Management of Mildly Reduced eGFR (77 mL/min/1.73 m²)
Your patient has Stage 2 chronic kidney disease (CKD) with mildly reduced kidney function (eGFR 77 mL/min/1.73 m²), which requires annual monitoring, blood pressure optimization, and evaluation for proteinuria—but does NOT require immunosuppressive therapy or nephrology referral at this stage. 1
Initial Assessment and Risk Stratification
Your first priority is determining whether this represents true kidney disease or a measurement artifact:
- Rule out exogenous creatinine elevation from creatine supplements, which can falsely elevate serum creatinine and reduce calculated eGFR without actual kidney dysfunction 2, 3
- Verify the eGFR calculation is appropriate for the patient's muscle mass, as both extremes (very high or very low muscle mass) can affect creatinine-based estimates 3
- Obtain baseline urinalysis with quantitative albumin measurement to assess for proteinuria, as this is essential for risk stratification and determines management intensity 1
Monitoring Strategy
For eGFR >60 mL/min/1.73 m² without significant proteinuria, annual monitoring is sufficient:
- Measure eGFR and quantitative urine albumin excretion annually 1
- Monitor serum potassium if using ACE inhibitors, ARBs, or diuretics 1
- Assess blood pressure at every clinical encounter 1
Blood Pressure Management
Target systolic blood pressure <120 mmHg using standardized office measurement 1:
- Use ACE inhibitor or ARB as first-line therapy if proteinuria is present (≥30 mg/24h), titrating to maximally tolerated dose 1
- Do not discontinue ACE inhibitor/ARB for serum creatinine increases up to 30% from baseline, as this represents appropriate hemodynamic changes rather than kidney injury 1
- Avoid ACE inhibitors/ARBs in patients without proteinuria and normal blood pressure, as they provide no benefit for primary prevention 1
Proteinuria-Based Treatment Algorithm
If proteinuria <30 mg/24h (normal):
- Conservative management with blood pressure control and cardiovascular risk reduction 1
- No specific kidney-protective medications indicated 1
If proteinuria 30-299 mg/24h:
- Initiate ACE inhibitor or ARB (but not both) titrated to maximum approved dose 1
- Target proteinuria reduction to <1 g/day 1
- Monitor serum creatinine and potassium 1-2 weeks after initiation or dose changes 1
If proteinuria ≥300 mg/24h:
- Requires further evaluation for underlying glomerular disease 1
- Consider nephrology referral for potential kidney biopsy 1
Cardiovascular Risk Management
At this level of kidney function, cardiovascular disease prevention is paramount:
- Initiate statin therapy for lipid management regardless of baseline cholesterol levels 4
- Consider SGLT2 inhibitor if diabetes is present, as these reduce cardiovascular and kidney disease progression risk 1, 4
- Optimize glycemic control if diabetic, targeting HbA1c individualized to patient factors 1
When NOT to Intervene Aggressively
Do not use immunosuppressive therapy at this level of kidney function unless there is biopsy-proven glomerulonephritis with active inflammation 1
Do not refer to nephrology unless: 1
- Proteinuria ≥300 mg/24h persists despite ACE inhibitor/ARB therapy
- eGFR declines by >30% within 6-12 months
- Unexplained hematuria accompanies the reduced eGFR
- Uncertainty exists about the etiology of kidney disease
Critical Monitoring Parameters
Accept modest creatinine increases (up to 30%) when initiating RAS blockade, as this reflects appropriate reduction in intraglomerular pressure rather than acute kidney injury 1
Stop ACE inhibitor/ARB only if: 1
- Serum creatinine continues to rise beyond 30%
- Refractory hyperkalemia develops (typically >5.5 mEq/L despite management)
- Acute kidney injury from another cause is suspected
Dietary and Lifestyle Modifications
- Restrict dietary sodium to <2 g/day (<90 mmol/day) to maximize blood pressure control and reduce proteinuria 1, 5
- Do not restrict dietary protein below usual intake, as this does not alter kidney disease progression at this stage 1
- Avoid nephrotoxins including NSAIDs and iodinated contrast when possible 1
Common Pitfalls to Avoid
- Do not assume elevated creatinine always means kidney disease—verify with repeat testing and consider non-renal causes like creatine supplementation 2, 3
- Do not combine ACE inhibitors with ARBs, as this increases adverse events without additional benefit 1
- Do not stop RAS blockade for modest creatinine increases unless other concerning features develop 1
- Do not delay cardiovascular risk reduction while focusing solely on kidney parameters, as cardiovascular disease is the leading cause of death in early CKD 4