It is a reversible or irreversible medical condition which occurs either due to toxic injury or due to an ischemic injury to the renal tubular cells. During this disorder the cells from the basement membrane either die or detach from the tubules that results in dysfunction of the tubules.
Patients suffering from ATN have no specific symptoms as such and most cases are found on incidental routine laboratory. Symptomatic patients may present with:
Besides these symptoms, there could be additional signs and symptoms pertaining to the underlying disease. For example, a patient with rhabdomyolysis may present with tender muscles with doughy consistency along with edema around the extremities involved. According to the 2011 UKRA AKI guidelines, a thorough physiological observation must be done on all patients suspected with AKI to be able to diagnose AKI and prevent from further deterioration. This also helps in prognosis and measures can be taken to keep it under control .
Complications of ATN
Besides these complications there are specific condition-related complications which are as follows:
Patients suspected of ATN should undergo the following diagnostic tests:
For a better outcome, an early consult with a nephrologist or an intensivist is preferred. The goals to be achieved while treating ATN are:
Some of the issues sought during an ATN treatment are:
There is no special treatment outlined for ATN and most of it is supportive. The following steps are taken in treating ATN:
Renal replacement therapy
If a patient suffers from conditions such as severe acidosis, volume overload that don't respond to diuretics administered, increased potassium in blood or uremia treatment methods like hemodialysis, peritoneal dialysis and hemofiltration are opted.
Patients who have lost renal function and need more than supportive therapy are examined along with their hemodynamic and laboratory evidence by a nephrologist who outlines the type of care needed to restore or minimize the damage.
In patients that are hemodynamically stable, hemodialysis is preferred. While in critically ill patients, an early intervention along with increased dose, increased frequency and time have shown better prognosis  .
But patients that are hemodynamically unstable or those who can't tolerate a 4 to 6 hour ultra-filtration hemodialysis treatment are then advised continuous renal replacement therapy (CRPT). Continuous renal replacement therapy is of two types: a) arteriovenous and b) venovenous with continuous venovenous being the most frequently used technique. In a continuous venovenous treatment, a large double lumen catheter is inserted into the central venous system through the internal jugular vein or the femoral vein. Hence the most commonly used treatment are continuous venovenous hemofiltration (CWH), continuous venovenous hemodialysis (CWHD) and continuous venovenous hemodiafiltration (CWHDF).
Patients that have suffered septic shock or severe heart failure with volume overload cannot be treated with the conventional hemodialysis. In such patients CRPT have shown beneficial. Studies evaluating high clearance volumes and addition of a dialysis dose to CWH has shown better outcomes   .
The prognosis of ATN depends largely on the necessity of intensive care unit.
Therefore an overall healthy patient suffering from ATN can have good prognosis when the main problem or the root cause is corrected. This can be seen with the serum creatinine level reaching normal in 1 to 3 weeks.
The predictors of prognosis of ATN are:
Various reasons could cause ATN:
Some of the most common nephrotoxic drugs are as follows :
It has been difficult to establish an appropriate occurrence rate of acute tubular necrosis due to changes in the definition and varied characteristics of examined patients. Acute renal failure (ARF) and acute tubular necrosis (ATN) are often used interchangeably even when they both are two different conditions . The incidence rates of ARF also aren't well established but as per the National Hospital Discharge Survey Data for the year 2001 that included 29,039,599 hospitalizations, suggested that 19.2 cases of ARF are seen in every 1000 patient hospitalizations in the US .
Acute tubular necrosis occurs in 3 stages namely initiation, maintenance, and recovery. Acute ischemia or toxic events usually are the cause for characteristic ATN features i.e tubular cell death. The ischemic ATN features overlap with the nephrotoxic forms as well.
Prereneal azotemia is known to be a predisposing factor that causes ischemic ATN even though the causes of prerenal azotemia are different than those of ischemic ATN. Ischemic ATN occurs due to a hypoperfused kidney which can be an added burden to the kidneys existing auto-regulatory defenses. Hypoperfusion is the main factor that initiates the process of cell injury but isn't the cause of cell death.
In ATN, the tubular cellular injury is more common at the straight portion of the proximal tubules and in the thick ascending limb of loop of Henle since it is embedded in the medulla that is comparatively more hypoxic. The most common mechanism of ATN is reduction of the glomerular filtration rate that occurs due to two reasons:
This blockade in the tubular lumen causes the filtrate to go back in to the system through the damaged epithelial lining of the glomerulus disrupting the whole procedure of filtration.
Microscopically, the first change to occur in ATN are the apical blebs which is followed by loss of brush border in the tubule and loss of polarity. Cells also show loss of tight junctions in ATN. Finally the epithelial lining of the glomerulus that controls the filtration is also damaged and this causes the filtered and unfiltered materials to go back into the system.
ATN brings about a disturbance in the anatomy of the glomerulus and the tubules. It affects the Na+/K+ -ATPase pumps which tends to move away from their original position and integrins too move apart into the apical membrane. It eventually leads to cell death due to necrosis and apoptosis. The shedding of live as well as dead cells causes the formation of casts and obstructs the tubules.
Ischemia not only leads to ATN but also causes decreased production of vasodilators like nitric oxide, prostacyclin. The vasodilators are produced by the tubular cells of the kidney and a decrease in these causes more vasoconstriction and hypoperfusion.
Ischemia biochemically also causes a decline in adenosine triphosphate (ATP), an increase in the cytosolic calcium along with an increase in free radicals. The free radicals when increased pose a threat to cells since they have deleterious and toxic effect on the cells. This damage caused by free radicals is worse on reperfusion.
It also leads to an increase of membrane phospholipid metabolism wherein the phospholipid membrane undergoes change and the membrane lipids end up in peroxidation. It also affects the cell volume regulation. The reduction of ATP hinders the cellular function especially the active transport.
All of the above mentioned pathophysiological process results in cellular swelling and intracellular accumulation of Na and Ca.
This phase usually lasts for 1-2 weeks. As the name suggests the maintenance phase is the period when the glomerular filtration rate tries to come back to its original physiological state.
During this phase, the afferent arterioles of the glomerulus detect the increased salt retention in the tubules and this leads to constriction of the arterioles that is carried out by the macula densa cells. This is the tubuloglomerular feedback mechanism that helps overcome the injury.
During this phase the damaged tubular cells begin to regenerate . As they recover, physiological disturbance such as abnormal diuresis may occur resulting in salt and water loss and depletion of volume. Though the exact process behind the diuresis hasn't been established but it is presumed to be due to the late recovery of the tubules especially when there is an increase in glomerular filtration. This phase might worsens if diuretics are added from an external source which are usually given during the initiation and maintenance phase.
ATN can be prevented by taking into following precautions:
It is difficult to comment on the efficacy of loop diuretics like mannitol or dopamine to help prevent ATN and no study has been able to prove it.
The kidney has two parts microscopically:
Acute tubular necrosis (ATN) is a condition affecting the tubules of the kidney which could be a reversible or an irreversible process, arising because of a toxic injury or an ischemic injury to the kidney. ATN occurs when the epithelial cells that line the tubule are damaged or die. ATN is known to be a very common disorder in acute kidney injury (AKI). The primary reasons for the occurrence of ATN are usually due to a toxin or decreased blood and oxygen flow to the tubules leading to ischemia.
ATN is difficult to diagnose since it doesn't present symptomatically. ATN is usually suspected when there are symptoms of AKI. These symptoms include decreased urine output, fluid retention, edema, nausea and vomiting, disoriented or decreased consciousness and lethargy. There are 2 types of ATN :
Acute tubular necrosis (ATN) is primarily caused due to lack of oxygen to the kidney tissues also known as ischemia of the kidneys.
Other factors include:
On a cellular level, the tubules present in the kidney either get damaged or destroyed due to ATN. This change in structure of the tubules is the most common cause that lands patients into acute renal failure. The most common cause of kidney failure in hospitalized patients is ATN.
Some of the risks associated with ATN are enumerated below:
ATN usually doesn't present with a lot of symptoms and often goes undiagnosed, but it can have other symptoms of the underlying disorder that are more pronounced.
A routine physical examination is carried out to analyze the systems. The doctor tries to listen to the heart sounds to make sure all is well with the heart. Sometimes abnormal sounds in lungs and heart can be heard due to excess fluid overload in the body. If any abnormalities are found following tests are recommended:
ATN is a reversible disorder of the kidneys. The main aim in treating ATN is to prevent any further complications that are life-threatening complications of acute kidney failure.
The treatment goals for ATN are:
Most of ATN treatment is supportive therapy, but if all of these fail and seem to not respond, dialysis may be the only option. Since ATN is a reversible disorder, the hemodialysis is temporary. Hemodialysis helps in removal of toxins and extra fluid. This technique decreases the burden of the kidneys and helps them to heal. Though it isn't necessary for all ATN patients to undergo dialysis but it has proven beneficial and is lifesaving especially in cases wherein the potassium levels are too high to manage.