Acute Tubular Necrosis

Below you will find more information about Acute Tubular Necrosis from Medigest. If you believe that you are suffering from any of the symptoms of Acute Tubular Necrosis it is important that you obtain an accurate diagnosis from a medical professional to ensure that you obtain the correct medication or treatment for your condition. There are medical conditions that carry similar symptoms associated with Acute Tubular Necrosis and therefore the information provided by Medigest is offered as a guideline only and should never be used in preference to seeking professional medical advice. The information relating to Acute Tubular Necrosis comes from a third party source and Medigest will not be held liable for any inaccuracies relating to the information shown.


Acute tubular necrosis (ATN) is a medical condition involving the death of tubular cells that form the tubule that transports urine to the ureters while reabsorbing 99% of the water, highly concentrating the salts and metabolic byproducts. Tubular cells continually replace themselves, and if the cause of ATN is taken out, then recovery is likely. ATN presents with acute renal failure and is one of the most frequent causes of ARF. The presence of "muddy brown casts" of epithelial cells present in the urine during urinalysis is pathognomonic for ATN. ATN may be classified as either toxic or ischemic. Toxic ATN arises when the tubular cells are exposed to a toxic substance (nephrotoxic ATN). Ischemic ATN occurs when the tubular cells do not get adequate amounts of oxygen, a condition they are highly sensitive to due to their very high metabolism.


The syndrome of ARF is present in about 5% of all hospital admissions. It occurs in up to 30% of patients admitted in the ICU. Prerenal causes are responsible for approximately 50% of all cases. The prevalence of each type of intrinsic renal disease varies depending on the population studied, but ATN (other than prerenal azotemia) is the most common cause of ARF in hospitalized patients.


Diagnosis is often supported by a positive history of risk factors. Yet the physician must rule out other factors for acute renal failure, such as prerenal, postrenal, and renal ARF. Distinguishing ATN from prerenal ARF can be extremely hard. Microscopic examination of the urine and urine chemistry and microscopic examination of the urine help to confirm the diagnosis. ATN does not quickly improve following the administration of large-volume intravenous fluid. Early diagnosis of ATN by exclusion of prerenal and postrenal causes of acute renal failure, analysis of urine measures (for example, fractional excretion of sodium in the absence of diuretics), and examination of urinary sediment can allow the early involvement of nephrologists and improve survival.


Management depends on aggressive treatment of the factors that precipitated ATN. One exception is the treatment of ATN related with the breakdown of muscle fibers caused by a crush injury. Aggressive, forced diuresis (that is, an increased excretion of urine) may improve the condition. Patients at high risk for developing ARF from contrast induced ATN should be treated with intravenous (IV) fluids before contrast exposure to prevent the ATN. There has been a recent report suggesting that pretreatment of these patients with a medication called mucomyst may also aid in preventing ARF in patients undergoing IV contrast exposure.

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