Management of Abnormal Microalbumin-to-Creatinine Ratio in Diabetes
For diabetic patients with an elevated urine albumin-to-creatinine ratio (UACR ≥30 mg/g), initiate an ACE inhibitor or ARB regardless of blood pressure status, optimize glycemic control to HbA1c <7%, and target blood pressure <130/80 mmHg. 1
Defining Abnormal UACR
- Normal UACR is <30 mg/g creatinine 1, 2
- Moderately elevated albuminuria (formerly "microalbuminuria") is defined as UACR 30-299 mg/g 1, 2
- Severely elevated albuminuria (formerly "macroalbuminuria") is UACR ≥300 mg/g 1, 2
- Albuminuria occurs on a continuum, and these categories represent increasing cardiovascular and renal risk 1
Initial Assessment and Confirmation
- Confirm abnormal UACR with 2-3 measurements over 3-6 months before initiating treatment, as up to 40% of patients with type 1 diabetes show spontaneous remission 1
- Measure serum creatinine and calculate eGFR using the CKD-EPI equation to stage chronic kidney disease 1
- Screen for complications when eGFR <60 mL/min/1.73 m² 1
- Use first morning void samples to minimize orthostatic proteinuria effects 2
Pharmacologic Management Algorithm
For UACR 30-299 mg/g (Moderately Elevated):
- Start either an ACE inhibitor or ARB even if blood pressure is normal 1, 2
- This recommendation carries a Grade C evidence level, meaning it's suggested but not as strongly supported as higher albuminuria levels 1
For UACR ≥300 mg/g (Severely Elevated):
- ACE inhibitor or ARB therapy is strongly recommended (Grade A evidence) 1
- These agents provide renoprotection beyond blood pressure lowering alone 1, 2
Important Caveat:
- Do NOT use ACE inhibitors or ARBs for primary prevention in diabetic patients with normal blood pressure and normal UACR (<30 mg/g) 1
Glycemic Optimization
- Target HbA1c <7% to reduce risk and slow progression of diabetic kidney disease 2, 3
- Optimize glucose control carries Grade A evidence for reducing diabetic kidney disease progression 1
Blood Pressure Management
- Target blood pressure <130/80 mmHg in all patients with diabetes and kidney disease 2, 3
- Blood pressure optimization carries Grade A evidence for slowing diabetic kidney disease progression 1
- When using ACE inhibitors, ARBs, or diuretics, monitor serum creatinine and potassium levels for hyperkalemia or acute kidney injury 1
Monitoring Strategy
- Continue annual UACR and eGFR monitoring to assess disease progression and treatment response 1, 2
- Some experts recommend monitoring every 6 months during the first year of treatment 3
- Patients with increasing albumin levels, declining GFR, worsening hypertension, or retinopathy are at higher risk for progression 1
Dietary Modifications
- Maintain protein intake at 0.8 g/kg/day based on ideal body weight 1
- Reducing protein below this level does not alter glycemic measures, cardiovascular risk, or GFR decline (Grade A evidence) 1
- Institute a low-salt, moderate-potassium diet 3
Nephrology Referral Triggers
Consider nephrology referral when: 1
- Uncertainty about etiology exists (heavy proteinuria, active urine sediment, absence of retinopathy, rapid GFR decline)
- eGFR reaches stage 4 CKD (eGFR 15-29 mL/min/1.73 m²)
- Difficult management issues arise (anemia, secondary hyperparathyroidism, resistant hypertension, electrolyte disturbances)
- Advanced kidney disease develops
Common Pitfalls to Avoid
- Do not rely solely on serum creatinine as it underestimates renal dysfunction until significant kidney damage has occurred 1, 4
- Do not assume all albuminuria in diabetes is diabetic nephropathy, especially with short diabetes duration, absence of retinopathy, or active urine sediment 1
- Do not combine ACE inhibitors with ARBs, as dual therapy increases adverse events without additional benefit 1
- Remember that 20-30% of patients with type 2 diabetes develop decreased GFR without increased albumin excretion 1