Main concern of doctors treating the patient suffering from acute tubular necrosis (usually shortened as ATN) is to prevent any further damage of the kidneys. In general, treatment is consisted of extracellular fluid (ECF) assessment and timely repletion of existing deficits. Patients receiving drugs toxic for the kidneys (nephrotoxic) should stop using these. In these patients, recommendation is the same for any of the drugs eliminated by the kidneys – quick cessation is advised by most doctors.
How to Treat Acute Tubular Necrosis?
Acute tubular necrosis is usually treated by correction of oliguria, dialysis, elimination of nephrotoxins and some dietary measures. Doctors will try to increase urine output using diuretic drugs like intravenous (IV) loop diuretics. This method is recommended only in patients whose ECF and cardiac function are found out to be adequate. A single high dose of bumetanide or furosemide (100 to 200mg) is commonly used to correct oliguria in these patients, but it usually doesn’t change anything for the patients. If they don’t improve the problem, loop diuretics should be stopped. Some doctors also used dopamine, but this is not recommended by modern medical practice, for it had no effects.
Early dialysis may be beneficial for ATN patients and hemodialysis is currently standard treatment for serious acute kidney injury. However, some studies show that this procedure has no positive effects on recovery or survival. Continuous hemodialysis is recommended for patients suffering from hemodynamic instability or multi-organ failure.
Cessation of nephrotoxic substances should prevent further kidney damage. Elimination of nephrotoxins – Cyclosporine may benefit from calcium channel blockers. This measure may cause hypotension and doctors avoid using it.
Dietary measures in form or adequate intake of proteins and calories can improve survival rate in ATN patients. ATN Prevention Methods
Acute tubular necrosis may be ischemic or nephrotoxic and these problems require different approach when it comes to prevention. Ischemic ATN is prevented by optimizing cardiovascular function and maintenance of intravascular volume. Doctors should be especially careful when prescribing nephrotoxic drugs or afterload reducers to these patients.
Nephrotoxic ATN may be prevented with careful neprotoxin consideration. Aminoglycosides, amphotericin B, tacrolimus, cisplatin and Cyclosporine are known to cause nephrotoxic acute tubular necrosis in some patients. One daily dose of aminoglycosides is discovered to be less likely to cause nephrotoxic effect than the same drug given three times per day. Lipid formulations of amphotericin B, such as colloid dispersion of this drug, complex or liposomal amphotericin B should be less toxic for the kidneys. Reduction of therapeutic dose is usually sufficient to reverse kidney damage due to the use of tacrolimus or Cyclosporine. Cisplatine can be less nephrotoxic if used with saline or amifostine, while some doctors recommend switching to carboplatin, considered to be less toxic for the kidneys.