Acute tubular necrosis

Acute tubular necrosis is a kidney disorder characterized by the destruction of renal tubular epithelial cells.

Renal tubular epithelial cells are a group of cells in the outer layer of the renal tubules (tiny tube-like structures of the kidneys where the blood is filtered). In acute tubular necrosis the cells in the proximal tubule are affected. As a consequence, reabsorption of water, electrolytes, glucose and amino acids is impaired.

Acute tubular necrosis is used to describe an intrinsic kidney failure associated with a urine sediment that has urinary casts and tubular epithelial cells.

Medically, it can be defined as an abrupt and sustained decline in GFR (glomerular filtration rate) caused by ischemia or a toxic event.

Acute tubular necrosis (ATN) is the most common cause of acute kidney injury (AKI).

Acute tubular necrosis, depending on the causes, can be classified as:

• Toxic: Due to the presence of toxic substances in the urinary filtrate.
• Ischemic: Produced by a decreased blood flow that causes a lack of oxygen presentation to the tubules.

Toxic acute tubular necrosis may be caused by exposure to a great variety of nephrotoxic agents (toxic to the kidneys).

• Exogenous
  • Aminoglycosides (bactericidal antibiotics such as gentamicin)
  • Cephalosporins (broad spectrum antibiotics)
  • Amphotericin B (antifungal medication)
  • Antiviral (cidofovir)
  • Antineoplastics (cisplatin, methotrexate)
  • Contrast media used in radiology (radiographic dye)
  • Organic solvents such as ethylene glycol
  • Heavy metals (lead, mercury)
  • Poisonous mushrooms
• Endogenous
  • Filtration of large amounts of hemoglobin and myoglobin

Disorders causing ischemic acute tubular necrosis include:

• Shock: It is a severe condition that decreases the flow of blood throughout the body. Disorders that may cause shock are cardiac failures, sepsis involving toxigenic bacteria (bacterial peritonitis), anaphylaxis, massive hemorrhage, and contact with high-voltage electricity.
• Trauma (such as crushing injuries).
• Surgical procedures.

Acute tubular necrosis is the most common cause of intrinsic acute renal failure (it is the cause of about 40 to 50% of all cases).

It is frequent in individuals with preexisting renal disease and/or diabetes mellitus and in the elderly population.

The disease course of acute tubular necrosis is variable characterized by a renal impairment that improves when the underlying cause is solved.

Urinalysis findings include mild proteinuria (a high level of proteins in the urine), microscopic hematuria (RBCs in the urine), and most noticeably the presence of renal tubular epithelial cells and urinary casts (mainly epithelial casts but also hyaline, granular or waxy casts).

It is necessary to remove the offending agent (medication, contrast medium, etc.) that can be toxic to the kidneys followed by a proper treatment of the symptoms related to the acute kidney failure.

Early dialysis is necessary in severe/rapidly progressing cases to prevent uremic syndrome.

Acute tubular necrosis is usually reversible with a proper management that results in a total recovery.

There are some measures that may help to reduce the possibility of suffering acute tubular necrosis:

• Keep a correct fluid balance before surgical procedures.
• In patients with chronic renal disease that require a radiographic contrast, give N-acetylcysteine and intravenous isotonic fluid before the procedure. In addition, avoid giving diuretics or cyclosporine the day of the procedure.
• Use renal-adjusted doses of nephrotoxic drugs in patients with renal insufficiency.