How should I evaluate and manage an elevated BUN (blood urea nitrogen) in a 77‑year‑old woman with diabetes mellitus (A1C 6.6 %), eGFR (estimated glomerular filtration rate) 58 mL/min/1.73 m², and serum creatinine 1.0 mg/dL?

Evaluation and Management of Elevated BUN in a 77-Year-Old Woman with Diabetes

The elevated BUN in this patient most likely reflects prerenal azotemia from volume depletion or medication effects, and you should assess hydration status, review medications (especially diuretics, ACE inhibitors, or ARBs), ensure adequate fluid intake, and recheck BUN/creatinine after rehydration before attributing this to progressive kidney disease. 1, 2

Understanding the Laboratory Pattern

This patient presents with an elevated BUN-to-creatinine ratio (assuming BUN is elevated while creatinine remains at 1.0 mg/dL), which creates a disproportionate pattern:

• The BUN rises disproportionately to creatinine in dehydration because 40-50% of filtered urea is reabsorbed in the proximal tubule, paralleling sodium and water reabsorption, whereas creatinine is not significantly reabsorbed 1
• When volume depleted, urea reabsorption increases significantly, leading to elevated BUN levels while creatinine elevation remains mild 1
• A BUN-to-creatinine ratio >20:1 suggests prerenal azotemia rather than intrinsic kidney injury, particularly in the context of dehydration, heart failure, or excessive diuresis 1, 3

The eGFR of 58 mL/min/1.73 m² places this patient in CKD Stage 3a (eGFR 45-59), which requires monitoring but does not necessarily explain an acute BUN elevation 4

Immediate Clinical Assessment

Evaluate Hydration Status

• Assess clinical signs of volume depletion: skin turgor, mucous membrane moisture, orthostatic vital signs, and jugular venous pressure 1, 2
• Check for signs of heart failure: elevated jugular venous pressure, peripheral edema, pulmonary rales, or S3 gallop 4
• Review recent fluid intake and urine output to identify inadequate hydration or excessive diuresis 2

Medication Review

• Identify medications that may cause prerenal azotemia: ACE inhibitors, ARBs, diuretics, or NSAIDs 1, 2
• ACE inhibitors/ARBs combined with diuretics can cause prerenal azotemia with elevated BUN-to-creatinine ratio due to excessive diuresis combined with RAAS inhibition 1
• Do NOT discontinue ACE inhibitors or ARBs for modest BUN/creatinine elevations (up to 30% increase in creatinine is acceptable), as these medications improve outcomes in diabetes and should be continued unless creatinine rises >30% or hyperkalemia develops 2, 4

Additional Laboratory Assessment

• Obtain urinalysis looking for proteinuria (>30 mg/g albumin-to-creatinine ratio) and hematuria; their presence suggests intrinsic renal pathology rather than a purely prerenal process 1, 4
• Check serum electrolytes, particularly potassium and sodium, as they may be affected by renal dysfunction and medications 2
• Measure urine sodium and fractional excretion of sodium (FENa) if diagnosis remains unclear; FENa <1% supports prerenal azotemia, though this finding is present in only a minority of cases 3

Management Strategy

Rehydration and Monitoring

• Ensure adequate hydration with appropriate fluid intake (typically 1.5-2 L/day unless contraindicated) to improve prerenal azotemia 2
• Recheck BUN and creatinine after 3-7 days of adequate rehydration to confirm resolution; persistent elevation suggests underlying kidney disease requiring further investigation 1, 2
• Monitor urine output during rehydration as an indicator of improving renal perfusion 1

Dietary Modifications

• Restrict dietary sodium to ≤2 g/day if hypertension or fluid retention is present 2, 1
• Consider dietary protein intake of approximately 0.8 g/kg body weight per day for patients with mild kidney dysfunction; avoid excessive protein intake which can further elevate BUN 2
• Avoid high protein intake >100 g/day, which is associated with disproportionate BUN elevation, particularly in elderly patients 3

Medication Adjustments

• Review and potentially discontinue nephrotoxic drugs such as NSAIDs or COX-2 inhibitors 2
• If on diuretics, consider temporary dose reduction during rehydration, but do not discontinue entirely if needed for volume management 1
• Continue ACE inhibitors or ARBs unless creatinine increases >30% from baseline or hyperkalemia develops 2, 4

Ongoing Monitoring for CKD Stage 3a

Given the eGFR of 58 mL/min/1.73 m²:

• Monitor kidney function at least annually with UACR (preferably morning spot) and eGFR 4
• Increase monitoring frequency to twice yearly if UACR >300 mg/g or if eGFR declines to <45 mL/min/1.73 m² 4
• Repeat testing more frequently if there is a change in clinical status or when new medications are started (such as SGLT2 inhibitors) 4

Glycemic Control Considerations

• The A1C of 6.6% indicates good glycemic control and is appropriate for this patient 4
• Target A1C <7.0% for most patients, with individualization based on hypoglycemia risk and comorbidities 4
• Note that poor glycemic control can overestimate eGFR in diabetic patients, so the current eGFR of 58 may be more accurate given the well-controlled A1C 5

Blood Pressure Management

• Target blood pressure <130/80 mmHg for most patients with diabetes and CKD 4
• Consider ACE inhibitor or ARB as first-line therapy for hypertension, which helps preserve kidney function 2, 4

Common Pitfalls to Avoid

• Do not rely solely on serum creatinine to assess renal function, as it may be falsely reassuring in elderly females with decreased muscle mass 2
• Do not discontinue ACE inhibitors/ARBs for small increases in creatinine (<30% rise), as these medications improve long-term outcomes 1, 2
• Avoid excessive fluid restriction, which can worsen prerenal azotemia and further elevate BUN 2
• Do not attribute elevated BUN solely to CKD Stage 3a without first excluding prerenal causes, as the eGFR of 58 represents only mild-to-moderate reduction 1, 4

When to Refer to Nephrology

• Consider referral if eGFR continues to decline or falls below 45 mL/min/1.73 m² for coordinated care 4
• Refer if persistent proteinuria (UACR ≥300 mg/g) is present despite optimal management 4
• Refer if BUN remains elevated after adequate rehydration and medication adjustment, suggesting intrinsic kidney disease 1, 2

Special Considerations in Elderly Diabetic Patients

• Elderly patients are particularly susceptible to dehydration-induced elevations in BUN and creatinine 1, 3
• Lower muscle mass in elderly patients contributes to disproportionate BUN-to-creatinine ratios and may mask true degree of renal impairment 3, 2
• Mortality is higher when disproportionate BUN elevation is associated with severe illness, infection, or hypercatabolic states 3
• Elevated BUN (>25 mg/dL) is independently associated with increased mortality risk in patients with diabetes and cardiovascular disease, even with preserved eGFR 6, 7