Acute tubular necrosis

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ATN Overview - Kidney's Downfall

Most common cause of acute kidney injury (AKI) in hospitalized patients, marked by tubular cell damage. It's often reversible.

FeatureIschemic ATNNephrotoxic ATN
Pathophysiology↓ Renal blood flow (hypoperfusion)Direct tubular cell toxin exposure
Key CausesShock, sepsis, major surgeryAminoglycosides, contrast, myoglobin
Tubular SegmentsProximal tubule & thick ascending limbPrimarily proximal tubule

Muddy brown casts in urine sediment are pathognomonic. The BUN:Cr ratio is often < 15:1 due to impaired urea reabsorption.

Pathophysiology - Cellular Chaos

Two major pathways converge on tubular epithelial cell injury:

  • Ischemic Injury: Most prominent in the proximal tubule (S3 segment) & thick ascending limb (TAL).
  • Nephrotoxic Injury: Primarily affects the proximal convoluted tubule (S1/S2) due to high reabsorptive function.

Pathophysiology of Acute Tubular Necrosis (ATN)

⭐ The S3 segment of the proximal tubule and the medullary thick ascending limb are classic sites for ischemic ATN due to high metabolic demand in a low-oxygen environment.

Morphology - Muddy Brown Mayhem

  • Gross: Enlarged, pale kidneys; swollen cortex, congested medulla.
  • Microscopy:
    • Tubular Injury: Necrosis and sloughing of proximal tubular epithelial cells, with loss of brush border and tubular dilation. The basement membrane is typically spared.
    • Casts: Pathognomonic muddy brown granular casts in distal tubules and collecting ducts.
    • Interstitial edema.

Acute Tubular Necrosis with muddy brown casts

⭐ The proximal straight tubule and the thick ascending limb of Henle's loop are the most susceptible segments to ischemic injury.

Clinical Phases - The 3-Act Tragedy

A clinical course defined by three stages, tracking the progression from injury to resolution. The timeline and electrolyte shifts are key.

⭐ The BUN:Cr ratio is characteristically < 15:1 in ATN, as tubular dysfunction impairs urea reabsorption, distinguishing it from pre-renal azotemia where the ratio is > 20:1.

Diagnosis & Management - The Clinician's Clues

  • Urinalysis: Key to differentiate from prerenal azotemia.
    • Microscopy: Muddy brown granular casts are pathognomonic.
FindingPrerenal AzotemiaAcute Tubular Necrosis (ATN)
BUN:Cr Ratio>20:1<15:1
Urine Na+<20 mEq/L>40 mEq/L
FeNa<1%>2%
Urine Osmolality>500 mOsm/kg<350 mOsm/kg
- Address underlying cause (e.g., stop nephrotoxic drugs, restore perfusion).
- Manage fluid & electrolytes; loop diuretics for fluid overload.
- Indications for dialysis: 📌 **A**cidosis, **E**lectrolytes (hyperkalemia), **I**ngestions, **O**verload (refractory), **U**remia.

⭐ FeNa may be <1% in early sepsis- or contrast-induced ATN due to initial vasospasm.

High‑Yield Points - ⚡ Biggest Takeaways

  • The most common cause of acute kidney injury (AKI) in hospitalized patients.
  • Caused by ischemic or nephrotoxic injury to the renal tubules, particularly the proximal tubule and thick ascending limb.
  • Muddy brown granular casts in the urine are pathognomonic.
  • Key lab findings include a BUN:Cr ratio < 15:1 and a FENa > 2%.
  • Presents in three phases: initiation, maintenance (oliguric, hyperkalemia), and recovery (polyuric, hypokalemia).
  • Unlike cortical necrosis, ATN is potentially reversible.

Practice Questions: Acute tubular necrosis

Test your understanding with these related questions

A 78-year-old man dies suddenly from complications of acute kidney failure. An autopsy is performed and microscopic evaluation of the kidneys shows pale, swollen cells in the proximal convoluted tubules. Microscopic evaluation of the liver shows similar findings. Which of the following is the most likely underlying mechanism of these findings?

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Flashcards: Acute tubular necrosis

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Acute tubular necrosis may be caused by _____-contrast dyes

TAP TO REVEAL ANSWER

Acute tubular necrosis may be caused by _____-contrast dyes

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