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A systematic workup of acute kidney injury is essential to distinguish between the three anatomic categories — prerenal, intrinsic renal, and postrenal — which have distinct etiologies, management approaches, and prognostic implications.
The kidney responds to different insults in characteristic ways detectable through urine studies. Prerenal states concentrate urine maximally (high osmolality, low sodium). ATN disrupts tubular reabsorption (low osmolality, high sodium, granular casts). Glomerular diseases release red blood cell casts into urine. Interstitial nephritis produces white cell casts and eosinophiluria. These patterns reflect underlying tubular, glomerular, or interstitial pathophysiology.
A focused AKI workup includes: basic metabolic panel with BUN/creatinine ratio, urinalysis with microscopy, urine electrolytes for FENa calculation, renal ultrasound for obstruction and chronicity assessment, and targeted serologic testing based on clinical suspicion (ANA, ANCA, complement, anti-GBM for glomerulonephritis). Medication reconciliation is critical — NSAIDs, ACE inhibitors, contrast agents, and aminoglycosides are common culprits. Kidney biopsy is reserved for unclear intrinsic AKI where diagnosis will change management.