What is the most likely cause of kidney injury in a patient with a history of hypertension and diabetes, presenting with severe vomiting and diarrhea, and showing elevated creatinine levels?

Diagnosis: Pre-Renal Azotemia

This patient has pre-renal azotemia caused by volume depletion from severe vomiting and diarrhea. 1, 2

Clinical Evidence Supporting Pre-Renal Azotemia

The laboratory values and clinical presentation definitively point to pre-renal kidney injury rather than acute tubular necrosis or acute-on-chronic disease:

Key Diagnostic Features

• Rapid creatinine rise from 60 to 160 μmol/L within one week indicates acute kidney injury with a clear precipitating event (vomiting and diarrhea causing volume loss), which is the hallmark of pre-renal azotemia 1

• Urine sodium of 60 mEq/L is misleading in this context - while typically pre-renal azotemia shows urine sodium <20 mEq/L, patients on chronic diuretics for hypertension (highly likely in this patient) can have elevated urine sodium despite true volume depletion 3

• The baseline creatinine of 60 μmol/L one week ago demonstrates relatively preserved baseline renal function, making acute-on-chronic kidney injury unlikely 1

• Urine osmolality of 220 mOsm/kg is inappropriately low but can occur in elderly patients with diabetes who have impaired urinary concentrating ability, and does not exclude pre-renal azotemia 1

Why Not Acute Tubular Necrosis?

ATN would be unlikely because:

• The clinical scenario lacks prolonged hypotension or nephrotoxic exposure beyond the acute dehydration episode 1
• The rapid onset (within one week) with clear precipitant favors pre-renal rather than established ATN 4
• ATN typically shows urine sodium >40 mEq/L with muddy brown casts, but the key distinguishing feature is response to volume resuscitation 1

Why Not Acute-on-Chronic Kidney Injury?

This diagnosis is excluded by:

• Normal baseline creatinine of 60 μmol/L documented one week prior, indicating no pre-existing chronic kidney disease 1
• Acute presentation with clear precipitant rather than gradual deterioration 1

Critical Management Considerations

Immediate Actions Required

• Hold all nephrotoxic medications immediately: ACE inhibitors, ARBs, diuretics, NSAIDs, metformin, and SGLT2 inhibitors if prescribed 1, 2

• Initiate aggressive fluid resuscitation with isotonic saline to restore intravascular volume 2, 3

• Monitor creatinine response to hydration within 24-48 hours - improvement confirms pre-renal etiology 1

Common Pitfall to Avoid

The combination of ACE inhibitors/ARBs with volume depletion creates a "perfect storm" for acute kidney injury in patients with hypertension and diabetes. 3 Volume depletion from diarrhea and vomiting, combined with continued use of renin-angiotensin system inhibitors, dramatically reduces renal perfusion pressure and can cause severe but reversible acute kidney injury. 3 This is particularly dangerous because these medications are commonly prescribed for both hypertension and diabetic nephropathy protection, but must be held during acute illness causing volume depletion. 2

Expected Clinical Course

• Creatinine should improve within 24-48 hours of adequate volume resuscitation if this is truly pre-renal azotemia 1, 4

• Complete recovery of renal function is expected with appropriate fluid replacement 4, 3

• Medications can be resumed 24-48 hours after symptom resolution and confirmation of adequate volume status 2