Workup of Acute Kidney Injury
Diagnose AKI using KDIGO criteria: serum creatinine increase ≥0.3 mg/dL within 48 hours OR ≥50% rise from baseline within 7 days OR urine output <0.5 mL/kg/h for >6 hours, then immediately discontinue all nephrotoxic medications and systematically determine if the cause is prerenal, intrinsic renal, or postrenal. 1, 2
Initial Diagnostic Steps
Immediate Laboratory Assessment
- Measure serum creatinine and compare to baseline to stage AKI severity using KDIGO criteria: Stage 1 (1.5-1.9× baseline or ≥0.3 mg/dL rise), Stage 2 (2.0-2.9× baseline), Stage 3 (≥3.0× baseline or Cr ≥4.0 mg/dL or need for RRT) 1
- Obtain complete blood count to assess for anemia suggesting chronic process or hemolysis 3
- Check serum electrolytes, BUN, and creatinine every 4-6 hours initially in severe cases to monitor for life-threatening complications 2, 4
Urinalysis and Urine Studies
- Perform urinalysis with microscopy to detect hematuria, proteinuria, casts (muddy brown casts suggest ATN, RBC casts suggest glomerulonephritis, WBC casts suggest interstitial nephritis) 1, 3, 5
- Calculate fractional excretion of sodium (FENa): FENa <1% suggests prerenal azotemia, FENa >2% suggests intrinsic renal disease (ATN) 3, 5
- Measure urine sodium and urea to differentiate prerenal (<20 mEq/L) from intrinsic causes (>40 mEq/L) 1
Imaging
- Obtain renal ultrasound in most patients, particularly older men, to rule out obstructive uropathy (postrenal causes) 3, 5
Determine the Etiology: Prerenal, Intrinsic, or Postrenal
History Taking - Specific Details to Elicit
- Identify nephrotoxic medication exposure: NSAIDs, ACE inhibitors, ARBs, diuretics, aminoglycosides, contrast agents, chemotherapy 1, 2, 3
- Assess for volume depletion: vomiting, diarrhea, bleeding, poor oral intake, excessive diuretic use 3, 5
- Screen for sepsis or infection: fever, hypotension, recent procedures, indwelling catheters 1, 6
- Evaluate for cardiac causes: heart failure exacerbation, recent cardiac surgery, cardiogenic shock 3, 6
- Check for urinary symptoms: hesitancy, frequency, flank pain suggesting obstruction 3, 5
Physical Examination - Key Findings
- Assess volume status: orthostatic vital signs, jugular venous pressure, skin turgor, mucous membranes, peripheral edema 2, 3, 5
- Examine for systemic illness: skin rashes (vasculitis, drug reaction), livedo reticularis (atheroemboli), palpable purpura 3
- Palpate bladder for distension suggesting urinary retention 3
Rigorous Infection Workup - Critical in All AKI Patients
- Perform diagnostic paracentesis in cirrhotic patients to evaluate for spontaneous bacterial peritonitis 1, 2
- Obtain blood cultures, urine cultures, and chest radiograph in all patients with suspected infection 1
- Start broad-spectrum antibiotics immediately when infection is strongly suspected, do not wait for culture results 1, 2
Immediate Management While Determining Cause
Medication Review and Discontinuation
- Stop all nephrotoxic drugs immediately: NSAIDs, ACE inhibitors, ARBs, diuretics, aminoglycosides, vancomycin 1, 2, 4
- Avoid the "triple whammy" combination of NSAIDs + diuretics + ACE inhibitors/ARBs, which more than doubles AKI risk 4
- Adjust all medication dosages based on reduced GFR and reassess frequently as kidney function changes 2, 4
Volume Management Based on Assessment
- For hypovolemic patients: administer isotonic crystalloids (normal saline or lactated Ringer's) for fluid repletion 2, 5
- For cirrhotic patients with AKI and doubling of creatinine: give albumin 1 g/kg/day (maximum 100 g/day) for 2 consecutive days 1, 2
- For volume-overloaded patients: implement fluid restriction and consider diuretics only after adequate perfusion is ensured 2, 4
Hemodynamic Support
- Maintain mean arterial pressure >65 mmHg to ensure adequate renal perfusion using vasopressors if needed 2
Special Considerations for Cirrhotic Patients
The workup differs significantly in cirrhosis because baseline creatinine overestimates GFR due to decreased muscle mass and creatinine production 1
- Use ICA-AKI criteria: increase in creatinine ≥0.3 mg/dL within 48 hours OR ≥50% from baseline, without the fixed 1.5 mg/dL threshold 1
- Hold diuretics and beta-blockers immediately when AKI is diagnosed 1
- Treat suspected hepatorenal syndrome (HRS-AKI) with albumin 1 g/kg IV on day 1, then 20-40 g daily, plus vasoactive agents (terlipressin preferred; or octreotide/midodrine; or norepinephrine) 2
Indications for Urgent Renal Replacement Therapy
Initiate RRT emergently for: severe oliguria unresponsive to fluid resuscitation, refractory hyperkalemia, severe metabolic acidosis, uremic complications (encephalopathy, pericarditis, pleuritis), volume overload causing pulmonary edema, or certain toxin ingestions 2, 4, 3, 5
Common Pitfalls to Avoid
- Delaying RRT when clear indications exist significantly increases mortality 2, 4
- Continuing nephrotoxic medications during AKI recovery leads to continued kidney damage 2, 4
- Overly aggressive fluid administration in non-hypovolemic patients worsens outcomes 4
- Failing to identify and treat underlying infection allows progression of AKI 1, 2
- Using urine output alone in cirrhotic patients is unreliable due to diuretic use and sodium retention 1
- Overly rapid correction of severe hyponatremia can cause osmotic demyelination syndrome 4
Monitoring and Follow-up
- Track strict input/output measurements and reassess volume status frequently 2, 4
- Monitor for uremic complications: altered mental status, pericardial friction rub, asterixis 4, 3
- Reassess need for continued RRT daily as kidney function may recover 2, 4
- Schedule close post-discharge follow-up for patients with moderate to severe AKI, with timing based on AKI severity 2