Renal · Year 2 · from Renal
Case 2: Acute Tubular Necrosis from Aminoglycosides
Patient Presentation
A 58-year-old male with endocarditis on IV gentamicin and ampicillin for 12 days presents with decreasing urine output. He was admitted with Enterococcus faecalis mitral valve endocarditis.
History of Present Illness
- Enterococcal endocarditis diagnosed 2 weeks ago
- Started on ampicillin and gentamicin
- Progressive decrease in urine output over past 3 days
- No hypotensive episodes documented
- No other nephrotoxic medications
Physical Examination
- Blood pressure: 128/76 mmHg
- Heart rate: 82 bpm
- Temperature: 37.2°C (afebrile)
- Mild lower extremity edema
- III/VI systolic murmur at apex
- Lungs with bibasilar crackles
Workup
Laboratory Studies:
- Baseline creatinine (admission): 1.0 mg/dL
- Day 7 creatinine: 1.3 mg/dL
- Day 12 creatinine: 2.8 mg/dL
- BUN: 42 mg/dL
- BUN:Creatinine ratio: 15:1
- Gentamicin trough: 2.8 mcg/mL (elevated, target <1)
- Urine sodium: 52 mEq/L
- FENa: 3.2%
- Urine osmolality: 320 mOsm/kg
- Urinalysis: Muddy brown granular casts, renal tubular epithelial cells
Diagnosis
Aminoglycoside-Induced Acute Tubular Necrosis
Discussion
This case demonstrates nephrotoxic ATN:
- Aminoglycoside Nephrotoxicity: The lecture describes how aminoglycosides accumulate in proximal tubular cells over days of therapy. Toxicity is dose- and duration-dependent, typically manifesting after 5-7 days.
- Non-Oliguric Pattern: Aminoglycoside ATN often presents with non-oliguric AKI and concentrating defect, as mentioned in the lecture.
- Laboratory Indices: Unlike prerenal AKI, ATN shows impaired tubular function: FENa >2%, urine sodium >40 mEq/L, inability to concentrate urine (<350 mOsm/kg), and near-normal BUN:Cr ratio.
- Muddy Brown Casts: The lecture identifies these as characteristic of ATN, representing degenerating tubular cells.
- Elevated Trough Levels: Poor drug clearance led to accumulation, worsening the injury.
Treatment
- Discontinue gentamicin immediately
- Switch to daptomycin monotherapy for enterococcal endocarditis
- Supportive care with fluid management
- Avoid additional nephrotoxins
- Infectious disease and cardiology consultation
- Monitor for recovery (typically 1-3 weeks)
Clinical Pearl
Aminoglycoside nephrotoxicity develops gradually over 5-7 days as the drug accumulates in proximal tubule cells. Monitor creatinine and drug levels closely. Non-oliguric AKI is typical, which may delay recognition. Once ATN is established, drug clearance decreases and levels rise further, creating a vicious cycle.