Workup of Acute Kidney Injury
Begin immediately with serum creatinine and urinalysis with microscopy—these two tests form the diagnostic foundation for AKI and guide all subsequent management decisions. 1, 2
Initial Laboratory Assessment
Essential First-Line Tests
Serum creatinine and BUN must be measured to diagnose AKI (defined as ≥0.3 mg/dL increase within 48 hours OR ≥50% rise within 7 days) and calculate estimated GFR using the CKD-EPI equation 1, 2
Complete blood count with differential to assess for anemia, infection, or systemic inflammatory processes that may contribute to or complicate AKI 1
Complete metabolic panel including electrolytes (sodium, potassium, calcium, chloride, phosphorus, magnesium) to detect life-threatening complications like hyperkalemia 2
Urinalysis with microscopy to examine for proteinuria, hematuria, cellular casts (red cell casts suggest glomerulonephritis, muddy brown casts suggest acute tubular necrosis), white blood cells (suggesting infection or interstitial nephritis), and crystals 1, 2
Urine Chemistry to Differentiate Prerenal from Intrinsic AKI
Urine sodium and fractional excretion of sodium (FENa) should be calculated from spot urine to distinguish prerenal AKI from intrinsic renal damage 2, 3
Urine specific gravity (USG) and renal failure index (RFI) provide high specificity (>85%) for prerenal AKI and are not confounded by diuretics or pre-existing CKD 3
Urine osmolality helps differentiate causes, with high osmolality (>500 mOsm/kg) suggesting prerenal AKI 3
Serial Monitoring Parameters
Serial serum creatinine every 4-6 hours initially to assess AKI progression and determine KDIGO stage (Stage 1: 1.5-1.9x baseline; Stage 2: 2.0-2.9x baseline; Stage 3: ≥3.0x baseline or ≥4.0 mg/dL or need for dialysis) 1, 2
Hourly urine output documentation with oliguria defined as <0.5 mL/kg/hour for >6 hours (Stage 1), >12 hours (Stage 2), or <0.3 mL/kg/hour for 24 hours (Stage 3) 1, 2
Imaging Studies
Renal ultrasound with Doppler is mandatory as the first-line imaging for all AKI patients to assess kidney size, cortical thickness, echogenicity, detect hydronephrosis (suggesting obstruction), and rule out renal artery stenosis 1, 2
Normal-sized kidneys support acute rather than chronic kidney disease, while small echogenic kidneys suggest underlying CKD 1
Ultrasound is non-nephrotoxic and should be performed before considering contrast-enhanced studies 1
Clinical Assessment Framework
History and Physical Examination Focus
Review all medications including over-the-counter drugs, NSAIDs, ACE inhibitors, ARBs, diuretics, and any nephrotoxic agents (aminoglycosides, vancomycin, contrast agents) 1, 2
Assess volume status clinically: look for hypotension, tachycardia, decreased skin turgor, dry mucous membranes (hypovolemia) versus jugular venous distension, peripheral edema, pulmonary crackles (volume overload) 1
Identify precipitating events: gastrointestinal bleeding, diarrhea, vomiting, sepsis, cardiac events, recent procedures with contrast exposure, or new medications 1
Examine for systemic disease: rash (vasculitis, drug reaction), joint pain (autoimmune disease), fever (infection, drug reaction) 1
Specialized Studies When Indicated
Infection Workup
Blood and urine cultures should be obtained before empirical antibiotics when infection is suspected, as sepsis is a common precipitant of AKI 2
Diagnostic paracentesis is mandatory in cirrhosis patients with AKI to exclude spontaneous bacterial peritonitis 1, 2
When to Consider Renal Biopsy
Renal biopsy is indicated when urinalysis shows proteinuria >500 mg/day, dysmorphic RBCs, red blood cell casts suggesting glomerulonephritis, or unexplained AKI with active sediment despite initial workup 1, 2
Biopsy helps differentiate nephritic syndromes, vasculitis, and interstitial nephritis when diagnosis remains unclear after initial evaluation 1
Categorization of AKI Etiology
The workup should systematically evaluate three categories:
Prerenal (>50% of cases)
- Suggested by FENa <1%, urine sodium <10 mEq/L, high urine osmolality, bland urine sediment, and clinical evidence of volume depletion or decreased effective circulating volume 1, 3
Intrinsic Renal (40-45% of cases)
- Acute tubular necrosis: FENa >1%, muddy brown casts, recent hypotension, sepsis, or nephrotoxin exposure 1, 3
- Glomerulonephritis: red cell casts, dysmorphic RBCs, proteinuria 1
- Interstitial nephritis: white blood cells, white cell casts, eosinophiluria, recent drug exposure 1
Postrenal (<3% of cases)
- Hydronephrosis on ultrasound, bladder distension, history of urinary obstruction 1
Critical Management Pitfalls to Avoid
Do not delay ultrasound to rule out obstruction, as this is immediately reversible and accounts for postrenal AKI 1, 2
Avoid iodinated contrast in AKI unless there is an overriding clinical indication that cannot be answered with alternative imaging, as contrast can worsen kidney injury 1
Do not rely solely on urine output for diagnosis, as changes may be physiologic; serum creatinine is more reliable for AKI diagnosis 1
Withdraw nephrotoxic medications immediately including NSAIDs, ACE inhibitors/ARBs (in appropriate clinical context), and diuretics while assessing volume status 1, 2
Follow-Up Recommendations
Repeat creatinine at 3 months after any AKI episode to assess for resolution or development of chronic kidney disease, as even transient AKI increases long-term risk for progressive kidney disease and cardiovascular events 2
Patients who respond to initial management require close monitoring with creatinine assessment every 2-4 days during hospitalization and every 2-4 weeks for the first 6 months after discharge 1