ACUTE TUBULAR INJURY

Kiran Shadentyra Akbari

 DEFINITION

Acute tubular necrosis (ATN) is a kidney disorder involving damage to the tubule
cells of the kidneys, which can lead to acute kidney failure. The most common
cause of acute kidney injury (AKI) is acute tubular injury (ATI) when the pattern
of injury lies within the kidney (intrinsic disease).
 ETIOLOGY

1. Ischemic ATI
pattern of ATI associated with generalized or localized reduction in blood
flow.
2. Nephrotoxic ATI
caused by a variety poisons, including heavy metals (mercury), organic
solvents (carbon tetrachloride), and a multitude of drugs such as gebtamicin
and other antibiotics, and radiographic contrast agents.
PATHOPHYSIOLOGY
 EVALUATION

• Urinalysis (UA)
In prerenal disease, the UA microscopy is normal or may contain hyaline casts. On
the other hand, the UA of acute tubular necrosis shows muddy brown casts or renal
tubular epithelial cells secondary to the sloughing of tubular cells into the lumen due
to ischemia or toxic injury.
• Fractional excretion of sodium (FENa)
This is a good test to differentiate between acute tubular necrosis and prerenal
disease with a value less than 1% favoring prerenal disease and more than 2%, acute
tubular necrosis. However, these values are not always accurate as in chronic
prerenal states such as congestive heart failure and cirrhosis in which there is an
overlap between both (ATN and prerenal AKI) having a value of less than 1%.[7]
 CONT’D

• Urine sodium concentration

This test determines that the kidney is sodium avid in hypovolemic states (prerenal) where kidneys
try to conserve sodium or lose sodium due to tubular injury with values more than 40 to 50 mEq/L
indicating acute tubular necrosis and less than 20 mEq/L suggestive of prerenal disease.
• Novel Biomarkers
Numerous biomarkers have evolved to detect AKI/acute tubular necrosis early as compared to
serum creatinine. These biomarkers include serum cystatin C to be an early and reliable marker of
renal injury as compared to serum creatinine which is often witnessed 48 to 72 hours after the initial
insult. Other markers include urinary alpha one microglobulin, beta-2 microglobulin, urinary liver-
type fatty acid-binding protein (L-FABP) and kidney injury molecule 1 (KIM-1) for the detection of
proximal tubular damage, urinary interleukin-18 (IL-18) is known to differentiate ATN from CKD,
urinary tract infection (UTI), and prerenal azotemia. Urinary biomarker neutrophil gelatinase-
associated lipocalin (NGAL) is upregulated in the renal ischemia after distal tubular injury.