Elevated BUN with Normal Creatinine and eGFR: Pre-Renal Azotemia
Your laboratory pattern—BUN 34 mg/dL with normal creatinine (1.20 mg/dL), normal eGFR (69 mL/min/1.73m²), and elevated BUN/creatinine ratio (28)—indicates pre-renal azotemia rather than intrinsic kidney disease, most commonly caused by dehydration, decreased renal perfusion from heart failure, or increased protein catabolism. 1
Understanding Your Laboratory Pattern
The disproportionately elevated BUN/creatinine ratio (>20:1) strongly suggests pre-renal causes rather than intrinsic kidney damage, where BUN and creatinine typically rise together 1, 2
Your eGFR of 69 mL/min/1.73m² confirms adequate glomerular filtration, ruling out significant chronic kidney disease 1
Unlike intrinsic renal disease, this pattern indicates factors affecting BUN independently of kidney filtration capacity 1
Most Likely Causes in Your Case
Dehydration/Volume Depletion:
- Inadequate fluid intake is the most common reversible cause in patients with this laboratory pattern 1
- Clinical signs to assess include orthostatic vital signs, dry mucous membranes, and decreased skin turgor 3
Cardiovascular Factors:
- Heart failure with reduced cardiac output causes elevated BUN through decreased renal perfusion and neurohormonal activation 1, 4
- BUN >19.6 mg/dL serves as a recognized marker of heart failure severity 1
- Check for signs of heart failure: peripheral edema, jugular venous distension, dyspnea on exertion 1
Increased Protein Catabolism:
- High protein intake (>100 g/day) can elevate BUN disproportionately 2
- Hypercatabolic states from infection, steroids, or tissue breakdown contribute 2
Immediate Actions Required
Assess Hydration Status:
- Check orthostatic vital signs (blood pressure and pulse lying and standing) 3
- Review fluid intake over the past 24-72 hours 3
- Examine for clinical dehydration signs 1
Evaluate Cardiovascular Function:
- Assess for heart failure symptoms: shortness of breath, leg swelling, exercise intolerance 1
- Check blood pressure for hypotension or orthostatic changes 1
Review Medications:
- Stop all NSAIDs immediately if you are taking them—they cause diuretic resistance and worsen renal perfusion 3
- If taking ACE inhibitors or ARBs with diuretics, consider temporarily reducing diuretic dose if dehydration is present 3
- Avoid nephrotoxic medications 1
Management Strategy
If Dehydration is Present:
- Increase oral fluid intake to 2-3 liters daily unless contraindicated by heart failure 1
- If severe, intravenous fluid repletion may be necessary 3
If Heart Failure is Suspected:
- Continue diuretics but monitor closely if fluid overload is present 3
- Reduce diuretic dosage only if hypovolemia/dehydration is confirmed 3
- BUN serves as a better predictor of outcomes than creatinine or eGFR in heart failure patients 1, 5
Dietary Modifications:
- If protein intake exceeds 100 g/day, consider moderate reduction 3
- Ensure adequate hydration with meals 3
Monitoring Plan
Follow-up Laboratory Testing:
- Recheck BUN, creatinine, and BUN/creatinine ratio in 3-7 days after addressing reversible causes 1
- Monitor serum electrolytes, particularly potassium 6
- If BUN normalizes with hydration, this confirms pre-renal etiology 1
Surveillance Schedule:
- At your eGFR of 69 mL/min/1.73m² (CKD stage 2), annual monitoring of kidney function is recommended 6
- More frequent testing (every 3-6 months) is warranted if BUN remains elevated or other risk factors develop 6
When to Seek Nephrology Referral
Refer if:
- Elevated BUN persists despite addressing dehydration and other reversible causes 1
- Creatinine subsequently rises or eGFR decreases to <45 mL/min/1.73m² 6
- Development of proteinuria or hematuria 1
- eGFR drops below 30 mL/min/1.73m² 6
- Rapid progression of kidney dysfunction or uncertainty about etiology 6
Critical Pitfalls to Avoid
Do not assume normal kidney function based solely on normal creatinine—BUN elevation warrants investigation even with preserved eGFR 1, 7
Do not discontinue ACE inhibitors or ARBs for isolated BUN elevation unless accompanied by significant creatinine rise (>30% from baseline) or volume depletion 6, 3
Do not ignore cardiovascular assessment—elevated BUN independently predicts cardiovascular mortality even with normal eGFR 7, 4
In elderly patients (you are 60), age-related muscle mass loss can cause inappropriately low creatinine that masks renal dysfunction, making BUN a more sensitive marker 3
Prognostic Significance
Higher BUN levels are independently associated with adverse outcomes including cardiovascular mortality, even when eGFR is preserved 8, 7
BUN reflects not only kidney function but also acute hemodynamic alterations and neurohumoral activation 7, 4
The BUN/creatinine ratio provides independent prognostic information beyond eGFR alone across the spectrum of cardiovascular disease 4