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?

Acute Kidney Injury: Pre-Renal Azotemia

The most likely cause of kidney injury in this patient is pre-renal azotemia (Option A), given the acute presentation with severe vomiting, diarrhea, clinical dehydration, and rapid rise in creatinine from 60 to 160 over a short period.

Clinical Reasoning

This patient presents with classic features of volume depletion leading to pre-renal acute kidney injury:

• Acute onset with clear precipitant: Severe vomiting and diarrhea causing volume loss 1
• Clinical dehydration: Physical signs of volume depletion are present 2
• Rapid creatinine rise: From 60 to 160 μmol/L (approximately 0.7 to 1.8 mg/dL) over days, consistent with acute kidney injury defined by rapid increase in serum creatinine 1
• Baseline kidney function: The creatinine of 60 one week ago suggests relatively preserved baseline renal function 1

Why Pre-Renal Azotemia (Not the Other Options)

Pre-Renal Azotemia is Most Likely Because:

• Volume depletion reduces renal perfusion: Severe vomiting and diarrhea cause intravascular volume depletion, reducing renal blood flow and glomerular filtration 1, 2
• Potentially reversible: Pre-renal azotemia typically resolves with fluid replacement, which is the expected trajectory here 3
• Disproportionate BUN rise: If BUN is disproportionately elevated compared to creatinine, this strongly suggests dehydration rather than intrinsic kidney injury 3

Why NOT Acute Tubular Necrosis (Option C):

• ATN requires prolonged ischemia: While severe volume depletion can progress to ATN if untreated, the clinical presentation suggests early intervention is still possible 2, 4
• ATN is less reversible: ATN represents structural tubular damage and takes longer to recover than simple pre-renal states 4
• Timing: The acute presentation with ongoing volume losses suggests functional rather than structural injury 2

Why NOT Acute-on-Chronic Kidney Injury (Option B):

• Baseline creatinine was 60: This is essentially normal kidney function, not consistent with pre-existing chronic kidney disease 1
• CKD typically develops over years: In diabetics, CKD usually develops after 10 years in type 1 diabetes or may be present at diagnosis in type 2 diabetes, but a creatinine of 60 one week ago argues against significant pre-existing CKD 1
• No mention of prior albuminuria or reduced eGFR: CKD diagnosis requires persistent albuminuria or eGFR <60 mL/min/1.73 m² 1

Important Caveats

Risk Factors Present:

• Diabetes and hypertension increase AKI risk: People with diabetes are at higher risk of acute kidney injury than those without 1
• Antihypertensive medications: If this patient takes ACE inhibitors, ARBs, or diuretics, these can exacerbate pre-renal azotemia by reducing intravascular volume and altering intrarenal hemodynamics 1

Progression Risk:

• Pre-renal can progress to ATN: If volume depletion is severe or prolonged without treatment, pre-renal azotemia can progress to acute tubular necrosis 2, 4
• Future CKD risk: Even after recovery, this AKI episode increases long-term risk of chronic kidney disease and cardiovascular events 5

Immediate Management Priorities

• Fluid resuscitation: Restore intravascular volume with appropriate crystalloid solutions 2
• Hold nephrotoxic medications: Temporarily discontinue ACE inhibitors, ARBs, diuretics, NSAIDs, and metformin if applicable 1
• Monitor response: Check if creatinine improves with hydration, confirming pre-renal etiology 3, 2
• Assess for complications: Monitor electrolytes, particularly potassium, and watch for volume overload during resuscitation 1, 2
• Calculate fractional excretion of sodium: FENa <1% supports pre-renal azotemia diagnosis 2