Renal · Year 2 · from Renal
Case 1: Prerenal AKI from Volume Depletion
Patient Presentation
A 78-year-old male with heart failure and hypertension presents to the emergency department with weakness and decreased oral intake for 5 days following a gastrointestinal illness. He continued taking his furosemide throughout his illness.
History of Present Illness
- Diarrhea and vomiting for 5 days (now resolved)
- Decreased appetite and fluid intake
- Progressive weakness and lightheadedness
- Continued all medications including furosemide 40 mg twice daily
- Also takes lisinopril 20 mg daily
Physical Examination
- Blood pressure: 88/52 mmHg (baseline 130/80)
- Heart rate: 108 bpm
- Orthostatic: Unable to stand due to dizziness
- Dry mucous membranes, poor skin turgor
- Flat neck veins
- Clear lungs, no peripheral edema
Workup
Laboratory Studies:
- Baseline creatinine (1 month ago): 1.2 mg/dL
- Current creatinine: 3.8 mg/dL
- BUN: 68 mg/dL
- BUN:Creatinine ratio: 18:1
- Sodium: 134 mEq/L
- Potassium: 5.4 mEq/L
- Urine sodium: 6 mEq/L
- FENa: 0.3%
- Urine osmolality: 620 mOsm/kg
- Urinalysis: Specific gravity 1.028, no blood, no protein, hyaline casts only
Diagnosis
Prerenal Acute Kidney Injury from Volume Depletion
Discussion
This case illustrates classic prerenal AKI:
- KDIGO Criteria: Creatinine rose from 1.2 to 3.8 mg/dL, representing more than 3x baseline within 7 days, meeting criteria for Stage 3 AKI.
- Intact Tubular Function: The lecture describes how prerenal AKI reflects decreased perfusion with preserved tubular function. The kidney responds appropriately by maximally conserving sodium (FENa <1%, urine Na <20 mEq/L) and concentrating urine (osmolality >500 mOsm/kg).
- BUN:Creatinine Ratio: The elevated ratio (>20:1) reflects enhanced urea reabsorption in the hypovolemic state.
- Contributing Factors: Continued diuretics during volume losses, plus ACE inhibitor removing compensatory efferent arteriolar constriction, created a "triple whammy" effect as described in the lecture.
- Bland Sediment: Hyaline casts only, without muddy brown casts or cellular elements, supports prerenal rather than intrinsic injury.
Treatment
- Hold furosemide and lisinopril
- IV normal saline 1 liter bolus, then 150 mL/hour
- Monitor urine output (goal >0.5 mL/kg/hour)
- Creatinine improved to 1.6 mg/dL after 48 hours of hydration
- Cautiously restart medications after recovery
Clinical Pearl
In prerenal AKI, laboratory indices reflect appropriate kidney responses to hypoperfusion: FENa <1%, urine sodium <20 mEq/L, concentrated urine, and BUN:Cr ratio >20:1. The rapid improvement after volume restoration confirms the diagnosis. If FENa remains low despite ATN (as with contrast or pigment nephropathy), consider using FEUrea (<35% suggests prerenal).