In a patient with chronic kidney disease stage 3 whose serum creatinine increased from 1.1 mg/dL to 1.8 mg/dL, what is the appropriate evaluation and management?

Acute Kidney Injury Evaluation and Management in CKD Stage 3

This patient meets KDIGO criteria for Stage 1 Acute Kidney Injury (AKI) superimposed on CKD and requires immediate evaluation to identify and reverse the underlying cause. 1

Diagnostic Classification

The creatinine rise from 1.1 to 1.8 mg/dL represents a 64% increase, which exceeds the 50% threshold required for Stage 1 AKI when occurring within 7 days. 1 This qualifies as acute-on-chronic kidney disease (ACKD), where an acute insult has occurred in a patient with pre-existing CKD Stage 3. 1

Importantly, this magnitude of creatinine rise (≥0.3 mg/dL and ≥50% from baseline) is independently associated with approximately fourfold increased hospital mortality, indicating that patients die "from AKI" not just "with AKI." 1

Immediate Evaluation Steps

Core Laboratory Assessment

• Order a complete metabolic panel (electrolytes, BUN, glucose, calcium, phosphate) and complete blood count immediately. 2
• Perform urinalysis with microscopy to identify proteinuria (>500 mg/day), hematuria (>50 RBCs per high-power field), or casts that differentiate prerenal from intrinsic renal causes. 1, 3
• Measure urine albumin-to-creatinine ratio on a first-morning void. 2
• Calculate fractional excretion of sodium; values <1% suggest prerenal azotemia. 3

Volume Status Assessment

Examine for clinical signs of prerenal azotemia: 3

• Orthostatic hypotension and tachycardia
• Dry mucous membranes
• Low jugular venous pressure
• BUN-to-creatinine ratio >20:1 supports volume depletion 3

Medication Review—Critical Priority

Immediately discontinue the following nephrotoxic agents: 1, 3

• NSAIDs (can independently cause AKI and potentiate injury when combined with ACE inhibitors) 3, 4
• ACE inhibitors or ARBs if the patient has started these within the past month or if baseline creatinine was >2.0 mg/dL 3, 4
• Diuretics temporarily if volume depletion is suspected 1, 3

Structural Evaluation

• Obtain renal ultrasound to exclude urinary obstruction. 1, 5

Management Algorithm

If Prerenal Azotemia Is Suspected:

1. Temporarily reduce or pause diuretic therapy 3
2. Administer cautious isotonic saline bolus of 250–500 mL 3
3. Reassess renal function within 48 hours 3

If Patient Has Cirrhosis with Ascites:

Consider hepatorenal syndrome-AKI (HRS-AKI) if: 1

• No response to diuretic withdrawal and 2-day volume challenge with albumin 20–25% at 1 g/kg/day 1
• Absence of shock 1
• No recent nephrotoxic drug exposure 1
• Normal renal ultrasound 1

Management for HRS-AKI: 1, 5

• Discontinue diuretics immediately 1
• Administer intravenous albumin 1 g/kg/day (maximum 100 g) for two consecutive days 1, 3
• Rule out spontaneous bacterial peritonitis before labeling as HRS-AKI 3
• Monitor fluid status closely due to risk of pulmonary edema 1

Special Consideration for ACE Inhibitor/ARB Therapy:

If the patient recently started an ACE inhibitor or ARB and baseline creatinine was <2.0 mg/dL, a 30% rise may represent acceptable hemodynamic adjustment rather than true kidney injury. 4 However, **this patient's 64% rise exceeds the 30% threshold and mandates temporary discontinuation.** 4 Research shows that in aggressive dual-RASI therapy, rises >30% can be tolerated long-term with favorable outcomes, but this applies to goal-directed therapy after initial stabilization, not acute evaluation. 6

Monitoring Strategy

• Repeat serum creatinine within 48 hours to determine if the rise is progressive or stabilizing. 3
• Monitor urine output daily during the acute phase. 3
• Do not use eGFR when creatinine is rapidly changing, as it substantially underestimates true kidney dysfunction in non-steady-state conditions. 3
• Consider measuring serum cystatin C if precise GFR estimation is needed to distinguish true AKI from pseudo-AKI. 2, 3

Prognostic Implications

Stage 1 AKI with serum creatinine ≥1.5 mg/dL (as in this patient at 1.8 mg/dL) carries a markedly worse prognosis than Stage 1 AKI at lower absolute values. 3 Even transient AKI increases the risk of progression to chronic kidney disease. 5, 3

Follow-Up Requirements

• Re-evaluate serum creatinine 3 months after the AKI episode to determine whether kidney function has returned to baseline or progressed to more advanced CKD. 3
• If eGFR remains <30 mL/min/1.73 m² and is expected to persist for at least 12 months, refer urgently to nephrology. 2

Common Pitfalls to Avoid

• Do not dismiss this as "normal variation"—the 0.7 mg/dL rise far exceeds the 14–17% biological variability of creatinine measurements. 5
• Do not continue ACE inhibitors/ARBs without reassessment when creatinine rises >30% from baseline. 4
• Do not rely on serum creatinine alone in elderly or malnourished patients; creatinine may underestimate kidney dysfunction due to reduced muscle mass. 2, 7
• In cirrhotic patients, hyperbilirubinemia causes inaccurate creatinine measurement by colorimetric methods. 1