Acute tubular necrosis (ATN), which occurs when a damage pattern occurs inside the kidney, is the most frequent reason for AKI (acute kidney injury). Tubular necrosis is a misnomer because actual cellular necrosis is typically mild and does not only affect protuberances.
The most common occurrence of acute tubular necrosis is in hospital admissions, which also have a higher risk of morbidity & fatality. Acute tubular necrosis is characterized by a pattern of trauma that involves death and damage to renal tubular cells.
An ischemia occurrence, a nephrotoxic process, or a combination of the two may be to blame for intrarenal vasoconstriction, which is also a direct result of medication toxicity.
Epidemiology
A sample of 618 patients in the (ICU with AKI participated in the ground-breaking PICARD (Program to improve care in acute renal disease) study, which was carried out at five American medical facilities.
Acute tubular necrosis due to ischemic reasons was found to be the documented etiology in 50 percent of cases of acute kidney failure, while nephrotoxic acute tubular necrosis was found to be the reported etiology in 25 percent of patients.
Acute tubular necrosis was shown to be the most common cause of AKI in 45 percent of hospitalized patients in multicentre Spanish research conducted in 13 tertiary care institutions in Madrid.
Anatomy
Pathophysiology
Reduced GFR is linked to acute tubular necrosis, which could result in 3 different ways that proximal tubules epithelial cells could be damaged:
Clinically, these damage patterns result in the following four phases:
Initiation
A sharp decline in GFR and an abrupt rise in creatinine levels & BUN values define the beginning phase.
Extension
The extension phase includes two significant occasions:
Continuous hypoxia after the ischemic episode
Inflammatory reaction
These occurrences are particularly evident in the kidney’s corticomedullary junction. The ischemic of the proximal tubules epithelial cell during this stage is brought on by injury to the renal vascular endothelium. The combination of apoptosis and necrosis causes the cells in the external medulla to sustain damage and die.
Cellular healing occurs when the blood flow in the external cortex layer nearly returns to normal. The GFR decreases when the lesion at the cortico-medullary junction (CMJ) develops because cytokines & chemokines are continuously released, worsening the inflammatory process.
Maintenance
Migration, apoptosis, cellular repair, & proliferation set up the maintenance stage to preserve cellular & tubule structure. As the cells heal and restructure, the cellular function gradually gets better. As the blood circulation returns to normal, intracellular equilibrium is established by the cells.
Recovery
The maintenance process continues in the recovery phase, during which epithelium polarity is restored, and cell differentiation proceeds, leading to an improvement in kidney function.
Etiology
Acute ischemia, toxic, or septic events can cause acute tubular necrosis.
ATN Caused by Ischemia
The spectrum of reasons for both ischemic ATN & prerenal azotemia is the same. Acute tubular ischemia can result from any factor that causes prerenal azotemia. Hypovolemic conditions such as vomiting, burns, diarrhea, dehydration, bleeding, renal losses from osmotic or diuretic diuresis & third fluid sequester are a few leading triggers. Impaired renal perfusion results from oedematous conditions such as cirrhosis and heart failure. Systemic vasodilation results from sepsis and anaphylaxis. ATN can also be brought on by coagulopathy, including disseminated intravascular coagulation.
ATN Caused by Nephrotoxic Agents
Many medications are excreted & metabolized by the kidney. ATN can result from certain of these medications’ extrinsic toxin-like behaviors, which can result in direct renal tubular injury or crystal-induced AKI. ATN can be brought on by medications such as amphotericin B, radiocontrast agents, sulfa medicines, acyclovir, aminoglycosides, calcineurin blockers (cyclosporine, tacrolimus), cisplatin, mammalian target of rapamycin mTOR blockers (temsirolimus, everolimus), ifosfamide, foscarnet.
Proteins containing heme pigments, like as hemoglobin & myoglobin, can act as endotoxins in one of three ways:
Resulting in kidney vasoconstriction, tubular blockage, and direct proximal tubular damage.
High cell turnover caused by crystals like uric acid and calcium phosphate stones might cause nephropathy when cancer treatment is still being administered.
When cancer treatment is still being used, high cell turnover brought on by crystals like calcium phosphate crystals & uric acid may result in nephropathy.
Acute Tubular Necrosis Caused by Sepsis
Because of systemic hypotension & kidney hypoperfusion, sepsis also contributes to the development of ATN. Endotoxemia, which causes AKI by constricting the blood vessels in the kidneys, and the production of inflammatory mediators, which increases the release of reactive oxygen species and causes renal damage, are two other pathways that remain poorly understood.
Genetics
Prognostic Factors
The underlying disease that causes ATN affects the death rate in people with the condition. Oliguria, male sex, inadequate nutrition, the requirement for mechanical breathing, seizures, stroke, & myocardial infarction acute are a few characteristics that contribute to poor survival in these patients.
As a result of the greater death rate in oliguric individuals compared to non-oliguric individuals, necrosis has been caused by a greater quantity of damage. Sepsis & surgical individuals have a high mortality rate (around 60%), which causes numerous organ failures.
Clinical History
Clinical History
The patient’s medical history is crucial in determining the cause of acute tubular necrosis (ATN), as it might identify potential contributing factors. The underlying issue of acute kidney damage (AKI) can frequently be determined by carefully reconstructing the past. The history frequently indicates nephrotoxic chemical exposure, hypotension, muscular necrosis, volume deficit, or sepsis.
ATN risk and severity are increased when several of them are present at once. Additionally, pre-existing diseases or drug use (such as multiple myeloma, NSAIDs, and diabetes mellitus) may aggravate renal dysfunction. Consequently, a complete medical and drug history may also be essential to the diagnosis.
Physical Examination
Physical examination
Physical examination results are frequently unimpressive, and regular laboratory tests occasionally reveal acute kidney damage (AKI) (i.e., increased BUN (blood urea nitrogen) and serum creatinine levels).
Findings may point to hypovolemia as a possible cause, such as low jugular venous return, skin turgor loss, dry mucous membranes, postural hypotension, and tachycardia.
Intra-abdominal hypertension & compartment syndrome may be raised as probable ATN caused by abdominal distension. Rhabdomyolysis, which can result in ATN and cause muscle pain, maybe the cause.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnosis
Medication-induced nephrotoxicity
Chronic renal disease
Tubulointerstitial nephritis
Azotemia
Acute glomerulonephritis
Acute renal injury
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
By identifying patients undergoing high-risk operations & possessing comorbidities such as cardiac failure, diabetes mellitus, atherosclerosis, CKD, and advanced cancer that might amplify the effects of ATN, the mainstay of care is the avoidance of ATN.
Some of the high-risk treatments & conditions include the following:
Hypovolemia
Major operations (heart bypass, vascular operation such as hepatobiliary surgery, urgent surgical investigation, surgery for a peripheral limb aortic aneurysm)
Sepsis
Severe burns
Pancreatitis
Hemorrhagic shock
Cardiogenic shock
Prevention of hypotension and hypovolemia, including stopping angiotensin II receptor inhibitors or ACEI in patients with low blood pressure, and optimization of fluid volume via IV fluids, including such crystalloids, to maintain optimal renal blood flow are interventions to reduce the risk of ATN in the aforementioned conditions.
Avoid using antibiotics such as aminoglycosides, amphotericin B vancomycin, tazobactam/piperacillin, radiocontrast medicines, and NSAIDs, as they can cause acute tubular necrosis. However, diuretics are not advised for the treatment of ATN in renal disease.
Diuretics are only used to control volume status: Guidelines for Improving Global Outcomes (KDIGO) 2012. In individuals with acute tubular necrosis, additional pharmaceuticals like fenoldopam, dopamine & atrial natriuretic peptide do not improve survival. The same indications apply to RRT (renal replacement therapy), which is utilized in cases of fluid overload resistant to hyperkalemia, diuretics symptoms of uremia, & metabolic acidosis. Continuous renal replacement therapy (CRRT) is the recommended treatment for critically unwell, hemodynamically unstable patients.
Acute tubular necrosis (ATN), which occurs when a damage pattern occurs inside the kidney, is the most frequent reason for AKI (acute kidney injury). Tubular necrosis is a misnomer because actual cellular necrosis is typically mild and does not only affect protuberances.
The most common occurrence of acute tubular necrosis is in hospital admissions, which also have a higher risk of morbidity & fatality. Acute tubular necrosis is characterized by a pattern of trauma that involves death and damage to renal tubular cells.
An ischemia occurrence, a nephrotoxic process, or a combination of the two may be to blame for intrarenal vasoconstriction, which is also a direct result of medication toxicity.
A sample of 618 patients in the (ICU with AKI participated in the ground-breaking PICARD (Program to improve care in acute renal disease) study, which was carried out at five American medical facilities.
Acute tubular necrosis due to ischemic reasons was found to be the documented etiology in 50 percent of cases of acute kidney failure, while nephrotoxic acute tubular necrosis was found to be the reported etiology in 25 percent of patients.
Acute tubular necrosis was shown to be the most common cause of AKI in 45 percent of hospitalized patients in multicentre Spanish research conducted in 13 tertiary care institutions in Madrid.
Reduced GFR is linked to acute tubular necrosis, which could result in 3 different ways that proximal tubules epithelial cells could be damaged:
Clinically, these damage patterns result in the following four phases:
Initiation
A sharp decline in GFR and an abrupt rise in creatinine levels & BUN values define the beginning phase.
Extension
The extension phase includes two significant occasions:
Continuous hypoxia after the ischemic episode
Inflammatory reaction
These occurrences are particularly evident in the kidney’s corticomedullary junction. The ischemic of the proximal tubules epithelial cell during this stage is brought on by injury to the renal vascular endothelium. The combination of apoptosis and necrosis causes the cells in the external medulla to sustain damage and die.
Cellular healing occurs when the blood flow in the external cortex layer nearly returns to normal. The GFR decreases when the lesion at the cortico-medullary junction (CMJ) develops because cytokines & chemokines are continuously released, worsening the inflammatory process.
Maintenance
Migration, apoptosis, cellular repair, & proliferation set up the maintenance stage to preserve cellular & tubule structure. As the cells heal and restructure, the cellular function gradually gets better. As the blood circulation returns to normal, intracellular equilibrium is established by the cells.
Recovery
The maintenance process continues in the recovery phase, during which epithelium polarity is restored, and cell differentiation proceeds, leading to an improvement in kidney function.
Acute ischemia, toxic, or septic events can cause acute tubular necrosis.
ATN Caused by Ischemia
The spectrum of reasons for both ischemic ATN & prerenal azotemia is the same. Acute tubular ischemia can result from any factor that causes prerenal azotemia. Hypovolemic conditions such as vomiting, burns, diarrhea, dehydration, bleeding, renal losses from osmotic or diuretic diuresis & third fluid sequester are a few leading triggers. Impaired renal perfusion results from oedematous conditions such as cirrhosis and heart failure. Systemic vasodilation results from sepsis and anaphylaxis. ATN can also be brought on by coagulopathy, including disseminated intravascular coagulation.
ATN Caused by Nephrotoxic Agents
Many medications are excreted & metabolized by the kidney. ATN can result from certain of these medications’ extrinsic toxin-like behaviors, which can result in direct renal tubular injury or crystal-induced AKI. ATN can be brought on by medications such as amphotericin B, radiocontrast agents, sulfa medicines, acyclovir, aminoglycosides, calcineurin blockers (cyclosporine, tacrolimus), cisplatin, mammalian target of rapamycin mTOR blockers (temsirolimus, everolimus), ifosfamide, foscarnet.
Proteins containing heme pigments, like as hemoglobin & myoglobin, can act as endotoxins in one of three ways:
Resulting in kidney vasoconstriction, tubular blockage, and direct proximal tubular damage.
High cell turnover caused by crystals like uric acid and calcium phosphate stones might cause nephropathy when cancer treatment is still being administered.
When cancer treatment is still being used, high cell turnover brought on by crystals like calcium phosphate crystals & uric acid may result in nephropathy.
Acute Tubular Necrosis Caused by Sepsis
Because of systemic hypotension & kidney hypoperfusion, sepsis also contributes to the development of ATN. Endotoxemia, which causes AKI by constricting the blood vessels in the kidneys, and the production of inflammatory mediators, which increases the release of reactive oxygen species and causes renal damage, are two other pathways that remain poorly understood.
The underlying disease that causes ATN affects the death rate in people with the condition. Oliguria, male sex, inadequate nutrition, the requirement for mechanical breathing, seizures, stroke, & myocardial infarction acute are a few characteristics that contribute to poor survival in these patients.
As a result of the greater death rate in oliguric individuals compared to non-oliguric individuals, necrosis has been caused by a greater quantity of damage. Sepsis & surgical individuals have a high mortality rate (around 60%), which causes numerous organ failures.
Clinical History
The patient’s medical history is crucial in determining the cause of acute tubular necrosis (ATN), as it might identify potential contributing factors. The underlying issue of acute kidney damage (AKI) can frequently be determined by carefully reconstructing the past. The history frequently indicates nephrotoxic chemical exposure, hypotension, muscular necrosis, volume deficit, or sepsis.
ATN risk and severity are increased when several of them are present at once. Additionally, pre-existing diseases or drug use (such as multiple myeloma, NSAIDs, and diabetes mellitus) may aggravate renal dysfunction. Consequently, a complete medical and drug history may also be essential to the diagnosis.
Physical examination
Physical examination results are frequently unimpressive, and regular laboratory tests occasionally reveal acute kidney damage (AKI) (i.e., increased BUN (blood urea nitrogen) and serum creatinine levels).
Findings may point to hypovolemia as a possible cause, such as low jugular venous return, skin turgor loss, dry mucous membranes, postural hypotension, and tachycardia.
Intra-abdominal hypertension & compartment syndrome may be raised as probable ATN caused by abdominal distension. Rhabdomyolysis, which can result in ATN and cause muscle pain, maybe the cause.
Differential Diagnosis
Medication-induced nephrotoxicity
Chronic renal disease
Tubulointerstitial nephritis
Azotemia
Acute glomerulonephritis
Acute renal injury
By identifying patients undergoing high-risk operations & possessing comorbidities such as cardiac failure, diabetes mellitus, atherosclerosis, CKD, and advanced cancer that might amplify the effects of ATN, the mainstay of care is the avoidance of ATN.
Some of the high-risk treatments & conditions include the following:
Hypovolemia
Major operations (heart bypass, vascular operation such as hepatobiliary surgery, urgent surgical investigation, surgery for a peripheral limb aortic aneurysm)
Sepsis
Severe burns
Pancreatitis
Hemorrhagic shock
Cardiogenic shock
Prevention of hypotension and hypovolemia, including stopping angiotensin II receptor inhibitors or ACEI in patients with low blood pressure, and optimization of fluid volume via IV fluids, including such crystalloids, to maintain optimal renal blood flow are interventions to reduce the risk of ATN in the aforementioned conditions.
Avoid using antibiotics such as aminoglycosides, amphotericin B vancomycin, tazobactam/piperacillin, radiocontrast medicines, and NSAIDs, as they can cause acute tubular necrosis. However, diuretics are not advised for the treatment of ATN in renal disease.
Diuretics are only used to control volume status: Guidelines for Improving Global Outcomes (KDIGO) 2012. In individuals with acute tubular necrosis, additional pharmaceuticals like fenoldopam, dopamine & atrial natriuretic peptide do not improve survival. The same indications apply to RRT (renal replacement therapy), which is utilized in cases of fluid overload resistant to hyperkalemia, diuretics symptoms of uremia, & metabolic acidosis. Continuous renal replacement therapy (CRRT) is the recommended treatment for critically unwell, hemodynamically unstable patients.
Acute tubular necrosis (ATN), which occurs when a damage pattern occurs inside the kidney, is the most frequent reason for AKI (acute kidney injury). Tubular necrosis is a misnomer because actual cellular necrosis is typically mild and does not only affect protuberances.
The most common occurrence of acute tubular necrosis is in hospital admissions, which also have a higher risk of morbidity & fatality. Acute tubular necrosis is characterized by a pattern of trauma that involves death and damage to renal tubular cells.
An ischemia occurrence, a nephrotoxic process, or a combination of the two may be to blame for intrarenal vasoconstriction, which is also a direct result of medication toxicity.
A sample of 618 patients in the (ICU with AKI participated in the ground-breaking PICARD (Program to improve care in acute renal disease) study, which was carried out at five American medical facilities.
Acute tubular necrosis due to ischemic reasons was found to be the documented etiology in 50 percent of cases of acute kidney failure, while nephrotoxic acute tubular necrosis was found to be the reported etiology in 25 percent of patients.
Acute tubular necrosis was shown to be the most common cause of AKI in 45 percent of hospitalized patients in multicentre Spanish research conducted in 13 tertiary care institutions in Madrid.
Reduced GFR is linked to acute tubular necrosis, which could result in 3 different ways that proximal tubules epithelial cells could be damaged:
Clinically, these damage patterns result in the following four phases:
Initiation
A sharp decline in GFR and an abrupt rise in creatinine levels & BUN values define the beginning phase.
Extension
The extension phase includes two significant occasions:
Continuous hypoxia after the ischemic episode
Inflammatory reaction
These occurrences are particularly evident in the kidney’s corticomedullary junction. The ischemic of the proximal tubules epithelial cell during this stage is brought on by injury to the renal vascular endothelium. The combination of apoptosis and necrosis causes the cells in the external medulla to sustain damage and die.
Cellular healing occurs when the blood flow in the external cortex layer nearly returns to normal. The GFR decreases when the lesion at the cortico-medullary junction (CMJ) develops because cytokines & chemokines are continuously released, worsening the inflammatory process.
Maintenance
Migration, apoptosis, cellular repair, & proliferation set up the maintenance stage to preserve cellular & tubule structure. As the cells heal and restructure, the cellular function gradually gets better. As the blood circulation returns to normal, intracellular equilibrium is established by the cells.
Recovery
The maintenance process continues in the recovery phase, during which epithelium polarity is restored, and cell differentiation proceeds, leading to an improvement in kidney function.
Acute ischemia, toxic, or septic events can cause acute tubular necrosis.
ATN Caused by Ischemia
The spectrum of reasons for both ischemic ATN & prerenal azotemia is the same. Acute tubular ischemia can result from any factor that causes prerenal azotemia. Hypovolemic conditions such as vomiting, burns, diarrhea, dehydration, bleeding, renal losses from osmotic or diuretic diuresis & third fluid sequester are a few leading triggers. Impaired renal perfusion results from oedematous conditions such as cirrhosis and heart failure. Systemic vasodilation results from sepsis and anaphylaxis. ATN can also be brought on by coagulopathy, including disseminated intravascular coagulation.
ATN Caused by Nephrotoxic Agents
Many medications are excreted & metabolized by the kidney. ATN can result from certain of these medications’ extrinsic toxin-like behaviors, which can result in direct renal tubular injury or crystal-induced AKI. ATN can be brought on by medications such as amphotericin B, radiocontrast agents, sulfa medicines, acyclovir, aminoglycosides, calcineurin blockers (cyclosporine, tacrolimus), cisplatin, mammalian target of rapamycin mTOR blockers (temsirolimus, everolimus), ifosfamide, foscarnet.
Proteins containing heme pigments, like as hemoglobin & myoglobin, can act as endotoxins in one of three ways:
Resulting in kidney vasoconstriction, tubular blockage, and direct proximal tubular damage.
High cell turnover caused by crystals like uric acid and calcium phosphate stones might cause nephropathy when cancer treatment is still being administered.
When cancer treatment is still being used, high cell turnover brought on by crystals like calcium phosphate crystals & uric acid may result in nephropathy.
Acute Tubular Necrosis Caused by Sepsis
Because of systemic hypotension & kidney hypoperfusion, sepsis also contributes to the development of ATN. Endotoxemia, which causes AKI by constricting the blood vessels in the kidneys, and the production of inflammatory mediators, which increases the release of reactive oxygen species and causes renal damage, are two other pathways that remain poorly understood.
The underlying disease that causes ATN affects the death rate in people with the condition. Oliguria, male sex, inadequate nutrition, the requirement for mechanical breathing, seizures, stroke, & myocardial infarction acute are a few characteristics that contribute to poor survival in these patients.
As a result of the greater death rate in oliguric individuals compared to non-oliguric individuals, necrosis has been caused by a greater quantity of damage. Sepsis & surgical individuals have a high mortality rate (around 60%), which causes numerous organ failures.
Clinical History
The patient’s medical history is crucial in determining the cause of acute tubular necrosis (ATN), as it might identify potential contributing factors. The underlying issue of acute kidney damage (AKI) can frequently be determined by carefully reconstructing the past. The history frequently indicates nephrotoxic chemical exposure, hypotension, muscular necrosis, volume deficit, or sepsis.
ATN risk and severity are increased when several of them are present at once. Additionally, pre-existing diseases or drug use (such as multiple myeloma, NSAIDs, and diabetes mellitus) may aggravate renal dysfunction. Consequently, a complete medical and drug history may also be essential to the diagnosis.
Physical examination
Physical examination results are frequently unimpressive, and regular laboratory tests occasionally reveal acute kidney damage (AKI) (i.e., increased BUN (blood urea nitrogen) and serum creatinine levels).
Findings may point to hypovolemia as a possible cause, such as low jugular venous return, skin turgor loss, dry mucous membranes, postural hypotension, and tachycardia.
Intra-abdominal hypertension & compartment syndrome may be raised as probable ATN caused by abdominal distension. Rhabdomyolysis, which can result in ATN and cause muscle pain, maybe the cause.
Differential Diagnosis
Medication-induced nephrotoxicity
Chronic renal disease
Tubulointerstitial nephritis
Azotemia
Acute glomerulonephritis
Acute renal injury
By identifying patients undergoing high-risk operations & possessing comorbidities such as cardiac failure, diabetes mellitus, atherosclerosis, CKD, and advanced cancer that might amplify the effects of ATN, the mainstay of care is the avoidance of ATN.
Some of the high-risk treatments & conditions include the following:
Hypovolemia
Major operations (heart bypass, vascular operation such as hepatobiliary surgery, urgent surgical investigation, surgery for a peripheral limb aortic aneurysm)
Sepsis
Severe burns
Pancreatitis
Hemorrhagic shock
Cardiogenic shock
Prevention of hypotension and hypovolemia, including stopping angiotensin II receptor inhibitors or ACEI in patients with low blood pressure, and optimization of fluid volume via IV fluids, including such crystalloids, to maintain optimal renal blood flow are interventions to reduce the risk of ATN in the aforementioned conditions.
Avoid using antibiotics such as aminoglycosides, amphotericin B vancomycin, tazobactam/piperacillin, radiocontrast medicines, and NSAIDs, as they can cause acute tubular necrosis. However, diuretics are not advised for the treatment of ATN in renal disease.
Diuretics are only used to control volume status: Guidelines for Improving Global Outcomes (KDIGO) 2012. In individuals with acute tubular necrosis, additional pharmaceuticals like fenoldopam, dopamine & atrial natriuretic peptide do not improve survival. The same indications apply to RRT (renal replacement therapy), which is utilized in cases of fluid overload resistant to hyperkalemia, diuretics symptoms of uremia, & metabolic acidosis. Continuous renal replacement therapy (CRRT) is the recommended treatment for critically unwell, hemodynamically unstable patients.
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