How should I manage an 80-year-old woman with chronic kidney disease stage 3 and a recent decline in estimated glomerular filtration rate to 46 mL/min/1.73 m2, normal electrolytes, mild metabolic acidosis, hyperglycemia, and lower-extremity edema currently on furosemide 20 mg daily?

Management of Progressive CKD Stage 3 with Edema in an 80-Year-Old Woman

Your current approach with furosemide 20 mg daily is appropriate for the lower extremity edema, but this patient requires urgent attention to several critical issues: worsening kidney function (eGFR decline from 58 to 46 mL/min/1.73 m²), uncontrolled hyperglycemia (glucose 171 mg/dL), and borderline metabolic acidosis (CO₂ 20 mmol/L). 1, 2

Immediate Priorities

1. Investigate the Cause of Declining Kidney Function

• The 12 mL/min/1.73 m² decline in eGFR over an unspecified timeframe warrants urgent evaluation. If this occurred over weeks to months, it represents rapid progression requiring nephrology referral. 1, 3

• Check for reversible causes immediately:

  • Obtain urinalysis with microscopy and urine albumin-to-creatinine ratio to assess for proteinuria and active sediment 1
  • Review all medications for nephrotoxins, particularly NSAIDs, which should be completely avoided in CKD stage 3 4, 3
  • Assess for volume depletion or overdiuresis from furosemide 2
  • Rule out urinary obstruction if clinically indicated 1

• Refer to nephrology promptly given eGFR <50 mL/min/1.73 m² with declining function, as recommended for patients at high risk of CKD progression. 1, 3

2. Address Uncontrolled Diabetes

• The fasting glucose of 171 mg/dL indicates inadequate glycemic control, which accelerates CKD progression. 1, 3

• Initiate or intensify diabetes management with CKD-appropriate agents:

  • Start an SGLT2 inhibitor (e.g., empagliflozin, dapagliflozin, or canagliflozin) immediately if not already prescribed, as these reduce CKD progression and cardiovascular events in patients with eGFR ≥20 mL/min/1.73 m² 1
  • Consider adding a GLP-1 receptor agonist for additional cardiovascular and renal protection 1
  • Avoid or adjust doses of oral hypoglycemics that accumulate in renal impairment 3

3. Manage Metabolic Acidosis

• The serum CO₂ of 20 mmol/L (lower limit of normal) represents early metabolic acidosis that accelerates CKD progression, causes muscle wasting, and bone demineralization. 5, 6, 7

• Initiate oral sodium bicarbonate 650 mg (approximately 8 mEq) twice daily to target serum bicarbonate 22-24 mmol/L, which has been shown to slow eGFR decline by approximately 4 mL/min/1.73 m² over 6-24 months. 6, 8

• Alternatively, increase dietary intake of fruits and vegetables while reducing animal protein intake, which provides base-producing foods and reduces dietary acid load. 6, 8

• Recheck serum bicarbonate, electrolytes, and creatinine in 2-4 weeks after initiating alkali therapy. 5, 7

Furosemide Management

Current Dosing Assessment

• Furosemide 20 mg daily is an appropriate starting dose for edema in CKD stage 3b per FDA labeling. 2

• The stable eGFR of 46 mL/min/1.73 m² does not require dose reduction unless acute kidney injury develops (creatinine rise >30% within 4 weeks) or symptomatic hypotension occurs. 9

• Monitor for signs of overdiuresis: orthostatic hypotension, worsening creatinine, hypokalemia, or metabolic alkalosis. 2

Monitoring Requirements

• Recheck serum electrolytes (especially potassium), CO₂, creatinine, and BUN within 2-4 weeks of initiating or adjusting furosemide, then every 3-6 months if stable. 9, 2

• Watch for hypokalemia (current potassium 4.5 mmol/L is acceptable), which can develop with loop diuretics, especially with inadequate oral intake or concurrent RAAS blockade. 2

• If edema persists on furosemide 20 mg daily, increase to 40 mg daily rather than adding a second dose, as once-daily dosing improves adherence. 2

Blood Pressure and RAAS Blockade

• Ensure the patient is on an ACE inhibitor or ARB (not specified in your labs) for renal protection, particularly if albuminuria is present. 1

• If starting or intensifying RAAS blockade, accept a creatinine increase up to 30% as this represents hemodynamic effect rather than harm, similar to SGLT2 inhibitor initiation. 1, 10

• Avoid the "triple whammy" combination of NSAID + ACE inhibitor/ARB + diuretic, which dramatically increases acute kidney injury risk. 4

Pain Management Considerations

• If this patient requires analgesia, use acetaminophen up to 3 grams daily as the first-line agent, avoiding all NSAIDs which are contraindicated in CKD stage 3. 4, 3

• For severe pain, consider low-dose opioids (fentanyl or buprenorphine preferred in renal impairment) or topical agents rather than NSAIDs. 4

Critical Pitfalls to Avoid

• Never use NSAIDs in this patient given CKD stage 3b, diabetes, and diuretic use—this combination creates unacceptable risk for acute kidney injury and cardiovascular events. 4, 3

• Do not attribute declining eGFR to "normal aging" without investigation, as decreased GFR is an independent predictor of mortality and cardiovascular disease even in the elderly. 1

• Do not delay nephrology referral for eGFR <50 mL/min/1.73 m² with declining function, as early specialist involvement improves outcomes. 1, 3

• Monitor for hyperglycemia worsening with furosemide, as loop diuretics can impair glucose tolerance. 2

Summary Algorithm

1. Obtain urinalysis with albumin-to-creatinine ratio and review medications for nephrotoxins 1, 3
2. Refer to nephrology for declining eGFR <50 mL/min/1.73 m² 1, 3
3. Start SGLT2 inhibitor for diabetes and renal protection 1
4. Initiate sodium bicarbonate 650 mg twice daily for metabolic acidosis 6, 8
5. Continue furosemide 20 mg daily, titrate to 40 mg if edema persists 2
6. Recheck labs (electrolytes, CO₂, creatinine, glucose) in 2-4 weeks 9, 2
7. Ensure ACE inhibitor or ARB is prescribed if not already on therapy 1
8. Avoid all NSAIDs permanently 4, 3