Acute Tubular Necrosis (ATN)
This patient has acute tubular necrosis (ATN), not prerenal azotemia. The urine sodium of 60 mEq/L and urine osmolality of 220 mOsm/kg definitively indicate tubular damage with loss of sodium conservation and concentrating ability, despite clinical evidence of volume depletion from vomiting and diarrhea 1, 2.
Diagnostic Reasoning
The urinary indices unequivocally point to ATN rather than prerenal azotemia:
Urine sodium >40 mEq/L has >85% specificity for ATN and effectively rules out prerenal causes 1, 2. This patient's urine sodium of 60 mEq/L far exceeds this threshold.
Urine osmolality of 220 mOsm/kg is inappropriately dilute for a dehydrated patient with vomiting and diarrhea 1. In true prerenal azotemia, urine osmolality should exceed 500 mOsm/kg as the kidneys attempt to conserve water 3.
The fractional excretion of sodium (FENa) calculation would likely exceed 1%, which indicates ATN rather than prerenal azotemia (FENa <1%) 1, 4.
Urine specific gravity of 0.900 (900) is inappropriately low for volume depletion, reflecting tubular inability to concentrate urine 2.
Why Not Prerenal Azotemia?
Prerenal azotemia requires:
This patient meets none of these criteria 3, 2.
Why Not Acute-on-Chronic?
The baseline creatinine of 0.6 mg/dL (60 μmol/L) is normal, indicating no preexisting chronic kidney disease 5. The acute rise to 1.6 mg/dL represents pure acute kidney injury, not acute-on-chronic 5.
Likely Etiology: Diuretic-Induced ATN
Valsartan combined with volume depletion from vomiting/diarrhea likely precipitated ATN 1, 6:
ARBs like valsartan reduce glomerular filtration pressure by blocking angiotensin II-mediated efferent arteriolar vasoconstriction 6.
Volume depletion from gastrointestinal losses further compromised renal perfusion, creating a "double hit" scenario 1, 4.
Prolonged renal hypoperfusion progressed from prerenal physiology to established ATN with tubular cell injury 1, 7.
Immediate Management
Stop valsartan immediately 1, 4. All nephrotoxic medications must be discontinued to prevent further kidney damage 1, 4.
Provide cautious volume resuscitation with crystalloids to correct dehydration 1, 4. Monitor closely for volume overload, as damaged tubules cannot appropriately handle sodium and water 4.
Consider albumin 1 g/kg (maximum 100 g) for two consecutive days if the patient fails to respond to initial crystalloid resuscitation 1, 4. Albumin is superior to crystalloids in patients with severe hypovolemia 4.
Monitor serum creatinine daily to assess AKI stage progression 1, 4. Measure urine output daily, as oliguria indicates poor prognosis 1, 4.
Common Pitfalls
Do not assume prerenal azotemia based solely on clinical dehydration 1, 2. The urinary indices trump clinical assessment when they diverge—this patient is clinically volume depleted but has established ATN 3, 2.
Do not give diuretics to "improve kidney function" 1. Diuretics have no role in treating ATN and may worsen outcomes 1.
Do not delay stopping the ARB 1, 4, 6. Valsartan can cause severe AIN or worsen ATN, and continuation will prevent recovery 6.
Prognosis
ATN carries significant mortality risk (37-55% in hospitalized patients) 4, 7. Mixed-cause ATN (ischemic plus nephrotoxic) has worse outcomes than pure ischemic ATN, with only 30% achieving complete renal recovery at discharge versus 74% for pure ischemic causes 7.
Long-term follow-up is essential 4. Patients should be evaluated for chronic kidney disease at 3 months, as CKD following AKI typically develops over 12-74 months 4.