Overview
This lecture covers acute tubular necrosis (ATN), focusing on its causes, pathophysiology, diagnosis, and management as the most common cause of acute kidney injury.
Definition and Pathophysiology
- Acute tubular necrosis (ATN) is the death (necrosis) of epithelial cells lining the renal tubules.
- ATN is the leading cause of acute kidney injury (AKI).
- Damage occurs due to ischemia (lack of blood flow) or nephrotoxic substances.
- The renal tubular epithelial cells can regenerate, making ATN usually reversible within 7–21 days.
Causes of Acute Tubular Necrosis
- Ischemic ATN arises from hypoperfusion, such as in shock, sepsis, or severe dehydration.
- Nephrotoxic ATN results from toxins, including radiology contrast dyes, gentamicin, and NSAIDs (e.g., naproxen).
Diagnosis
- Urinalysis may reveal "muddy brown casts," which are pathognomonic (specific) for ATN.
- Renal tubular epithelial cells may be found in urine due to their detachment from damaged tubules.
Management
- Supportive management is the mainstay of treatment.
- Administer intravenous fluids to correct dehydration and restore kidney perfusion.
- Discontinue nephrotoxic drugs such as NSAIDs and gentamicin.
- Treat any arising complications associated with ATN.
Key Terms & Definitions
- Acute tubular necrosis (ATN) — necrosis of tubular epithelial cells in the kidney leading to acute kidney injury.
- Ischemia — inadequate blood supply to an organ or tissue.
- Nephrotoxic — damaging or destructive to kidney cells.
- Pathognomonic — a sign or finding specific to a particular disease.
Action Items / Next Steps
- Review urinalysis findings, especially recognizing muddy brown casts.
- Memorize common ischemic and nephrotoxic causes of ATN.
- Study AKI management, focusing on supportive care and avoidance of nephrotoxins.