- Urinalysis:
- Granular ("muddy brown") casts and tubular epithelial cells are characteristic.
- Low Specific Gravity reflects impaired urine concentration.
- Blood Tests:
- Elevated creatinine and blood urea nitrogen (BUN), hyperkalemia, and metabolic acidosis.
- Fractional Excretion of Sodium (FeNa):
- FeNa >2% indicates ATN due to impaired sodium reabsorption.
- Management:
- Supportive Care:
- Volume resuscitation in hypovolemic patients and diuretics for volume overload. Correct hyperkalemia and acidosis as needed.
- Nephrotoxin Avoidance:
- Discontinue nephrotoxic agents and hydrate before contrast use.
- Renal Replacement Therapy (RRT):
- Dialysis may be needed for severe cases of electrolyte imbalance or volume overload.
Key Points
- Acute tubular necrosis is a common cause of acute kidney injury, usually triggered by ischemia or nephrotoxic agents.
- Clinical features include oliguria, fluid overload, hyperkalemia, and metabolic acidosis.
- Diagnosis involves identifying granular casts on urinalysis and elevated creatinine levels.
- Management includes supportive care, nephrotoxin avoidance, and dialysis for severe cases.