With a blood urea nitrogen of 13 mmol/L and a serum creatinine of 339 µmol/L, is this acute kidney injury or chronic kidney disease?

Distinguishing AKI from CKD with Urea 13 mmol/L and Creatinine 339 µmol/L

This presentation is most consistent with acute kidney injury (AKI) superimposed on possible chronic kidney disease (CKD), and you must immediately obtain prior creatinine values to confirm the diagnosis and determine AKI staging. 1, 2

Immediate Diagnostic Steps

The single most critical action is to retrieve all available prior creatinine measurements from the past 3–12 months to establish whether a baseline exists and to calculate the magnitude of acute change. 1, 2 Without a documented baseline, you cannot definitively distinguish pure AKI from acute-on-chronic kidney disease or stable CKD. 1

Apply KDIGO AKI Criteria

• AKI is diagnosed when any one of the following occurs:

  • Creatinine rise ≥26.5 µmol/L (≥0.3 mg/dL) within any 48-hour window, or
  • Creatinine increase to ≥1.5× baseline within 7 days, or
  • Urine output <0.5 mL/kg/h for ≥6 consecutive hours 1, 2

• If prior creatinine values show the current level of 339 µmol/L represents a ≥26.5 µmol/L rise within 48 hours or a ≥50% increase within 7 days, this confirms AKI. 1, 2

• If no prior values exist and you must back-calculate assuming normal baseline GFR (75 mL/min/1.73 m²), recognize this may overestimate AKI severity in populations with high CKD prevalence. 2

Staging the Kidney Injury

Once you confirm AKI by comparing to baseline:

• Stage 1: Creatinine 1.5–1.9× baseline or absolute rise ≥26.5 µmol/L 1, 3, 2
• Stage 2: Creatinine 2.0–2.9× baseline 1, 3, 2
• Stage 3: Creatinine ≥3.0× baseline or absolute creatinine ≥354 µmol/L (4.0 mg/dL) with acute rise ≥26.5 µmol/L, or initiation of dialysis 1, 3, 2

A creatinine of 339 µmol/L (3.8 mg/dL) approaches the Stage 3 threshold if there is documented acute rise; this carries approximately four-fold higher in-hospital mortality. 2, 4

Clinical Context Clues Favoring AKI

Look for these features that suggest acute rather than chronic injury:

• Recent nephrotoxic medication exposure (NSAIDs, ACE inhibitors, ARBs, diuretics, aminoglycosides, contrast agents) 1, 2
• Volume depletion (vomiting, diarrhea, poor oral intake, diuretic overuse) 1, 2
• Sepsis or infection (fever, hypotension, elevated white count) 2, 5
• Acute illness within the past 7 days (hospitalization, surgery, acute heart failure) 1, 2

Clinical Context Clues Favoring CKD

• Bilateral small kidneys on ultrasound (<9 cm in length) suggest chronicity 1
• Anemia and hyperphosphatemia out of proportion to the creatinine level indicate long-standing kidney disease 1
• Diabetic retinopathy in a patient with diabetes makes diabetic nephropathy (CKD) more likely, though its absence does not rule out diabetic kidney disease in type 2 diabetes 1
• Prior creatinine values consistently elevated for >3 months confirm CKD 1

Urea-to-Creatinine Ratio: Limited Utility

The blood urea nitrogen-to-creatinine ratio (BUN:Cr or urea:creatinine) is not reliable for distinguishing prerenal AKI from intrinsic AKI and should not guide your diagnosis. 6 A study of 1,103 ED patients with creatinine >133 µmol/L found no statistical difference in BUN:Cr between prerenal and intrinsic AKI groups (area under ROC curve = 0.5). 6

• Urea 13 mmol/L (BUN ~36 mg/dL) with creatinine 339 µmol/L (3.8 mg/dL) yields a ratio of approximately 9.5:1 (or ~38:3.8 in mg/dL units), which is nonspecific. 6
• Elevated urea disproportionate to creatinine may reflect dehydration, gastrointestinal bleeding, high protein intake, or catabolism—not necessarily prerenal physiology. 1, 6

Immediate Management Actions

While awaiting prior records:

• Discontinue all nephrotoxic medications immediately (NSAIDs, ACE-I/ARBs, diuretics). 1, 2
• Assess volume status clinically (orthostatic vitals, jugular venous pressure, mucous membranes, skin turgor) and initiate isotonic crystalloid resuscitation if hypovolemic. 2, 5
• Order urinalysis with microscopy to differentiate causes: muddy-brown casts suggest acute tubular necrosis, red-cell casts indicate glomerulonephritis, white-cell casts point to pyelonephritis or interstitial nephritis. 1, 2, 5
• Measure urine sodium and fractional excretion of sodium (FENa): FENa <1% suggests prerenal azotemia, FENa >2% supports intrinsic renal injury. 2
• Obtain renal ultrasound to rule out obstruction (postrenal AKI) and assess kidney size. 1

When to Consult Nephrology

• Obtain nephrology consultation promptly if:
  • AKI reaches Stage 2 or Stage 3 (creatinine ≥2× baseline) 3, 2
  • AKI persists >48 hours despite initial management 1, 2
  • Glomerulonephritis, vasculitis, or rapidly progressive AKI is suspected 2
  • The underlying cause cannot be identified 2

Follow-Up and Monitoring

• Repeat creatinine and electrolytes every 4–6 hours initially if Stage 2–3 AKI to track trajectory and detect complications. 2, 5
• Reassess kidney function at 3 months after the episode to determine if AKI has progressed to CKD or acute kidney disease (AKD). 2
• Patients with Stage 3 AKI require nephrology follow-up within 1–2 weeks due to high risk of CKD progression. 3, 2

Common Pitfalls to Avoid

• Do not assume CKD based on a single elevated creatinine without prior values or imaging evidence of chronicity. 1
• Do not dismiss a modest absolute creatinine rise as "insignificant" in patients with pre-existing CKD; the KDIGO absolute criterion (≥26.5 µmol/L) captures clinically relevant AKI across all baseline renal functions. 2, 4
• Do not rely on estimated GFR equations (MDRD, CKD-EPI) during acute changes in kidney function; they require steady-state creatinine and were validated only in stable CKD. 1, 2
• Do not use the BUN:Cr ratio to differentiate prerenal from intrinsic AKI; it lacks diagnostic accuracy. 6