How should I interpret a normal complete blood count, low‑normal serum sodium, normal serum potassium, and impaired renal function (elevated serum creatinine) in an emergency department patient?

Laboratory Interpretation: Acute Kidney Injury in the Emergency Department

This patient has acute kidney injury (AKI) with a serum creatinine of 3 mg/dL, which represents significantly impaired renal function requiring immediate evaluation for the underlying cause and potential complications. 1

Key Laboratory Findings

Renal Function

• Creatinine 3 mg/dL is markedly elevated and indicates severe renal impairment, though the absolute value must be interpreted in context of the patient's baseline, age, sex, and muscle mass 2, 3, 4
• Serum creatinine alone underestimates the severity of renal dysfunction, particularly in elderly patients with reduced muscle mass who may have severe renal failure despite "normal-appearing" creatinine values 5
• The rate of creatinine rise matters: a rapid increase suggests acute tubular necrosis, pre-renal azotemia from volume depletion, or obstructive uropathy, while chronic elevation indicates underlying chronic kidney disease 1, 6

Electrolytes

• Sodium 136 mEq/L is low-normal and may indicate volume overload, SIADH, or diuretic use; in the context of AKI, this suggests possible volume depletion or heart failure 1, 7
• Potassium 4.5 mEq/L is reassuringly normal but requires close monitoring because hyperkalemia is a life-threatening complication of AKI that can develop rapidly 1

Complete Blood Count

• Normal CBC helps exclude several important diagnoses: no anemia rules out acute hemorrhage as a cause of pre-renal AKI; normal white count makes sepsis less likely; normal platelets exclude thrombotic microangiopathy 1

Immediate Clinical Actions Required

Determine AKI Etiology

• Assess volume status clinically: check for orthostatic hypotension, tachycardia, dry mucous membranes, flat jugular venous pressure, and skin turgor to identify pre-renal azotemia from volume depletion 6
• Obtain urine studies immediately: urinalysis with microscopy to look for muddy-brown granular casts (acute tubular necrosis), red cell casts (glomerulonephritis), or white cell casts (interstitial nephritis); fractional excretion of sodium <1% supports pre-renal etiology 1, 6
• Calculate BUN:creatinine ratio: a ratio >20:1 suggests pre-renal azotemia from volume depletion 6

Additional Laboratory Tests Needed

• Blood urea nitrogen (BUN) to calculate the BUN:creatinine ratio and assess for uremia 1, 6
• Serum bicarbonate and arterial blood gas to evaluate for metabolic acidosis, a common complication of AKI 1
• Serum chloride because hypochloremia can worsen diuretic resistance if heart failure is present 1, 6
• Liver enzymes and albumin to assess for hepatorenal syndrome if liver disease is suspected 1
• Lactate level to identify tissue hypoperfusion or bowel ischemia if abdominal pathology is suspected 1
• Urinalysis and urine culture to exclude urinary tract infection or obstruction 1

Medication Review

• Identify nephrotoxic medications: NSAIDs, ACE inhibitors, ARBs, aminoglycosides, contrast agents, and diuretics can all precipitate AKI 1, 7
• Check for recent diuretic use: aggressive diuresis can cause pre-renal azotemia through intravascular volume depletion, particularly in patients with heart failure or cirrhosis 1, 6
• Review ACE inhibitor/thiazide combinations: this combination substantially increases the risk of severe hyponatremia and hyperkalemia, especially in elderly diabetic patients 7

Monitoring Strategy

Frequency of Reassessment

• Measure serum creatinine every 48 hours during the acute phase to detect worsening AKI, defined as an increase ≥0.3 mg/dL within 48 hours 6
• Check electrolytes daily because potassium can rise rapidly in AKI and cause life-threatening arrhythmias 1
• Monitor urine output closely: oliguria (<400 mL/day) indicates severe AKI and may require renal replacement therapy 1

Imaging Considerations

• Renal ultrasound to exclude obstructive uropathy (hydronephrosis) and assess kidney size (small kidneys suggest chronic kidney disease) 1
• CT scan without contrast if obstruction, nephrolithiasis, or abdominal catastrophe is suspected; avoid IV contrast given the elevated creatinine 1

Common Pitfalls to Avoid

• Do not assume "normal" CBC rules out serious pathology: inflammatory bowel disease, bowel obstruction, and early sepsis can present with normal white counts 1
• Do not rely solely on serum creatinine to assess renal function: it is insensitive to mild-moderate GFR reductions and is affected by age, sex, muscle mass, and creatinine production rate 2, 3, 5
• Do not overlook the low-normal sodium: in combination with AKI, this may indicate heart failure with volume overload or SIADH requiring specific management 1, 7
• Do not delay imaging if clinical suspicion for obstruction or perforation exists: free air on plain radiographs or CT indicates perforation requiring emergency surgery 1