What is the most likely cause of acute kidney injury in a patient with 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 acute presentation with severe vomiting and diarrhea causing volume depletion, signs of dehydration, and a rapid creatinine rise in a patient with previously preserved baseline renal function. 1

Clinical Reasoning

This patient presents with the classic triad for pre-renal acute kidney injury:

• Acute volume loss from severe vomiting and diarrhea causing intravascular volume depletion and reduced renal perfusion 1
• Preserved baseline kidney function (creatinine 60 μmol/L one week ago) indicating no significant pre-existing chronic kidney disease 1
• Clear temporal relationship between the gastrointestinal losses and the acute creatinine rise to 160 μmol/L 1

The creatinine increase from 60 to 160 μmol/L represents KDIGO Stage 2 AKI (>2.0 times baseline), but the clinical context strongly favors a reversible pre-renal etiology rather than established tubular injury 2

Why Not Acute Tubular Necrosis (ATN)?

While ATN is possible if pre-renal injury is prolonged, several factors argue against established ATN as the primary diagnosis:

• ATN typically requires additional urinary indices for diagnosis, specifically urine sodium >40 mEq/L and low urine osmolality (<350 mOsm/kg), which indicate loss of tubular concentrating ability 2
• The acute presentation with clear precipitant (vomiting/diarrhea) and signs of dehydration favor pre-renal physiology that should respond to volume resuscitation 1
• Community-acquired AKI is predominantly pre-renal (70% of cases), with intrinsic renal failure accounting for only 11% 3

Why Not Acute-on-Chronic Kidney Injury?

The baseline creatinine of 60 μmol/L one week ago indicates relatively preserved baseline renal function, making pure acute-on-chronic injury less likely as the primary diagnosis 1. However, the patient's diabetes and hypertension do increase long-term risk for both AKI and progression to chronic kidney disease 1, 4

Critical Management Steps

Immediate actions to confirm pre-renal etiology and prevent progression to ATN:

• Hold all 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
• Initiate aggressive volume resuscitation with isotonic fluids as first-line therapy 2
• Monitor creatinine response to hydration within 24-48 hours - improvement confirms pre-renal etiology, while lack of response suggests progression to ATN 1

Important Caveats

The distinction between pre-renal azotemia and ATN exists on a continuum:

• If volume depletion is severe or prolonged, pre-renal injury can progress to ischemic ATN 2
• Patients with diabetes and hypertension have impaired renal autoregulation, making them more susceptible to ischemic tubular injury even with moderate hypoperfusion 2
• Age (50s-60s) further increases susceptibility to progression from pre-renal to intrinsic renal injury 2

Even if creatinine fully recovers, this AKI episode significantly increases long-term risks of recurrent AKI, progression to chronic kidney disease, and cardiovascular events 2. Mandatory follow-up with creatinine monitoring every 2-4 weeks for 6 months is recommended, with nephrology referral if creatinine fails to return to within 115% of baseline 2

The key to diagnosis is the response to volume resuscitation - rapid improvement confirms pre-renal azotemia, while persistent elevation despite adequate hydration suggests established ATN 1