Acute Tubular Necrosis (ATN)
This patient has acute tubular necrosis (ATN), not simple prerenal azotemia, as evidenced by the elevated urine sodium of 60 mEq/L and low urine osmolality of 220 mOsm/kg despite severe volume depletion from vomiting and diarrhea.
Diagnostic Reasoning
The laboratory values definitively point to intrinsic renal injury rather than functional prerenal azotemia:
Urine sodium of 60 mEq/L indicates tubular dysfunction - In true prerenal azotemia, the kidneys should avidly retain sodium (urine Na <20 mEq/L) in response to volume depletion 1, 2. This patient's urine sodium >40 mEq/L demonstrates the tubules have lost their ability to conserve sodium, which is pathognomonic for ATN 1.
Low urine osmolality (220 mOsm/kg) confirms loss of concentrating ability - The specific gravity of 900 (which translates to approximately 1.009) and osmolality of 220 indicate the kidneys cannot concentrate urine appropriately despite severe dehydration 3. In prerenal states, urine osmolality should exceed 500 mOsm/kg 3.
The clinical context supports progression from prerenal to ATN - While the initial insult was volume depletion from gastrointestinal losses, the duration and severity allowed progression from functional prerenal injury to structural tubular damage 3. The creatinine rise from 60 to 160 μmol/L represents KDIGO Stage 2 AKI (>2.0 times baseline) 4.
Why Not Prerenal Azotemia
Prerenal azotemia would show urine sodium <20 mEq/L, fractional excretion of sodium (FENa) <1%, and urine osmolality >500 mOsm/kg 1, 2. This patient's urinary indices are completely inconsistent with preserved tubular function. The distinction is critical because while prerenal AKI responds rapidly to volume repletion, ATN requires supportive care and takes days to weeks for tubular regeneration 3.
High-Risk Features in This Patient
Several factors predisposed this patient to ATN rather than reversible prerenal injury:
Age (50s-60s) with diabetes and hypertension - These comorbidities impair renal autoregulation and increase susceptibility to ischemic tubular injury 4.
Likely continuation of RAAS inhibitors and diuretics during illness - Patients with diabetes and hypertension are commonly on ACE inhibitors/ARBs and diuretics. Failure to hold these "sick day medications" during volume depletion accelerates progression from prerenal to ATN 4, 5.
Duration of volume depletion - The week-long interval between the last physician visit (creatinine 60) and presentation allowed sustained renal hypoperfusion, causing ischemic tubular necrosis 3.
Critical Management Points
Volume resuscitation remains first-line therapy even in ATN, as some component of prerenal physiology may be reversible 1. However, expect slower recovery than pure prerenal azotemia.
Immediately discontinue all nephrotoxic medications including NSAIDs, and hold RAAS inhibitors and diuretics until volume status normalizes 4, 1.
Monitor for dialysis indications - With Stage 2 AKI and ongoing gastrointestinal losses, watch for hyperkalemia, metabolic acidosis, uremia, or volume overload requiring renal replacement therapy 4.
Avoid the "triple whammy" - The combination of volume depletion, RAAS inhibitors, and NSAIDs creates particularly severe risk for ATN progression 5.
Common Diagnostic Pitfall
The most critical error is assuming all AKI with volume depletion is prerenal 1. Up to 86% of patients with intrinsic kidney disease can initially present with clinical features suggesting prerenal causes 1. The urinary indices are essential for distinguishing functional from structural injury. This patient's urine sodium >40 mEq/L definitively excludes simple prerenal azotemia and confirms tubular damage has occurred 1, 2.
Prognosis and Follow-Up
Even with complete creatinine recovery, this patient faces significantly increased long-term risks of recurrent AKI, progression to chronic kidney disease, and cardiovascular events 1. Mandatory follow-up includes creatinine monitoring every 2-4 weeks for 6 months, with nephrology referral if creatinine fails to return to within 115% of baseline 1.