What are the typical urinalysis findings in patients with Acute Tubular Necrosis (ATN)?

Typical Urinalysis Findings in Acute Tubular Necrosis

The hallmark urinalysis findings in ATN include tubular epithelial cells, renal tubular epithelial cell casts, and granular (muddy brown) casts in the urine sediment, which distinguish it from prerenal azotemia and other causes of acute kidney injury. 1

Microscopic Sediment Examination

The urine sediment examination is the cornerstone of ATN diagnosis and provides direct evidence of tubular injury:

• Renal tubular epithelial cells are present in the urine sediment, with higher numbers correlating with more severe tubular damage and predicting non-recovery of AKI and need for dialysis 2
• Renal tubular epithelial cell casts are pathognomonic for ATN and indicate active tubular injury 1, 2
• Granular casts (often described as "muddy brown" casts) are characteristic findings that result from tubular cell debris and protein aggregation 1, 2
• The presence and quantity of these cellular elements can be used in a scoring system to predict severity and outcomes in ATN 2

Biochemical Urinary Indices

Several urinary biochemical parameters help differentiate ATN from prerenal causes:

• Fractional excretion of sodium (FENa) >1% indicates tubular damage and inability to reabsorb sodium, distinguishing ATN from prerenal azotemia (FENa <1%) 1
• Urinary sodium concentration typically >20 mEq/L in ATN, compared to <10 mEq/L in prerenal AKI 1
• Fractional excretion of urea (FEUrea) >50% suggests ATN, while <35% suggests prerenal causes; this is particularly useful when diuretics confound FENa interpretation 1, 3

Proteinuria and Hematuria

• Proteinuria is typically <500 mg/day and does not include significant albuminuria, which helps exclude glomerular diseases 4, 5
• Absence of significant hematuria (<50 RBCs per high-power field) helps distinguish ATN from glomerulonephritis 4
• Absence of microhematuria is part of the diagnostic criteria to differentiate ATN from structural kidney diseases like acute glomerulonephritis 4

Clinical Context and Differential Diagnosis

When interpreting urinalysis findings, consider the clinical context:

• Prerenal azotemia shows benign urinary sediment with hyaline casts, FENa <1%, and responds to volume expansion 1
• Hepatorenal syndrome demonstrates absence of proteinuria, absence of hematuria, and normal urinary sediment despite severe AKI 4
• Acute glomerulonephritis presents with dysmorphic RBCs, RBC casts, and significant proteinuria, which are absent in ATN 4

Important Caveats

• Urine microscopy findings may be less prominent early in ATN before significant tubular cell sloughing occurs 2
• Diuretic use can falsely elevate FENa, making FEUrea a more reliable marker in these patients 1, 3
• The absence of typical sediment findings does not completely rule out ATN, particularly in early or mild cases 2
• Emerging urinary biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and interleukin-18 (IL-18) may provide earlier and more specific diagnosis of tubular injury, though these are not yet standard practice 4, 3