In a patient with an estimated glomerular filtration rate (eGFR) ≥90 mL/min/1.73 m², blood urea nitrogen (BUN) 29 mg/dL, a BUN‑to‑creatinine ratio of about 30:1, and a urine albumin‑creatinine ratio (ACR) of 825 mg/g, does the normal eGFR indicate healthy kidneys and what management is recommended?

Normal eGFR Does NOT Indicate Healthy Kidneys in This Patient

This patient has established chronic kidney disease (CKD) Stage G1A3 despite the normal eGFR of ≥90 mL/min/1.73 m², because the severely elevated urinary albumin‑to‑creatinine ratio (UACR) of 825 mg/g confirms kidney damage. The elevated BUN‑to‑creatinine ratio of 30:1 suggests a prerenal component or early hyperfiltration, but does not negate the CKD diagnosis. 1

Why Normal eGFR Does Not Equal Healthy Kidneys

• CKD is diagnosed when either eGFR <60 mL/min/1.73 m² OR UACR ≥30 mg/g persists for at least 3 months, meaning albuminuria alone establishes the diagnosis regardless of filtration rate. 1, 2

• An eGFR ≥90 mL/min/1.73 m² represents only 90% or more of expected kidney function in a young adult, but this measurement provides no information about structural kidney damage, which is precisely what albuminuria reveals. 3

• Normal‑sized kidneys on imaging do not exclude CKD, particularly in diabetic kidney disease, minimal change disease, focal segmental glomerulosclerosis, and infiltrative disorders where kidney architecture remains preserved despite progressive damage. 2

• A UACR of 825 mg/g places this patient in the A3 category (severely increased albuminuria, ≥300 mg/g), which carries very high risk for CKD progression, cardiovascular events, and mortality even when eGFR remains normal. 1

Risk Stratification and Prognosis

• According to the KDIGO heat map, this patient falls into the highest risk category (dark red zone: G1A3), requiring treatment and immediate nephrology referral with monitoring 3–4 times per year. 1

• The presence of severely increased albuminuria increases 10‑year all‑cause mortality substantially, with cardiovascular disease being the leading cause of death rather than progression to kidney failure itself. 2

• Diabetes accounts for 40–50% of all cases requiring dialysis worldwide, and this patient's severely elevated albuminuria suggests diabetic kidney disease if diabetes is present, or another glomerular pathology requiring urgent evaluation. 2

Immediate Management Priorities

Blood Pressure Control

• Target blood pressure <130/80 mmHg is strongly recommended for all patients with UACR ≥300 mg/g, regardless of baseline blood pressure, to slow CKD progression and reduce cardiovascular risk. 1

• An ACE inhibitor or ARB is strongly recommended (Grade A evidence) for patients with UACR ≥300 mg/g and/or eGFR <60 mL/min/1.73 m², even in the absence of hypertension, to prevent kidney disease progression and reduce cardiovascular events. 1

• Do not discontinue renin‑angiotensin system blockade for mild to moderate increases in serum creatinine (≤30%) in the absence of volume depletion, as this is an expected hemodynamic effect that does not indicate harm. 1

• Monitor serum creatinine and potassium within 2–4 weeks after initiating ACE inhibitors or ARBs, then periodically thereafter to detect hyperkalemia or excessive creatinine elevation. 1

Glucose Management (If Diabetic)

• Optimize glucose control to reduce the risk or slow CKD progression (Grade A recommendation), with individualized hemoglobin A1c targets based on patient factors. 1

• For patients with type 2 diabetes and CKD, use of an SGLT2 inhibitor is strongly recommended (Grade A) to reduce CKD progression and cardiovascular events in individuals with eGFR ≥20 mL/min/1.73 m² and urinary albumin ≥200 mg/g. 1

Cardiovascular Risk Reduction

• Initiate statin therapy immediately for cardiovascular risk reduction, as CKD patients have 5–10 times higher cardiovascular mortality risk than risk of progression to end‑stage kidney disease. 2

Diagnostic Evaluation to Determine Underlying Cause

Confirm Chronicity

• Review historical eGFR and UACR measurements to verify that abnormalities have persisted for ≥3 months, which is required to distinguish CKD from acute kidney injury. 2

• If duration is unclear, repeat serum creatinine, eGFR, and UACR within 2–4 weeks to confirm persistence. 2

Identify the Etiology

• Obtain a detailed history focusing on diabetes duration (typically >10 years for type 1, may be present at diagnosis for type 2), hypertension history, family history of kidney disease, and systemic symptoms such as rash, arthritis, or hearing loss that suggest vasculitis or hereditary conditions. 2

• Screen for diabetes immediately if not already diagnosed, using hemoglobin A1c ≥6.5%, fasting plasma glucose ≥126 mg/dL, or 2‑hour oral glucose tolerance test ≥200 mg/dL, as diabetes accounts for 30–40% of CKD cases. 2

• Perform autoimmune work‑up including complement levels (C3, C4), antinuclear antibody, ANCA, and anti‑GBM antibodies to identify glomerulonephritis if clinical features suggest systemic disease. 2

• Obtain serum and urine protein electrophoresis with immunofixation and serum free‑light‑chain assays to exclude monoclonal gammopathies such as multiple myeloma or MGRS. 2

• Check hepatitis B and C serologies when an infectious etiology is considered. 2

Consider Kidney Biopsy

• Kidney biopsy is indicated when the underlying cause is uncertain or when results will influence management, particularly in this patient with severely elevated albuminuria and normal eGFR. 2

• Specific biopsy indications include diabetic individuals with atypical features (absence of diabetic retinopathy, short disease duration, rapid eGFR decline, active urinary sediment, or nephrotic‑range proteinuria without retinopathy), suspicion of primary glomerulonephritis, nephrotic syndrome (UACR >3000 mg/g with hypoalbuminemia and edema), or rapidly progressive loss of kidney function. 2

• Up to 30% of patients with presumed diabetic kidney disease have other causes of CKD on kidney biopsy, making biopsy particularly valuable when clinical features are atypical. 2

Monitoring Frequency

• Monitor eGFR and UACR 3–4 times per year (every 1–3 months) for patients in the G1A3 category, as this represents very high risk for progression and complications. 1

• Screen for CKD complications systematically, including serum electrolytes, hemoglobin, serum calcium and phosphate, intact PTH, and 25‑hydroxyvitamin D, though these are typically not abnormal until eGFR falls below 45–60 mL/min/1.73 m². 2

Nephrology Referral

• Immediate referral to nephrology is strongly recommended for this patient based on UACR ≥300 mg/g with ongoing increase in albuminuria despite optimal therapy, unclear etiology requiring potential kidney biopsy, and very high risk for progression. 1, 2

• **Additional referral indications include eGFR <30 mL/min/1.73 m²**, eGFR decline >5 mL/min/1.73 m² per year, difficulty managing CKD complications (anemia, mineral‑bone disorder, resistant hypertension, hyperkalemia), or consideration of kidney biopsy to clarify diagnosis. 1, 2

Common Pitfalls to Avoid

• Never assume normal eGFR means healthy kidneys—albuminuria is an independent marker of kidney damage and cardiovascular risk that requires aggressive treatment regardless of filtration rate. 1, 4

• Do not delay ACE inhibitor or ARB therapy while awaiting nephrology consultation in patients with UACR ≥300 mg/g, as early initiation is critical for slowing progression. 1

• Avoid combining ACE inhibitors with ARBs, as this increases adverse events without additional benefit. 2

• Do not discontinue renin‑angiotensin system blockade for creatinine increases ≤30% in the absence of volume depletion, as this represents expected hemodynamic effects. 1

• Never rely on serum creatinine or BUN alone—always calculate eGFR using validated equations (CKD‑EPI 2021) and measure UACR, as both provide independent prognostic information. 2