ACUTE TUBULAR NECROSIS (ACUTE RENAL SHUT DOWN)
is a medical condition involving the death of tubular cells that transport urine to the ureters.Tubular cells continually replace themselves and if the cause of ATN is removed then recovery is likely. ATN is commonly defined as an abrupt decline in renal function, manifested by acute elevation in plasma blood urea nitrogen (BUN) and serum creatinine, occurring in hours to days to weeks.The presence of "muddy brown casts" of epithelial cells found in the urine during urinalysis is pathognomonic for ATN.
It may be classified as either toxic or ischemic. Toxic ATN occurs when the tubular cells are exposed to a nephrotoxic substance Ischemic ATN occurs when the tubular cells do not get enough oxygen, a condition that they are highly sensitive and susceptible to, due to their very high metabolism.
Toxic ATN can be caused by free hemoglobin or myoglobin, by medication such as aminoglycosides, drugs such as cisplatin,amphoterecin, or by intoxication with ethylene glycol etc.Toxic ATN is characterized by proximal tubular epithelium necrosis, Necrotic cells fall into the tubule lumen, obturating it, and determining acute renal failure.Ischemic ATN can be caused when the kidneys are not sufficiently perfused for a long period of time as in renal artery stenosis or during shock. Hypoperfusion can also be caused by embolism of the renal arteries. Ischemic ATN specifically causes skip lesions through the tubules.
There are other causes like mis-matched blood transfusion,iodine-contrast induced reaction,extensive muscle damage,septic shock , diabetics.
The symptoms are common to any acute renal shut down like, nausea,vomiting,generalised swelling,decreased/no urine out put,delirium,coma etc.
The following tests confirm the diagnosis of ATN:
is a medical condition involving the death of tubular cells that transport urine to the ureters.Tubular cells continually replace themselves and if the cause of ATN is removed then recovery is likely. ATN is commonly defined as an abrupt decline in renal function, manifested by acute elevation in plasma blood urea nitrogen (BUN) and serum creatinine, occurring in hours to days to weeks.The presence of "muddy brown casts" of epithelial cells found in the urine during urinalysis is pathognomonic for ATN.
It may be classified as either toxic or ischemic. Toxic ATN occurs when the tubular cells are exposed to a nephrotoxic substance Ischemic ATN occurs when the tubular cells do not get enough oxygen, a condition that they are highly sensitive and susceptible to, due to their very high metabolism.
Toxic ATN can be caused by free hemoglobin or myoglobin, by medication such as aminoglycosides, drugs such as cisplatin,amphoterecin, or by intoxication with ethylene glycol etc.Toxic ATN is characterized by proximal tubular epithelium necrosis, Necrotic cells fall into the tubule lumen, obturating it, and determining acute renal failure.Ischemic ATN can be caused when the kidneys are not sufficiently perfused for a long period of time as in renal artery stenosis or during shock. Hypoperfusion can also be caused by embolism of the renal arteries. Ischemic ATN specifically causes skip lesions through the tubules.
There are other causes like mis-matched blood transfusion,iodine-contrast induced reaction,extensive muscle damage,septic shock , diabetics.
The symptoms are common to any acute renal shut down like, nausea,vomiting,generalised swelling,decreased/no urine out put,delirium,coma etc.
The following tests confirm the diagnosis of ATN:
- BUN and serum creatinine
- Fractional excretion of sodium
- Kidney biopsy
- Urinalysis
- Urine sodium
- Urine specific gravity and osmolarity urine
In most people, ATN is reversible. The goal of treatment is to prevent life-threatening complications of acute kidney failure.Treatment focuses on preventing the excess buildup of fluids and wastes, while allowing the kidneys to heal. Patients should be watched closely for deterioration of kidney function.
Treatment can include:
- Identifying and treating the underlying cause of the problem
- Restricting fluid intake to a volume equal to the volume of urine produced
- Taking medications to help control potassium levels in the bloodstream
- Medicines taken by mouth or through an IV to help remove excess fluid from the body
- Most of the times there may be a block in the ureters due to necrotic material from kidney.This is managed by placing a DJ stent to allow proper functioning of kidneys.This is done by a urologist under anaesthesiologist cover.
Temporary dialysis can remove toxins and excess fluids. This can make the kidney failure easier to control. Dialysis may not be necessary for all people, but is often lifesaving.
Dialysis may be needed in the following cases:
- Decreased mental status
- Fluid overload
- Increased potassium levels
- Pericrditis
- To remove toxins that are dangerous to the kidneys
- Total lack of urine production
- Uncontrolled buildup of nitrogen waste products
There is less urine for a few days to 6 weeks,and this may be followed by a period of high urine output (diuretic phase). This occurs because the healed and newly functioning kidneys try to clear the body of fluid and waste.
One or two days after urine out put increases, symptoms reduce and test results begin to return to normal.
At the time of Blood transfusions blood should be crossmatched by two people to reduce the risk of incompatibility reactions.Control the diseases like as diabetes, liver disorders, and cardiac disorders to reduce the risk of acute tubular necrosis.Drink a lot of fluids after having any radiocontrast dyes to allow them to be removed from the body and reduce the risk of kidney damage.
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