What is the basic renal workup for an adult patient with Chronic Kidney Disease (CKD) stage 3 and rising creatinine levels?

Basic Renal Workup for Rising Creatinine in CKD Stage 3

The first critical step is to distinguish whether the rising creatinine represents acute kidney injury (AKI) superimposed on CKD versus progression of underlying CKD by comparing current creatinine to baseline values within the past 48 hours to 7 days. 1

Immediate Assessment to Rule Out AKI

• Compare current creatinine to baseline values to determine if AKI criteria are met: an increase ≥0.3 mg/dL within 48 hours or ≥50% increase from baseline within 7 days defines AKI. 1, 2
• Monitor urine output closely, as oliguria (<0.5 mL/kg/h for >6 hours) indicates Stage 1 AKI requiring immediate intervention. 1, 3
• Review medication list immediately for nephrotoxic agents including NSAIDs, aminoglycosides, vancomycin, and assess whether ACE inhibitors/ARBs should be temporarily held if volume depletion or acute hemodynamic instability is present. 1, 3

Core Laboratory Evaluation

Essential baseline tests include:

• Serum creatinine with eGFR calculation using the CKD-EPI equation rather than relying on creatinine alone, as creatinine underestimates CKD severity particularly in older adults. 4, 1
• Spot urine albumin-to-creatinine ratio (ACR) or protein-to-creatinine ratio, as albuminuria is the strongest predictor of CKD progression and guides treatment decisions. 4, 1
• Serum electrolytes including sodium, potassium, bicarbonate, and chloride to assess for metabolic acidosis and electrolyte abnormalities. 4
• Complete blood count to evaluate for anemia, which becomes prevalent when eGFR falls below 60 mL/min/1.73 m². 4
• Serum calcium, phosphate, and parathyroid hormone (PTH) to screen for metabolic bone disease. 4
• Vitamin 25(OH)D level as part of mineral metabolism assessment. 4

Urinalysis and Imaging

• Urinalysis with microscopy to detect urine sediment abnormalities, hematuria, pyuria, or casts that may indicate glomerular disease or acute tubular injury. 4
• Renal ultrasound to assess for structural abnormalities, hydronephrosis (post-renal obstruction), kidney size, and cortical thickness. 4

Determine Cause and Duration of CKD

• Review past creatinine measurements to determine if kidney disease duration exceeds 3 months, which confirms CKD diagnosis. 4
• Assess clinical context including personal and family history, diabetes status, hypertension control, social and environmental factors, and medication history to determine the underlying cause of CKD. 4
• Assign GFR category (G3a: 45-59 mL/min/1.73 m² or G3b: 30-44 mL/min/1.73 m²) and albuminuria category (A1: <30 mg/g, A2: 30-300 mg/g, A3: >300 mg/g) to stratify risk. 4

Monitoring Frequency for Stage 3 CKD

• Laboratory evaluations every 6-12 months for stage 3a CKD and every 3-5 months for stage 3b CKD, or more frequently if indicated by symptoms or therapy changes. 4
• Blood pressure and weight assessment at every clinical contact to evaluate for volume overload and hypertension. 4
• Serum potassium monitoring for patients on ACE inhibitors, ARBs, or diuretics due to risk of hyperkalemia or hypokalemia. 4

Critical Pitfall: Distinguishing Acceptable Creatinine Rise from True AKI

A creatinine increase up to 30% from baseline when initiating or intensifying ACE inhibitors/ARBs should not be confused with AKI and does not require discontinuation of these medications. 4, 5 This represents hemodynamic adjustment rather than kidney injury, and patients with such increases do not have increased mortality or progressive kidney disease. 4 However, increases beyond 30% in the context of aggressive RASI therapy may be tolerable if volume status is optimized and BP/proteinuria goals are achieved, though this requires close monitoring. 5

When to Suspect Superimposed Acute Process

• Rapid creatinine rise (≥0.3 mg/dL within 48 hours) suggests AKI rather than CKD progression. 1, 2
• New oliguria, volume overload, or electrolyte derangements indicate acute deterioration requiring immediate intervention. 1, 3
• Recent contrast exposure, new medications, or acute illness should raise suspicion for contrast-induced nephropathy, drug-induced AKI, or acute tubular necrosis. 1