In an adult patient with baseline serum creatinine 1.2 mg/dL who had lisinopril (angiotensin‑converting enzyme inhibitor) stopped, diuretics held, NSAIDs discontinued, and received intravenous isotonic fluids, the creatinine has now risen to approximately 1.5 mg/dL; what further management steps should be taken?

Further Management of Rising Creatinine Despite Initial Interventions

Continue holding the ACE inhibitor (lisinopril), diuretics, and NSAIDs while pursuing urgent diagnostic evaluation to differentiate between volume-responsive acute kidney injury, acute tubular necrosis, and intrinsic renal disease. 1

Immediate Diagnostic Workup

The creatinine rise from 1.2 to 1.5 mg/dL represents a 25% increase, which meets KDIGO criteria for Stage 1 AKI (≥0.3 mg/dL increase within 48 hours OR ≥1.5 times baseline within 7 days). 1 This progression despite appropriate initial management requires systematic evaluation:

Essential Laboratory Studies

• Urinalysis with microscopy: Look specifically for proteinuria (>500 mg/day suggests glomerular disease), hematuria (red cell casts indicate glomerulonephritis), and granular casts (suggest acute tubular necrosis). 1

• Urine sodium and fractional excretion of sodium (FENa): FENa <1% suggests prerenal azotemia that may still respond to volume expansion, while FENa >2% indicates intrinsic renal injury or acute tubular necrosis. 1

• Serum electrolytes with particular attention to potassium: Hyperkalemia (K+ ≥5.6 mmol/L) would necessitate immediate intervention and confirms that ACE inhibitor discontinuation was appropriate. 1, 2

• Urine output monitoring: Document whether output is <0.5 mL/kg/hour for >6 hours, which independently predicts worse outcomes. 1

Imaging and Structural Assessment

• Renal ultrasound: Mandatory to exclude obstructive uropathy (hydronephrosis), assess kidney size (small kidneys suggest chronic disease), and evaluate for structural abnormalities. 1

• Bladder scan post-void residual: Rule out bladder outlet obstruction, particularly in older male patients. 1

Volume Status Reassessment

Despite initial fluid administration, reassess volume status rigorously:

• Physical examination findings: Check for jugular venous distension (suggests volume overload), orthostatic vital signs (suggests ongoing volume depletion), peripheral edema, and pulmonary crackles. 1, 3

• If volume depleted: Administer additional isotonic crystalloid (normal saline or lactated Ringer's) with target mean arterial pressure >65 mmHg and urine output >0.5 mL/kg/hour. 1

• If euvolemic or volume overloaded: Avoid further fluid administration as this risks pulmonary edema without improving renal perfusion. 1

Critical Decision Point: ACE Inhibitor Management

The American Heart Association guidelines provide clear thresholds for ACE inhibitor discontinuation versus continuation: 1

• Discontinue permanently if: Creatinine rises >30% from baseline (your patient is at 25%, approaching this threshold), hyperkalemia develops (K+ ≥5.6 mmol/L), or progressive increase continues beyond 2 months. 1, 2

• Your patient's 25% rise is borderline: Given the rise occurred despite stopping lisinopril and other interventions, this suggests either the injury was already established before discontinuation OR there is an alternative cause beyond ACE inhibitor-mediated hemodynamic changes. 1, 2

• Do NOT restart lisinopril until creatinine stabilizes or decreases, and only if creatinine returns to within 30% of baseline. 1

Exclude Specific High-Risk Scenarios

Bilateral Renal Artery Stenosis or Solitary Kidney

• High suspicion if: Flash pulmonary edema history, refractory hypertension, abdominal bruit, or asymmetric kidney sizes on ultrasound. 1

• Diagnostic approach: Consider CT angiography or MR angiography if clinical suspicion is high, as ACE inhibitors cause acute renal failure in this setting. 1, 4

Hepatorenal Syndrome (if cirrhosis present)

• Diagnostic criteria: Cirrhosis with ascites, creatinine >1.5 mg/dL, no improvement after 2 days of diuretic withdrawal and volume expansion with albumin, absence of shock, no nephrotoxic drugs, and no parenchymal kidney disease (normal urinalysis). 1

• Management if HRS confirmed: Albumin 1 g/kg on day 1 followed by 40 g/day PLUS vasoconstrictor therapy (terlipressin 1 mg every 4-6 hours, increased to 2 mg every 4-6 hours if no response by day 3). 1

• Treatment goal: Reduce creatinine to <1.5 mg/dL, typically requiring 14 days of therapy. 1

Acute Tubular Necrosis

• Suspect if: Recent hypotensive episode, sepsis, contrast exposure, or nephrotoxic drug exposure (aminoglycosides, vancomycin). 1

• Urinalysis findings: Muddy brown granular casts, tubular epithelial cells, FENa >2%. 1

• Management: Supportive care, avoid further nephrotoxic insults, maintain euvolemia. 1

Monitoring Protocol

• Repeat creatinine and electrolytes: Every 24-48 hours until stabilization or downward trend established. 1

• Daily weights and strict intake/output: Essential for volume management decisions. 1

• Blood pressure monitoring: Maintain MAP >65 mmHg but avoid excessive hypertension that could worsen proteinuria if present. 1, 3

Indications for Nephrology Consultation

Urgent nephrology consultation is warranted if: 1

• Creatinine continues rising despite interventions
• Stage 2 AKI develops (creatinine ≥2.4 mg/dL or doubling from baseline)
• Oliguria persists (<0.5 mL/kg/hour for >12 hours)
• Hyperkalemia develops (K+ >5.5 mmol/L)
• Active urinary sediment suggests glomerulonephritis
• Consideration of renal replacement therapy needed

Renal Replacement Therapy Considerations

Initiate dialysis if: 1

• Severe hyperkalemia refractory to medical management (K+ >6.5 mmol/L with ECG changes)
• Severe metabolic acidosis (pH <7.1)
• Volume overload with pulmonary edema unresponsive to diuretics
• Uremic complications (pericarditis, encephalopathy, bleeding)
• Creatinine >4 mg/dL with oliguria in appropriate clinical context

Common Pitfalls to Avoid

• Do not restart ACE inhibitor prematurely: Wait until creatinine returns to within 30% of baseline and underlying cause is identified. 1

• Avoid NSAIDs completely: Even short courses dramatically increase AKI risk in this setting (3.3% incidence with triple therapy of NSAIDs + diuretics + RAAS inhibitors). 5

• Do not assume prerenal azotemia: The lack of response to initial fluid resuscitation suggests intrinsic renal injury or another process. 1

• Monitor for volume overload with albumin: If hepatorenal syndrome is being treated, albumin administration carries pulmonary edema risk and requires careful monitoring. 1

Prognosis and Long-Term Implications

Even if this AKI episode resolves, the patient faces increased risk of: 6, 3

• Progression to chronic kidney disease
• Recurrent AKI episodes
• Cardiovascular events

Therefore, establish long-term monitoring with creatinine, eGFR, and urine albumin-to-creatinine ratio at least every 3-6 months after resolution. 6, 3