What is the appropriate workup for a patient with acute kidney injury?

Acute Kidney Injury Workup

Diagnostic Criteria and Staging

Diagnose AKI when any one of the following KDIGO criteria is met: serum creatinine rise ≥0.3 mg/dL within 48 hours, creatinine increase to ≥1.5× baseline within 7 days, or urine output <0.5 mL/kg/h for ≥6 consecutive hours. 1, 2, 3

• Stage 1: Creatinine 1.5–1.9× baseline OR ≥0.3 mg/dL increase OR urine output <0.5 mL/kg/h for 6–12 hours 1, 4
• Stage 2: Creatinine 2.0–2.9× baseline OR urine output <0.5 mL/kg/h for ≥12 hours 1, 4
• Stage 3: Creatinine ≥3.0× baseline OR ≥4.0 mg/dL OR initiation of dialysis OR urine output <0.3 mL/kg/h for ≥24 hours 1, 4

Initial Laboratory Evaluation

Order a comprehensive metabolic panel immediately to measure serum creatinine, BUN, sodium, potassium, calcium, magnesium, chloride, and bicarbonate to identify life-threatening metabolic derangements. 1, 2

• Obtain complete blood count to screen for anemia and thrombocytopenia 1
• Measure serum creatinine every 4–6 hours initially in Stage 2–3 AKI to track progression 1
• Review all prior creatinine values to establish true baseline and confirm chronicity (>3 months indicates pre-existing CKD) 1

Urinalysis and Urine Studies

Perform urinalysis with microscopy to differentiate AKI etiology: muddy-brown casts suggest acute tubular necrosis, red-cell casts indicate glomerulonephritis, and white-cell casts point to interstitial nephritis. 1, 2

• Calculate fractional excretion of sodium (FENa): <1% suggests prerenal azotemia; >2% supports intrinsic renal injury such as ATN 1, 2
• Measure urine sodium: <20 mEq/L favors prerenal causes; >40 mEq/L supports intrinsic kidney injury 1
• Obtain urine albumin-to-creatinine ratio (UACR) on early-morning specimen; UACR ≥30 mg/g warrants confirmation 1

Medication History and Nephrotoxin Assessment

Conduct a thorough medication review to identify exposure to NSAIDs, ACE inhibitors, ARBs, diuretics, aminoglycosides, vancomycin, contrast media, and chemotherapeutic agents—these are common precipitants of AKI. 5, 1, 6, 2

• Discontinue all identified nephrotoxic medications immediately upon AKI diagnosis 5, 1, 6
• Assess for the "triple whammy" combination of NSAIDs + diuretics + ACE inhibitor/ARB, which more than doubles AKI risk 5, 6
• Adjust doses of all renally eliminated medications based on current kidney function, not baseline 1, 6

Volume Status Assessment

Assess intravascular volume through jugular venous pressure examination, lung auscultation for crackles, presence of orthopnea, and evaluation of peripheral edema to distinguish prerenal from intrinsic or postrenal causes. 7, 2

• For hypovolemic patients, provide fluid repletion with isotonic crystalloids (lactated Ringer's or normal saline) rather than colloids 1, 6
• Avoid aggressive fluid administration in euvolemic or hypervolemic patients with edema 7
• In cirrhotic patients with AKI and creatinine doubling, administer albumin 1 g/kg/day (maximum 100 g) for two consecutive days 5, 1, 7

Imaging Studies

Obtain renal ultrasonography in most patients, particularly older men, to rule out urinary tract obstruction as a postrenal cause of AKI. 6, 2, 8

• Perform ultrasound after correcting hypovolemia if present 6
• Imaging is especially important when risk factors for obstruction exist (prostatic hypertrophy, pelvic malignancy, nephrolithiasis history) 2, 8

Infection Evaluation

In all AKI patients, especially when infection is suspected, obtain blood cultures, urine cultures, and chest radiograph; for cirrhotic patients, perform diagnostic paracentesis to rule out spontaneous bacterial peritonitis. 1

• Initiate empiric broad-spectrum antibiotics promptly when infection is strongly suspected, without awaiting culture results 1
• Recognize that failure to promptly treat underlying infection markedly increases risk of AKI progression 1

Etiologic Classification

Classify AKI as prerenal (volume depletion, decreased cardiac output, medications altering glomerular hemodynamics), intrinsic renal (acute tubular necrosis, glomerulonephritis, acute interstitial nephritis, atheroembolic disease), or postrenal (urinary tract obstruction). 5, 1, 2, 8

• Prerenal causes account for most community-acquired AKI and typically reverse within 48 hours with appropriate fluid resuscitation 1
• Intrinsic renal causes include ATN (most common in hospitalized patients), glomerulonephritis, and interstitial nephritis 1, 2
• Postrenal obstruction must be excluded early, particularly in older men with prostatic disease 2, 8

Indications for Nephrology Consultation

Consult nephrology immediately for Stage 2–3 AKI (creatinine ≥2.0× baseline), AKI without clear cause after initial evaluation, AKI persisting >48 hours despite appropriate management, or pre-existing CKD Stage 4 or higher. 1, 7, 8

• Obtain nephrology input when glomerulonephritis, vasculitis, or rapidly progressive AKI is suspected 1
• Refer patients with severe metabolic acidosis (pH <7.2 or bicarbonate <12 mEq/L) 1, 7
• Consult for consideration of renal replacement therapy when indicated 1, 8

Monitoring Electrolytes and Complications

Monitor serum potassium, bicarbonate, calcium, magnesium, and phosphate levels to detect and treat hyperkalemia, metabolic acidosis, and other electrolyte disturbances that may require urgent intervention. 1, 2, 8

• Administer intravenous sodium bicarbonate for severe metabolic acidosis; consider dialysis when acidosis is refractory 1
• Treat hyperkalemia urgently with calcium gluconate, insulin/dextrose, and sodium polystyrene sulfonate or dialysis if refractory 1

Common Pitfalls to Avoid

• Do not apply eGFR equations (MDRD or CKD-EPI) during acute changes in kidney function because they require steady-state creatinine and were validated only in stable CKD patients. 1
• Do not dismiss a modest absolute creatinine rise (≥0.3 mg/dL) in CKD patients as "insignificant" merely because the percentage change is small; this absolute criterion captures clinically relevant AKI across all baseline renal functions and is associated with four-fold higher mortality. 1, 4
• Avoid assuming chronic kidney disease based on a single abnormal creatinine; chronicity requires repeat measurements beyond 3 months or corroborating imaging/pathology evidence. 1
• Do not delay nephrology consultation when clear indications exist (Stage 2–3 AKI, unclear etiology, persistent AKI >48 hours), as delayed specialist input worsens outcomes. 1, 8

Nuances in Clinical Application

The KDOQI commentary emphasizes that while KDIGO staging provides an important epidemiologic tool, management should be based on overall clinical status—including specific AKI cause, trends in kidney function over time, comorbid conditions, volume status, and electrolyte disturbances—rather than stage alone. 5 The stage-based management approach proposed in KDIGO guidelines lacks adequate evidence validation for clinical decision-making, and the extreme heterogeneity of AKI makes rigid protocolization clinically unhelpful. 5 However, the KDIGO diagnostic criteria remain the standard for AKI recognition and should guide initial workup. 1, 3, 4

For cirrhotic patients, baseline creatinine underestimates true GFR due to reduced muscle mass; therefore, use the absolute creatinine rise criterion (≥0.3 mg/dL within 48 hours or ≥50% from baseline) without fixed thresholds. 1 Urine output alone is unreliable for AKI assessment in cirrhosis due to frequent diuretic use and altered sodium handling. 1

Follow-Up Planning

Evaluate kidney function at 3 months post-AKI to assess for progression to CKD or development of acute kidney disease (AKD), with Stage 3 AKI requiring earlier follow-up (within 1–2 weeks) due to higher risk of CKD progression. 5, 7, 6

• Patients with pre-existing CKD, heart failure, cirrhosis, or malignancy need more intensive monitoring 5, 7
• Recognize that AKI increases long-term risk of CKD, cardiovascular disease, and mortality even after apparent creatinine recovery 5, 7, 9
• Document the AKI episode prominently in the medical record and educate patients to avoid NSAIDs and seek prompt medical attention during intercurrent illnesses 6