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    Acute Tubular Injury: Kiran Shadentyra Akbari

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    Kiran tyra
    Acute tubular injury, also known as acute tubular necrosis, is damage to the tubule cells of the kidneys that can lead to acute kidney failure. It is most commonly caused by acute tubular injury when the damage is intrinsic to the kidneys. Acute tubular injury can be ischemic, due to reduced blood flow, or nephrotoxic, caused by poisons like heavy metals, organic solvents, antibiotics, or radiographic contrast agents. Urinalysis can detect muddy brown casts or renal cells shed into the urine. Novel biomarkers like NGAL can now detect acute kidney injury earlier than serum creatinine.

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    Acute Tubular Injury: Kiran Shadentyra Akbari

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    Kiran tyra
    58 views6 pages
    Acute tubular injury, also known as acute tubular necrosis, is damage to the tubule cells of the kidneys that can lead to acute kidney failure. It is most commonly caused by acute tubular injury when the damage is intrinsic to the kidneys. Acute tubular injury can be ischemic, due to reduced blood flow, or nephrotoxic, caused by poisons like heavy metals, organic solvents, antibiotics, or radiographic contrast agents. Urinalysis can detect muddy brown casts or renal cells shed into the urine. Novel biomarkers like NGAL can now detect acute kidney injury earlier than serum creatinine.

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    Acute Tubular Injury

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    Acute tubular injury, also known as acute tubular necrosis, is damage to the tubule cells of the kidneys that can lead to acute kidney failure. It is most commonly caused by acute tubular injury when the damage is intrinsic to the kidneys. Acute tubular injury can be ischemic, due to reduced blood flow, or nephrotoxic, caused by poisons like heavy metals, organic solvents, antibiotics, or radiographic contrast agents. Urinalysis can detect muddy brown casts or renal cells shed into the urine. Novel biomarkers like NGAL can now detect acute kidney injury earlier than serum creatinine.

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    58 views6 pages

    Acute Tubular Injury: Kiran Shadentyra Akbari

    Uploaded by

    Kiran tyra
    Acute tubular injury, also known as acute tubular necrosis, is damage to the tubule cells of the kidneys that can lead to acute kidney failure. It is most commonly caused by acute tubular injury when the damage is intrinsic to the kidneys. Acute tubular injury can be ischemic, due to reduced blood flow, or nephrotoxic, caused by poisons like heavy metals, organic solvents, antibiotics, or radiographic contrast agents. Urinalysis can detect muddy brown casts or renal cells shed into the urine. Novel biomarkers like NGAL can now detect acute kidney injury earlier than serum creatinine.

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    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.

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