Internal Medicine · Year 3 · from Internal Medicine
Case 2: Intrinsic AKI - Acute Tubular Necrosis
Patient Presentation
A 62-year-old man with a history of diabetes and peripheral vascular disease underwent aortic aneurysm repair 3 days ago. He had intraoperative hypotension requiring vasopressors and received IV contrast for preoperative imaging. His urine output has progressively decreased over the past 24 hours despite fluid resuscitation.
Vital Signs
- Blood Pressure: 118/72 mmHg (on norepinephrine)
- Heart Rate: 88 bpm
- Respiratory Rate: 18/min
- Oxygen Saturation: 96% on 2L NC
- Temperature: 37.2°C
- Urine output: 180 mL in past 12 hours
Physical Examination
- General: Sedated, intubated
- Cardiovascular: Regular rhythm, no murmurs, CVP 12 cmH2O
- Pulmonary: Bilateral crackles at bases
- Abdomen: Midline surgical incision, soft
- Extremities: Trace edema
Laboratory Results
- Creatinine: 4.8 mg/dL (baseline 1.4, was 2.8 yesterday)
- BUN: 52 mg/dL
- BUN/Cr ratio: 11:1
- Potassium: 6.1 mEq/L
- Bicarbonate: 18 mEq/L
- Urinalysis: Muddy brown granular casts, renal tubular epithelial cells
- Urine sodium: 48 mEq/L
- FENa: 3.2%
Clinical Image
Figure 2: Urine microscopy demonstrating muddy brown granular casts, pathognomonic for acute tubular necrosis.
Image Source: Educational illustration for teaching purposes.
Questions
- What urine findings are characteristic of acute tubular necrosis?
- A) Bland sediment with low urine sodium
- B) Muddy brown granular casts, renal tubular epithelial cells, high urine sodium, FENa >2%
- C) RBC casts and dysmorphic RBCs
- D) White blood cell casts
- What are the likely causes of ATN in this patient?
- A) Glomerulonephritis
- B) Ischemia (intraoperative hypotension) and nephrotoxin (contrast)
- C) Obstructive uropathy
- D) Interstitial nephritis
- What is the typical clinical course of ATN?
- A) Immediate recovery
- B) Initiation (insult) → Extension → Maintenance (oliguria) → Recovery phases over 1-3 weeks
- C) Permanent kidney failure
- D) Fluctuating course
- What indications for renal replacement therapy (dialysis) are present or developing?
- What preventive measures could have reduced the risk of contrast-induced nephropathy?
Answers
- B) Muddy brown granular casts, renal tubular epithelial cells, high urine sodium, FENa >2% - These findings indicate tubular damage with loss of ability to reabsorb sodium. Muddy brown casts are composed of degenerating tubular cells and are pathognomonic for ATN.
- B) Ischemia (intraoperative hypotension) and nephrotoxin (contrast) - This patient has multifactorial ATN from ischemic insult (prolonged hypotension during surgery) and contrast nephropathy. These are the two most common causes of ATN in hospitalized patients.
- B) Initiation (insult) → Extension → Maintenance (oliguria) → Recovery phases over 1-3 weeks - ATN typically evolves through phases. Maintenance phase with oliguria lasts 1-2 weeks. Recovery with polyuria follows as tubules regenerate. Most patients recover if they survive the underlying illness.
- Indications for RRT (AEIOU):
- Acidemia: Severe metabolic acidosis (pH <7.1) refractory to bicarbonate
- Electrolytes: Refractory hyperkalemia (6.1 mEq/L is concerning)
- Ingestion: Toxic ingestions (not applicable here)
- Overload: Volume overload refractory to diuretics
- Uremia: Uremic symptoms (encephalopathy, pericarditis, bleeding)
- This patient has hyperkalemia and oliguria - may need RRT if not responsive to medical management
- Prevention of contrast-induced nephropathy:
- Pre-procedural volume expansion with IV isotonic crystalloid
- Use of low-osmolar or iso-osmolar contrast agents
- Minimizing contrast volume
- Holding nephrotoxic medications (NSAIDs, ACE inhibitors) before procedure
- Avoiding repeated contrast exposure within 48-72 hours
- N-acetylcysteine (limited evidence, sometimes used)