Published on Aug 09, 2022 and last reviewed on Mar 10, 2023 - 5 min read
Abstract
The damage to the tubular cells occurs as a result of compromised blood and oxygen flow to the kidney causing acute tubular necrosis. Read the article to know more about it.
The kidneys contain millions of microscopic structures called the nephron. It is the filtering unit of the kidney. A nephron is made up of a renal corpuscle and a connecting tubule. The renal corpuscle contains a glomerulus and a bowman's capsule. The renal tubule extends from this capsule and is divided into the proximal convoluted tubule, the collecting loop, and the distal convoluted loop. The cells of the glomerulus have a special ability to filter the blood. Blood entities like red blood cells, white blood cells, platelets, and proteins are not filtered in the bowman's capsule.
The rest of the renal tubule consists of the endothelial cells, which add to the filtration. The filtration takes place by four mechanisms, namely - filtration, reabsorption, secretion, and excretion. Substances that are secreted include urea, uric acid, creatinine, potassium, and hydrogen. Substances that are observed from the renal tubule are water, glucose, amino acids, calcium phosphate, bicarbonate, and sodium chloride. A kidney contains 1 to 1.5 million nephrons.
The death of the cells or tissue is called necrosis. It can occur due to the less supply of blood or oxygen in the body. External injury or trauma can cause necrosis. Irreversible injury and cell death are possible outcomes of necrosis. It occurs when the stimulus is from outside the cell and is always associated with the inflammatory response. Necrosis can be caused by -
Hypoxia - A condition that occurs due to a lack of oxygen. It can occur due to ischemia, shock, or respiratory failure.
Physical Injury - External injuries such as trauma, extreme temperatures, radiation exposure, or electric shock.
Chemical Compounds - It includes poison, occupational exposure, and drug toxicities.
Biological Agents - Bacterias, fungi, and viruses.
Immunological Reactions - Autoimmune responses.
Tubular cells are cells present in the filtering unit of the kidney called the nephron. Acute tubular necrosis is a kidney disorder that occurs when the tubular cells of the kidneys are damaged due to the lack of blood flow or oxygen to the tissues. A chronic hypoxic condition can lead to the necrosis of the tubular cells, which further causes impairment in the filtration process. It can also occur when the kidney cells are damaged by a poison or harmful substance. Any irreversible structural changes can lead to acute kidney failure. Kidney failure occurs when the fluid and electrolyte balance is disturbed, and the waste products get accumulate in the body. There are three types of acute tubular necrosis based on the cause -
Nephrotoxin-Induced Acute Tubular Necrosis - Certain medications, poisons, and chemicals that can damage the kidney act as nephrotoxins. Drugs that can cause nephrotoxicity include Amphotericin B, Aminoglycoside, Radiocontrast media, Sulfa drugs, Acyclovir, and Cyclosporine.
The Ischemia-Induced Acute Tubular Necrosis - Any factor that can lead to a lack of oxygen supply to the tubular cells can cause ischemia-induced acute tubular necrosis.
Sepsis-Induced Acute Tubular Necrosis - Sepsis is a condition of bacterial infection throughout the body. This condition can lead to hypovolemia and hypotension.
Stroke - Stroke or heart attack are the two conditions in the body that can cause hypoxia in the kidneys.
Hypoxia - Hypoxia is a condition caused due to a lack of oxygen.
Blood Clots - Blood clots can hamper the flow of blood and oxygen and can cause necrosis.
Septic Shock - A severe bacterial infection that occurs throughout the body leading to low blood pressure.
Blood Transfusion Reaction - The reaction that occurs when there is a mismatch in the blood group during transfusion.
Major Surgery - Patients with a history of major surgery or at risk of acute tubular necrosis.
Hypotension - Low blood pressure that lasts for more than 30 minutes.
Trauma - Injury or trauma to the muscles causes the damage and destruction of the cells.
Systemic Diseases - Diabetic nephropathy is supposed to have a damaging effect on the kidney and liver.
Nephrotoxic Substances - Acute play necrosis can be caused by poisons and some nephrotoxic medications also. The medications include Aminoglycoside antibiotics and antifungal drugs like Amphotericin.
Reduction in the total urine output.
Fluid retention in the body.
Swelling in the extremities and face.
Drowsiness or trouble waking up.
Feeling of confusion.
Nausea and vomiting.
Confusion or delirium.
Lethargy or feeling of low energy.
Blood Analysis- A blood test can be done to check for the presence of blood urea nitrogen, creatinine and electrolyte levels such as potassium in the blood. A rise in the level of these substances can indicate damage to the kidneys. The biomarker of acute kidney injury is the presence of serum cystatin levels compared to serum creatinine.
Urinalysis - Microscopic examination of the urine can present brown-colored renal tubular cells, which are found secondary to the necrosis. Urinary biomarkers of acute kidney injury include beta-2 microglobulin, urinary liver-type fatty-acid binding protein, and kidney injury molecule one.
The first step in the management of acute tubular necrosis involves the identification of the risk factor associated with it.
Patients having a history of shock or undergoing major surgery should be monitored well from time to time.
Interventions to decrease the risk of acute tubular necrosis in patients with cardiogenic shock, hemorrhagic shock, severe burns, sepsis, and pancreatitis should be done by correcting the hypotension and hypovolemia.
Hypertension can be controlled by cessation of the Angiotensin II receptor blocker in patients with low blood pressure.
Hypovolaemia can be corrected by intravenous infusion of fluid such as crystalloids.
Complete withdrawal of the drugs that can cause acute tubular necrosis or neurotoxins are NSAIDs, antibiotics such as Aminoglycosides, Vancomycin, and antifungal agents such as Amphotericin.
Dialysis and kidney transplant therapy can be done in cases where the symptoms of acute tubular necrosis do not react to the treatment.
Conclusion :
The most effective measure to prevent the initiation of acute tubular necrosis is the identification and treatment of systemic diseases such as diabetes mellitus, heart failure, atherosclerosis, and malignancy. Daily measurement of fluid balances, electrolyte balance, and urine output can help in the diagnosis of acute kidney injury. Acute tubular necrosis can last for several weeks to a month. The disease cannot be reversed, but the progression can be slowed down. It is relatively easily curable in patients who are free from any underlying systemic disease.
Acute tubular necrosis (ATN) is a kidney problem including harm to the tubule cells of the kidneys, which can prompt intense kidney damage. Tubules help in blood filtration while passing through the kidney.
Three stages of ATN are:
- Initiation.
- Maintenance.
- Recovery.
In the renal category, acute tubular necrosis (ATN) is the commonest cause of acute kidney injury (AKI), or AKI, in which the pathology is located within the kidney.
ATN is thought when serum creatinine rises ≥ 0.3 mg/dL/day (26.5 micromol/liter [μmol/L]) above standard or a 1.5 to 2.0 expansion in serum creatinine from pattern after an evident trigger.
From a few days to six weeks or more, ATN can occur. As the kidneys recover, this may be followed by one or two days of unusually high urine production. The kidney's capability frequently returns to normal, yet other complex issues and problems may persist.
ATN is commonly seen in hospitalized patients and can cause ischemia, toxin exposure, or sepsis. High mortality and morbidity are associated with acute tubular necrosis.
The following are included in ATN:
- Overload of volume specifically, hyperkalemia, acidosis, hyperphosphatemia, and hypocalcemia are acid-base and electrolyte imbalances.
- Problems like prolonged bleeding, altered mental state, and pericardial disease can result from urination.
Nephrotoxic medications like NSAIDs, antibiotics like amphotericin B, aminoglycosides, vancomycin, piperacillin/tazobactam, and radiocontrast agents should be avoided because they can cause acute tubular necrosis.
A creatinine level higher than 1.4 in men and 1.2 in women typically indicates that the kidneys are not functioning properly.
Following are the clinical indicators of ATN.
- A decreased urine output.
- Swelling.
- Fluid retention.
- Nausea and vomiting.
- Drowsiness.
The patient requires dialysis when the creatinine clearance falls below 10-12 cc/minute.
Creatinine levels above 1.3 mg/dL are dangerous.
Antioxidant-rich fruits such as cranberries, kiwis, apples, and blueberries are suitable for creatinine levels.
Intravenous Furosemide or Bumetanide is used in a single high dose (100-200 mg of Furosemide) to alter the course of ATN. These medicines should be given slowly because high doses can result in hearing loss.
Two kinds of ATN are toxic and ischemic. Toxic ATN develops when tubular cells are exposed to a toxic substance (nephrotoxic ATN). Due to their rapid metabolism, tubular cells are susceptible to oxygen deprivation, resulting in ischemic ATN.
Last reviewed at:
10 Mar 2023 - 5 min read
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