Renal · Year 2 · from Renal
Case 1: NSAID-Induced Acute Kidney Injury
Patient Presentation
A 72-year-old male with osteoarthritis presents to his primary care physician with fatigue and decreased urine output over the past week. He has been taking ibuprofen 800 mg three times daily for the past 2 weeks for a flare of knee pain.
History of Present Illness
- Started high-dose ibuprofen 2 weeks ago
- Noticed decreased urine output 5 days ago
- Mild swelling in ankles
- Currently taking lisinopril for hypertension and metformin for type 2 diabetes
- Also recently started a low-sodium diet for blood pressure control
Physical Examination
- Blood pressure: 158/94 mmHg
- Heart rate: 72 bpm
- Weight: 2 kg increase from baseline
- Trace bilateral pedal edema
- Lungs clear to auscultation
Workup
Laboratory Studies:
- Baseline creatinine (3 weeks ago): 1.2 mg/dL
- Current creatinine: 2.8 mg/dL
- BUN: 42 mg/dL
- BUN:Creatinine ratio: 15:1
- Potassium: 5.4 mEq/L
- Urinalysis: Specific gravity 1.025, no blood, no protein, no casts
- Urine sodium: 8 mEq/L
- Fractional excretion of sodium (FENa): 0.4%
Diagnosis
NSAID-Induced Prerenal Acute Kidney Injury
Discussion
This case illustrates the determinants of GFR from the lecture:
- Afferent Arteriolar Regulation: Prostaglandins normally cause afferent arteriolar dilation, particularly important when renal perfusion is compromised. NSAIDs block prostaglandin synthesis, removing this protective vasodilation.
- Combined NSAID + ACE Inhibitor Effect: The patient is also on lisinopril, which dilates the efferent arteriole. The combination creates a "perfect storm" - reduced inflow (blocked prostaglandin dilation) and reduced efferent constriction removes the ability to maintain glomerular capillary pressure.
- Low FENa: The FENa <1% indicates intact tubular function with appropriate sodium conservation, confirming prerenal etiology rather than acute tubular necrosis.
Starling Forces Analysis
- Reduced renal perfusion (dehydration from low-sodium diet, reduced cardiac preload)
- Blocked afferent dilation (NSAID effect)
- Blocked efferent constriction (ACE inhibitor effect)
- Net effect: Marked reduction in glomerular capillary hydrostatic pressure (PGC) and GFR
Treatment
- Discontinue ibuprofen immediately
- Hold lisinopril temporarily
- Gentle IV fluid resuscitation with normal saline
- Monitor creatinine daily
- Creatinine improved to 1.4 mg/dL after 5 days
Clinical Pearl
The "triple whammy" of NSAID + ACE inhibitor/ARB + diuretic or volume depletion is a common cause of prerenal AKI. All three factors reduce GFR: NSAIDs block afferent dilation, RAAS blockers remove efferent constriction, and volume depletion reduces perfusion pressure.