Acute Tubular Necrosis

Background

Early Stage squareAcute Tubular Necrosis (ATN) is a condition involving the death of epithelial cells that form the tubules of the kidney and is one of the most common forms of acute kidney injury (AKI). The cell death that characterizes ATN is usually the result of ischemia (lack of blood flow/oxygen) or a toxin affecting the kidney.

ATN is usually asymptomatic, but may cause symptoms of AKI such as decreased consciousness/lethargy, decreased or no urine output, fluid retention, and nausea and vomiting.

Risk factors for ATN include blood transfusion reaction, injury or trauma that damages the muscles, low blood pressure (hypotension) for >30 mins, recent surgery, sepsis due to severe infection, or exposure to agents that are toxic to the kidney (i.e. aminoglycoside antibiotics, amphotericin, contrast dye for radiological studies).

Current Treatment

Treatment for ATN focuses on averting further injury to the kidney by preventing excess build-up of fluids and wastes, as well as preventing the life-threatening complications of acute kidney failure. Treatment can include:

  • Restricting fluid intake to a volume equal to the volume of urine produced
  • Restricting substances normally removed by the kidneys (such as protein, sodium, potassium) to minimize their buildup in the body
  • Stopping all nephrotoxic drugs
  • Medications to help keep potassium levels within normal range in the bloodstream
  • Medications to help remove excess fluid from the body:

Temporary dialysis may be a life-saving approach in some patients and should be started once the diagnosis of AKI is established, but before any serious complications arise.

Focused Ultrasound Treatment

Pre-clinical research is being conducted around the globe to explore the potential of focused ultrasound to treat ATN. As one of the major triggers for developing ATN is ischemia (lack of blood flow) to the kidney, therapies that enhance kidney perfusion through vasodilation (widening of the blood vessels) may be beneficial. Focused ultrasound has been shown to cause a change in pressure at a precise location in a targeted blood vessel, which causes the endothelium (cells lining the blood vessel wall) to release nitric oxide, a chemical that causes vasodilation through relaxing the smooth muscle in blood vessels. This vasodilation is reversible and trials have shown no permanent damage to the targeted tissue thus far.

In addition, it has been shown that renal artery sonication with FUS temporarily enhances the permeability of the downstream glomerulus, which is the site of major filtration within the kidney. Also, sonication of the kidney itself revealed increased glomerular filtration, with improved urine flow and enhanced clearance of large molecular weight agents that are not normally filtered by the kidney. Improvements in the glomerular filtration rate may prevent the build-up of toxic wastes and fluids that occur in ATN. Further research is needed to determine whether these effects can be observed in kidneys affected by or are at risk for ATN.

Notable Papers

Yang FY, Chiu WH. Focused ultrasound-modulated glomerular ultrafiltration assessed by functional changes in renal arteries. PLoS One. 2013.

Fischer K, McDannold NJ, Zhang Y, Kardos M, Szabo A, Szabo A, Reusz GS, Jolesz FA. Renal ultrafiltration changes induced by focused US. Radiology. 2009

F.-Y. Yang, W.-H. Chiu, S.-H. Liu, G.-L. Lin, and F.-M. Ho, Functional changes in arteries induced by pulsed high-intensity focused ultrasound. IEEE Trans. Ultrason. Ferroelectr. Freq. Control., vol. 56, no. 12, pp. 2643–2649, Dec. 2009.

A. Maruo, C. E. Hamner, A. J. Rodrigues, T. Higami, J. F. Greenleaf, and H. V. Schaff, Nitric oxide and prostacyclin in ultrasonic vasodilatation of the canine internal mammary artery. Ann. Thorac. Surg., vol. 77, no. 1, pp. 126–132, Jan. 2004.

 

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