What is the cause of kidney injury in a patient with a history of hypertension and diabetes, presenting with dehydration, severe vomiting, and diarrhea, and an elevated creatinine level from 60 to 160 over a week?

Acute Tubular Necrosis (ATN)

This patient has acute tubular necrosis (ATN), not prerenal azotemia, as evidenced by the urine sodium of 60 mEq/L, urine osmolality of 220 mOsm/kg, and the clinical context of prolonged dehydration in a high-risk patient with diabetes and hypertension. 1

Diagnostic Reasoning

The laboratory findings definitively distinguish ATN from prerenal azotemia:

• Urine sodium >40 mEq/L is pathognomonic for tubular dysfunction and indicates ATN, as the damaged tubular cells cannot reabsorb sodium appropriately 1
• Urine osmolality of 220 mOsm/kg confirms loss of concentrating ability, which is inconsistent with preserved tubular function seen in prerenal states 1
• In true prerenal azotemia, the kidneys retain their ability to concentrate urine (>500 mOsm/kg) and avidly reabsorb sodium (urine sodium <20 mEq/L) 1

The creatinine rise from 60 to 160 μmol/L represents KDIGO Stage 2 AKI (>2.0 times baseline), meeting criteria for acute kidney injury by showing more than a 50% increase within 7 days 2, 1

Why This Is ATN and Not Prerenal Azotemia

The low BUN of 11 mg/dL argues strongly against prerenal azotemia, as prerenal states typically show disproportionate BUN elevation (BUN:Cr ratio >20:1) due to enhanced urea reabsorption in the proximal tubule 3. This patient's BUN:Cr ratio is inappropriately low, suggesting tubular dysfunction preventing normal urea reabsorption 3

The clinical scenario reveals progression from prerenal physiology to established ATN:

• Initial dehydration from vomiting/diarrhea likely caused prerenal injury 2
• Age (50s-60s) with diabetes and hypertension impairs renal autoregulation, making these patients highly susceptible to ischemic tubular injury when perfusion drops 1
• One week of illness provided sufficient time for ischemic injury to damage tubular cells, converting reversible prerenal azotemia into established ATN 1, 4

Management Priorities

Immediate volume resuscitation remains first-line therapy even in established ATN, as some component of prerenal physiology may still be reversible 1:

• Administer isotonic saline (0.9% NaCl) initially to restore intravascular volume 2
• Monitor hemodynamic response, urine output, and mental status during fluid replacement 2

Discontinue all nephrotoxic medications immediately 1:

• Stop NSAIDs if being used 2
• Hold ACE inhibitors/ARBs until volume status normalizes 2, 1
• Hold diuretics during acute illness 1

Monitor for dialysis indications including hyperkalemia, metabolic acidosis, uremia, or volume overload requiring renal replacement therapy 1

Critical Pitfall to Avoid

Do not assume this is simple prerenal azotemia based solely on the clinical history of dehydration 1. The urinary indices (high urine sodium, low urine osmolality) override the clinical presentation and indicate established tubular damage 1. Treating this as prerenal azotemia alone without recognizing ATN could delay appropriate monitoring for complications and nephrology consultation 1

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 1:

• Creatinine monitoring every 2-4 weeks for 6 months
• Nephrology referral if creatinine fails to return to within 115% of baseline (approximately 69 μmol/L in this case)
• Long-term surveillance for CKD development given underlying diabetes and hypertension 2