What is the likely cause of kidney injury in a patient with a history of hypertension (HTN) and diabetes mellitus (DM) presenting with dehydration, severe vomiting, and diarrhea, and an elevated creatinine level from 60 to 160?

Pre-Renal Azotemia

The most likely cause of kidney injury in this patient is pre-renal azotemia (Option A), given the clear precipitant of severe vomiting and diarrhea causing volume depletion, signs of dehydration on examination, and the rapid rise in creatinine from a relatively preserved baseline just one week prior. 1

Clinical Reasoning

Acute Presentation with Clear Precipitant

• Severe vomiting and diarrhea directly cause volume loss, leading to pre-renal acute kidney injury with acute onset and a clear precipitating event 1
• The rapid creatinine rise from 60 to 160 μmol/L over one week meets criteria for acute kidney injury, defined by rapid increase in serum creatinine 1
• Volume depletion reduces renal perfusion by causing intravascular volume depletion, which reduces renal blood flow and glomerular filtration 1

Evidence Against Acute Tubular Necrosis (ATN)

• ATN typically requires more severe or prolonged ischemic insult, and the clinical presentation here suggests reversible hemodynamic changes rather than established tubular damage 2
• The presence of clear dehydration signs and recent baseline creatinine of 60 suggests the injury is functional rather than structural 1
• Pre-renal azotemia should be confirmed by checking if creatinine improves with hydration—if it does, this confirms the pre-renal etiology 1

Evidence Against Acute-on-Chronic Kidney Injury

• The baseline creatinine of 60 one week ago suggests relatively preserved baseline renal function, not chronic kidney disease 1
• While diabetes and hypertension are risk factors that increase the risk of acute kidney injury 1, a creatinine of 60 indicates the patient did not have significant chronic kidney disease at baseline
• Acute-on-chronic kidney injury would require evidence of pre-existing CKD, which is not supported by the recent normal creatinine 3

Immediate Management Priorities

Medication Review

• Hold nephrotoxic medications immediately, including ACE inhibitors, ARBs, diuretics, NSAIDs, and metformin, as these can exacerbate pre-renal azotemia by reducing intravascular volume and altering intrarenal hemodynamics 1
• Antihypertensive medications are particularly problematic in volume-depleted states 1

Diagnostic Confirmation

• Check BUN-to-creatinine ratio: a disproportionate rise in BUN compared to creatinine suggests dehydration rather than intrinsic kidney injury 4
• Obtain fractional excretion of sodium to help distinguish pre-renal from intrinsic causes 2
• Assess for absence of proteinuria, hematuria, or abnormal urinary sediment, which helps distinguish transient elevation from intrinsic kidney disease 4

Treatment Response

• Initiate fluid resuscitation and monitor creatinine response 2
• In pure dehydration/pre-renal azotemia, creatinine elevation typically resolves with fluid replacement 4
• If creatinine improves with hydration, this confirms the pre-renal etiology 1

Important Caveats

• If the patient fails to respond to adequate fluid resuscitation within 24-48 hours, consider that pre-renal azotemia may have progressed to ATN 2
• The patient's diabetes and hypertension place them at higher risk for AKI complications and potential progression 1, 3
• Close monitoring is essential, as frequency and severity of kidney injury episodes are risk factors for eventual progression to chronic kidney disease 3