Management of Impaired Renal Function with GFR 60 mL/min and Elevated Albumin-to-Creatinine Ratio
For a patient with GFR 60 mL/min (Stage G3a CKD) and elevated ACR, initiate an ACE inhibitor or ARB immediately as first-line therapy, target blood pressure <140/90 mmHg (or <130/80 mmHg if tolerated), monitor kidney function annually, and treat this patient actively rather than simply observe, as the combination of reduced GFR and albuminuria significantly increases risk for cardiovascular mortality, ESRD progression, and all-cause death. 1, 2
Risk Stratification and Classification
Classify this patient as Stage G3a CKD (GFR 45-59 mL/min/1.73 m²) combined with albuminuria category based on the specific ACR value: A1 if ACR <30 mg/g, A2 if ACR 30-299 mg/g, or A3 if ACR ≥300 mg/g. 1
The combination of Stage G3a with any degree of albuminuria (A2 or A3) places this patient in at least the "yellow" or "orange" risk category, requiring active treatment rather than observation alone, with measurements at least 1-2 times per year. 1
Both reduced eGFR and elevated albuminuria are independent, additive risk factors for ESRD, acute kidney injury, progressive CKD, cardiovascular disease, and mortality—they do not simply overlap but compound each other's risk synergistically. 3, 4
Confirm chronicity by documenting that abnormalities persist for >3 months with repeat testing before finalizing the CKD diagnosis, as transient elevations can occur. 1, 5
Primary Pharmacologic Intervention: RAAS Blockade
Start either an ACE inhibitor (such as lisinopril) or an ARB (such as losartan) immediately as first-line therapy, as both are equally effective for reducing albuminuria, slowing CKD progression, and reducing cardiovascular events in patients with Stage G3a CKD and albuminuria. 2, 6, 7
ACE inhibitors and ARBs are safe at GFR 60 mL/min and do not require dose adjustment until GFR falls below 30 mL/min/1.73 m². 7
Target a ≥30% reduction in urinary albumin within 3-6 months of initiating RAAS blockade, as this degree of albuminuria reduction predicts slower long-term CKD progression and improved outcomes. 2
Expect and tolerate serum creatinine increases up to 30% from baseline after starting ACE inhibitors or ARBs—this is not acute kidney injury but rather reflects hemodynamic changes from reduced intraglomerular pressure, and patients with these increases do not experience increased mortality or progressive kidney disease. 1
Never combine an ACE inhibitor with an ARB (dual RAAS blockade), as this increases risks of hyperkalemia, hypotension, and acute kidney injury without providing additional benefit, as demonstrated in the VA NEPHRON-D trial. 6
Blood Pressure Management
Target blood pressure <140/90 mmHg at minimum, with consideration of <130/80 mmHg in patients with albuminuria, to slow CKD progression and reduce cardiovascular risk. 2
If the ACE inhibitor or ARB alone does not achieve blood pressure goals, add a thiazide-like diuretic or dihydropyridine calcium channel blocker as second-line agents. 2
Avoid NSAIDs (including COX-2 inhibitors) in this population, as they can cause deterioration of renal function, including acute renal failure, and attenuate the antihypertensive effects of RAAS blockade, particularly in elderly or volume-depleted patients. 6
Glucose Management (If Diabetic)
Metformin is safe and appropriate at GFR 60 mL/min/1.73 m² and should be continued until eGFR falls below 30 mL/min/1.73 m². 2
Consider adding an SGLT2 inhibitor or GLP-1 receptor agonist if additional glucose control is needed beyond metformin, as these agents provide direct kidney protection independent of glucose lowering, reduce CKD progression, and lower cardiovascular risk. 2
Monitoring Schedule and Follow-Up
Measure eGFR and urine ACR at least annually (once per year for Stage G3a with A1 albuminuria, twice per year for A2, three times per year for A3), with confirmation of albuminuria using 2-3 specimens collected over 3-6 months before making major treatment decisions. 1, 2, 5
Increase monitoring frequency if eGFR declines >5 mL/min/1.73 m² per year, if albuminuria increases despite treatment, or if new medications are added that affect kidney function. 2, 5
Define rapid progression as ≥30% decrease in eGFR over 2 years or sustained decline ≥5 mL/min/1.73 m²/year, and a 25% reduction in eGFR plus change in GFR category confirms true progression rather than normal fluctuation. 5
Monitor serum potassium regularly after initiating RAAS blockade, as hyperkalemia risk increases, particularly when combined with other potassium-raising agents. 6
Evaluation for CKD Complications
Screen for complications of CKD including elevated blood pressure, volume overload, electrolyte abnormalities, metabolic acidosis, anemia, and metabolic bone disease by checking serum electrolytes, hemoglobin, calcium, and phosphorus. 1
Note that albuminuria itself is not independently associated with concurrent CKD complications (anemia, acidosis, hyperphosphatemia) after controlling for GFR—these complications are driven primarily by the level of GFR rather than albuminuria. 8
Nephrology Referral Criteria
Do not refer to nephrology at Stage G3a unless specific complications arise, such as eGFR falling below 30 mL/min/1.73 m² (Stage G4), rapid progression as defined above, difficult-to-control hypertension or hyperkalemia, or uncertainty about CKD etiology. 2
The KDIGO risk grid indicates "Treat" rather than "Refer" for Stage G3a with any degree of albuminuria, meaning primary care management is appropriate at this stage. 1
Key Clinical Pitfalls to Avoid
Do not discontinue ACE inhibitors or ARBs if creatinine rises up to 30% from baseline—this hemodynamic effect is expected, not harmful, and discontinuation removes the kidney-protective benefit. 1
Do not ignore albuminuria in patients with preserved or mildly reduced GFR—albuminuria independently predicts mortality and cardiovascular events even when GFR is normal or only mildly reduced. 3, 4, 9
Do not assume that elderly patients with "normal" creatinine have normal kidney function—age-related muscle mass loss can mask significant GFR reductions, and eGFR should always be calculated. 5
Do not use cystatin C routinely, but consider measuring it for confirmation in patients with eGFR 45-59 mL/min/1.73 m² (G3a) without albuminuria or other kidney damage markers, as this represents an area of controversy regarding disease labeling. 5