Acute kidney injury (AKI) is a sudden decline in kidney function, which can cause an imbalance in the mineral composition and build-up of fluid and waste products in the body.
It can be caused by various factors, like reduced blood flow to the kidneys from dehydration, blood loss, trauma, medications or toxins, and other autoimmune or systemic conditions.
AKI is more common in hospitalized patients, particularly those critically ill or with underlying health conditions such as diabetes or high blood pressure. AKI can be treated and reversed in some cases; in others, it can lead to permanent kidney damage or failure.
Epidemiology
Acute kidney injury is a common condition that affects individuals of all ages and occurs both in the community and hospital settings. The incidence is highest in critically ill patients (about 40%) and up to 7% in noncritically ill patients in the hospital and those with underlying chronic kidney disease.
The majority of cases occur in the setting of surgery, with an estimated incidence of up to 20%. AKI is also more common in older adults and the presence of comorbidities such as hypertension, diabetes, and heart disease. The incidence of AKI is also higher in specific ethnic populations, such as African Americans and Native Americans.
Anatomy
Pathophysiology
The pathophysiology of acute kidney injury is complex and multifactorial. The main mechanisms leading to AKI can be divided into three categories: prerenal, intrinsic, and post-renal. Prerenal AKI occurs as a result of decreased blood flow to the kidneys. This can be caused by conditions such as dehydration from vomiting, diarrhea, blood loss, sepsis, heart failure, or cardiac failure, which reduces the perfusion pressure in the kidneys.
This leads to a decrease in the glomerular filtration rate (GFR) and can lead to the accumulation of waste products in the bloodstream. Intrinsic AKI is caused by damage to the kidney’s renal parenchyma or functional tissue. This can occur due to conditions such as acute tubular necrosis (ATN), the most common cause of intrinsic AKI.
ATN is caused by various factors, including ischemia, nephrotoxins, and sepsis, which can cause injury and death of renal tubular cells, resulting in decreased GFR. Another important cause of intrinsic AKI is allergic interstitial nephritis due to a local allergic reaction to medications, such as antibiotics, nonsteroidal inflammatory drugs, or viruses.
Obstruction of the urine flow from the kidneys causes post-renal AKI. This can occur due to obstruction of the ureters, bladder, or urethra, leading to a backup of urine and a decrease in GFR. Some examples of post-renal AKI include kidney stones, ureteral stenosis, strictures from previous surgery or radiation, and obstruction from benign prostatic hypertrophy or prostate cancer.
Etiology
The acute prerenal kidney injury is caused by reduced blood flow to the kidneys. This can be due to systemic hypoperfusion, such as from hypovolemia or hypotension, or it can be due to selective hypoperfusion of the kidneys, such as from renal artery stenosis or aortic dissection. Prerenal AKI is characterized by normal tubular and glomerular function and can be caused by various factors, including hypovolemia, hypotension, septic shock, anaphylaxis, and certain medications.
Various factors, including trauma or unaccustomed exertion, blood loss or transfusions, exposure to toxic substances like alcohol or ethylene glycol, and heavy metals like mercury, lead, and cadmium, can cause AKI. These heavy metals can be found in occupational settings such as welding and mining and can drive AKI in workers exposed to them.
It is important to consider all possible causes of AKI. Identifying and addressing the underlying cause of prerenal AKI is important to treat and manage the condition effectively.
Genetics
Prognostic Factors
The prognosis of acute kidney injury depends on diverse factors, including the underlying cause, the severity of the injury, and the patient’s overall health status. The prognosis for AKI is generally better for patients with prerenal and postrenal causes than those with intrinsic causes.
In patients with prerenal and postrenal causes of AKI, the prognosis is generally good if the underlying cause is identified and treated promptly. Most patients with prerenal and postrenal causes recover their kidney function without any long-term complications. In patients with intrinsic causes of AKI, the prognosis is generally less favorable.
Intrinsic causes of AKI are often more severe and can lead to permanent loss of kidney function. Recovery of kidney function can be slow, and some patients may require dialysis or kidney transplantation.
Clinical History
Clinical History
When evaluating a patient for AKI, it is important to note their history of urine output and medications. Oliguria, or decreased urine output, is a strong indicator of AKI. Sudden anuria, or complete lack of urine output, can suggest several serious causes, such as acute urinary tract obstruction, acute glomerulonephritis (inflammation of the kidneys), or vascular catastrophe.
On the other hand, a gradually diminishing urine output may be caused by more chronic issues such as urethral stricture or bladder outlet obstruction caused by conditions such as prostate enlargement. Overall, monitoring urine output can provide valuable clues to determine the underlying cause of AKI.
Differentiating AKI from chronic kidney disease (CKD) is crucial, but it can be challenging. This is because CKD is a significant risk factor for AKI. A patient with a history of prolonged symptoms such as fatigue, weight loss, anorexia, nocturia, sleep disturbance, and pruritus is likely to suffer from chronic kidney disease.
However, AKI can also cause similar symptoms over a shorter period. Therefore, it is important to carefully consider the symptoms’ duration and nature when distinguishing between AKI and CKD.
Physical Examination
Physical Examination
During an abdominal examination, certain findings can help identify obstruction at the bladder outlet as a possible cause of AKI. This obstruction can be caused by cancer or an enlarged prostate. The presence of tense ascites can also suggest elevated intra-abdominal pressure, which can impede renal venous return and lead to AKI. If an epigastric bruit is present, it may indicate renal vascular hypertension, increasing the risk of AKI.
Furthermore, on physical examination, specific cutaneous changes like livido reticularis, digital ischemia, butterfly rash, and palpable purpura could indicate systemic vasculitis. A maculopapular rash can indicate allergic interstitial nephritis, and track marks can indicate endocarditis, all possible causes of AKI.
Petechiae, purpura, ecchymosis, and livedo reticularis can also provide clues to AKI’s inflammatory and vascular causes. Infectious diseases can cause these cutaneous changes, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation DIC, and embolic phenomena, all potential causes of AKI. A thorough examination, including abdominal and physical examinations, can provide clues to the underlying cause of AKI.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnoses
Sickle cell anemia
Renal calculi
Dehydration
Heart failure
Diabetic ketoacidosis
Urinary tract infection
Protein overloading
Chronic renal failure
Gastrointestinal bleeding
Urinary obstruction
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
It is crucial to address the underlying causes of acute kidney injury as soon as kidney dysfunction is detected. The relationship between glomerular filtration rate and serum creatinine level is not linear, particularly in the early stages of the disease, so an abnormal increase in serum creatinine may only be evident when 50% of GFR is lost.
It is important to note that the current treatment for AKI is mainly supportive. The main goals of treatment are to maintain volume homeostasis and correct biochemical abnormalities, which can include measures such as correcting fluid overload with furosemide, correcting severe acidosis with bicarbonate administration, correcting hyperkalemia, and correcting hematologic abnormalities like anemia and uremic platelet dysfunction with transfusions or administration of desmopressin or estrogens.
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Media Gallary
References
https://www.ncbi.nlm.nih.gov/books/NBK441896/
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Acute kidney injury (AKI) is a sudden decline in kidney function, which can cause an imbalance in the mineral composition and build-up of fluid and waste products in the body.
It can be caused by various factors, like reduced blood flow to the kidneys from dehydration, blood loss, trauma, medications or toxins, and other autoimmune or systemic conditions.
AKI is more common in hospitalized patients, particularly those critically ill or with underlying health conditions such as diabetes or high blood pressure. AKI can be treated and reversed in some cases; in others, it can lead to permanent kidney damage or failure.
Acute kidney injury is a common condition that affects individuals of all ages and occurs both in the community and hospital settings. The incidence is highest in critically ill patients (about 40%) and up to 7% in noncritically ill patients in the hospital and those with underlying chronic kidney disease.
The majority of cases occur in the setting of surgery, with an estimated incidence of up to 20%. AKI is also more common in older adults and the presence of comorbidities such as hypertension, diabetes, and heart disease. The incidence of AKI is also higher in specific ethnic populations, such as African Americans and Native Americans.
The pathophysiology of acute kidney injury is complex and multifactorial. The main mechanisms leading to AKI can be divided into three categories: prerenal, intrinsic, and post-renal. Prerenal AKI occurs as a result of decreased blood flow to the kidneys. This can be caused by conditions such as dehydration from vomiting, diarrhea, blood loss, sepsis, heart failure, or cardiac failure, which reduces the perfusion pressure in the kidneys.
This leads to a decrease in the glomerular filtration rate (GFR) and can lead to the accumulation of waste products in the bloodstream. Intrinsic AKI is caused by damage to the kidney’s renal parenchyma or functional tissue. This can occur due to conditions such as acute tubular necrosis (ATN), the most common cause of intrinsic AKI.
ATN is caused by various factors, including ischemia, nephrotoxins, and sepsis, which can cause injury and death of renal tubular cells, resulting in decreased GFR. Another important cause of intrinsic AKI is allergic interstitial nephritis due to a local allergic reaction to medications, such as antibiotics, nonsteroidal inflammatory drugs, or viruses.
Obstruction of the urine flow from the kidneys causes post-renal AKI. This can occur due to obstruction of the ureters, bladder, or urethra, leading to a backup of urine and a decrease in GFR. Some examples of post-renal AKI include kidney stones, ureteral stenosis, strictures from previous surgery or radiation, and obstruction from benign prostatic hypertrophy or prostate cancer.
The acute prerenal kidney injury is caused by reduced blood flow to the kidneys. This can be due to systemic hypoperfusion, such as from hypovolemia or hypotension, or it can be due to selective hypoperfusion of the kidneys, such as from renal artery stenosis or aortic dissection. Prerenal AKI is characterized by normal tubular and glomerular function and can be caused by various factors, including hypovolemia, hypotension, septic shock, anaphylaxis, and certain medications.
Various factors, including trauma or unaccustomed exertion, blood loss or transfusions, exposure to toxic substances like alcohol or ethylene glycol, and heavy metals like mercury, lead, and cadmium, can cause AKI. These heavy metals can be found in occupational settings such as welding and mining and can drive AKI in workers exposed to them.
It is important to consider all possible causes of AKI. Identifying and addressing the underlying cause of prerenal AKI is important to treat and manage the condition effectively.
The prognosis of acute kidney injury depends on diverse factors, including the underlying cause, the severity of the injury, and the patient’s overall health status. The prognosis for AKI is generally better for patients with prerenal and postrenal causes than those with intrinsic causes.
In patients with prerenal and postrenal causes of AKI, the prognosis is generally good if the underlying cause is identified and treated promptly. Most patients with prerenal and postrenal causes recover their kidney function without any long-term complications. In patients with intrinsic causes of AKI, the prognosis is generally less favorable.
Intrinsic causes of AKI are often more severe and can lead to permanent loss of kidney function. Recovery of kidney function can be slow, and some patients may require dialysis or kidney transplantation.
Clinical History
When evaluating a patient for AKI, it is important to note their history of urine output and medications. Oliguria, or decreased urine output, is a strong indicator of AKI. Sudden anuria, or complete lack of urine output, can suggest several serious causes, such as acute urinary tract obstruction, acute glomerulonephritis (inflammation of the kidneys), or vascular catastrophe.
On the other hand, a gradually diminishing urine output may be caused by more chronic issues such as urethral stricture or bladder outlet obstruction caused by conditions such as prostate enlargement. Overall, monitoring urine output can provide valuable clues to determine the underlying cause of AKI.
Differentiating AKI from chronic kidney disease (CKD) is crucial, but it can be challenging. This is because CKD is a significant risk factor for AKI. A patient with a history of prolonged symptoms such as fatigue, weight loss, anorexia, nocturia, sleep disturbance, and pruritus is likely to suffer from chronic kidney disease.
However, AKI can also cause similar symptoms over a shorter period. Therefore, it is important to carefully consider the symptoms’ duration and nature when distinguishing between AKI and CKD.
Physical Examination
During an abdominal examination, certain findings can help identify obstruction at the bladder outlet as a possible cause of AKI. This obstruction can be caused by cancer or an enlarged prostate. The presence of tense ascites can also suggest elevated intra-abdominal pressure, which can impede renal venous return and lead to AKI. If an epigastric bruit is present, it may indicate renal vascular hypertension, increasing the risk of AKI.
Furthermore, on physical examination, specific cutaneous changes like livido reticularis, digital ischemia, butterfly rash, and palpable purpura could indicate systemic vasculitis. A maculopapular rash can indicate allergic interstitial nephritis, and track marks can indicate endocarditis, all possible causes of AKI.
Petechiae, purpura, ecchymosis, and livedo reticularis can also provide clues to AKI’s inflammatory and vascular causes. Infectious diseases can cause these cutaneous changes, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation DIC, and embolic phenomena, all potential causes of AKI. A thorough examination, including abdominal and physical examinations, can provide clues to the underlying cause of AKI.
Differential Diagnoses
Sickle cell anemia
Renal calculi
Dehydration
Heart failure
Diabetic ketoacidosis
Urinary tract infection
Protein overloading
Chronic renal failure
Gastrointestinal bleeding
Urinary obstruction
It is crucial to address the underlying causes of acute kidney injury as soon as kidney dysfunction is detected. The relationship between glomerular filtration rate and serum creatinine level is not linear, particularly in the early stages of the disease, so an abnormal increase in serum creatinine may only be evident when 50% of GFR is lost.
It is important to note that the current treatment for AKI is mainly supportive. The main goals of treatment are to maintain volume homeostasis and correct biochemical abnormalities, which can include measures such as correcting fluid overload with furosemide, correcting severe acidosis with bicarbonate administration, correcting hyperkalemia, and correcting hematologic abnormalities like anemia and uremic platelet dysfunction with transfusions or administration of desmopressin or estrogens.
https://www.ncbi.nlm.nih.gov/books/NBK441896/
medtigo
Acute Kidney Injury (AKI)
Updated :
January 20, 2023
Acute kidney injury (AKI) is a sudden decline in kidney function, which can cause an imbalance in the mineral composition and build-up of fluid and waste products in the body.
It can be caused by various factors, like reduced blood flow to the kidneys from dehydration, blood loss, trauma, medications or toxins, and other autoimmune or systemic conditions.
AKI is more common in hospitalized patients, particularly those critically ill or with underlying health conditions such as diabetes or high blood pressure. AKI can be treated and reversed in some cases; in others, it can lead to permanent kidney damage or failure.
Acute kidney injury is a common condition that affects individuals of all ages and occurs both in the community and hospital settings. The incidence is highest in critically ill patients (about 40%) and up to 7% in noncritically ill patients in the hospital and those with underlying chronic kidney disease.
The majority of cases occur in the setting of surgery, with an estimated incidence of up to 20%. AKI is also more common in older adults and the presence of comorbidities such as hypertension, diabetes, and heart disease. The incidence of AKI is also higher in specific ethnic populations, such as African Americans and Native Americans.
The pathophysiology of acute kidney injury is complex and multifactorial. The main mechanisms leading to AKI can be divided into three categories: prerenal, intrinsic, and post-renal. Prerenal AKI occurs as a result of decreased blood flow to the kidneys. This can be caused by conditions such as dehydration from vomiting, diarrhea, blood loss, sepsis, heart failure, or cardiac failure, which reduces the perfusion pressure in the kidneys.
This leads to a decrease in the glomerular filtration rate (GFR) and can lead to the accumulation of waste products in the bloodstream. Intrinsic AKI is caused by damage to the kidney’s renal parenchyma or functional tissue. This can occur due to conditions such as acute tubular necrosis (ATN), the most common cause of intrinsic AKI.
ATN is caused by various factors, including ischemia, nephrotoxins, and sepsis, which can cause injury and death of renal tubular cells, resulting in decreased GFR. Another important cause of intrinsic AKI is allergic interstitial nephritis due to a local allergic reaction to medications, such as antibiotics, nonsteroidal inflammatory drugs, or viruses.
Obstruction of the urine flow from the kidneys causes post-renal AKI. This can occur due to obstruction of the ureters, bladder, or urethra, leading to a backup of urine and a decrease in GFR. Some examples of post-renal AKI include kidney stones, ureteral stenosis, strictures from previous surgery or radiation, and obstruction from benign prostatic hypertrophy or prostate cancer.
The acute prerenal kidney injury is caused by reduced blood flow to the kidneys. This can be due to systemic hypoperfusion, such as from hypovolemia or hypotension, or it can be due to selective hypoperfusion of the kidneys, such as from renal artery stenosis or aortic dissection. Prerenal AKI is characterized by normal tubular and glomerular function and can be caused by various factors, including hypovolemia, hypotension, septic shock, anaphylaxis, and certain medications.
Various factors, including trauma or unaccustomed exertion, blood loss or transfusions, exposure to toxic substances like alcohol or ethylene glycol, and heavy metals like mercury, lead, and cadmium, can cause AKI. These heavy metals can be found in occupational settings such as welding and mining and can drive AKI in workers exposed to them.
It is important to consider all possible causes of AKI. Identifying and addressing the underlying cause of prerenal AKI is important to treat and manage the condition effectively.
The prognosis of acute kidney injury depends on diverse factors, including the underlying cause, the severity of the injury, and the patient’s overall health status. The prognosis for AKI is generally better for patients with prerenal and postrenal causes than those with intrinsic causes.
In patients with prerenal and postrenal causes of AKI, the prognosis is generally good if the underlying cause is identified and treated promptly. Most patients with prerenal and postrenal causes recover their kidney function without any long-term complications. In patients with intrinsic causes of AKI, the prognosis is generally less favorable.
Intrinsic causes of AKI are often more severe and can lead to permanent loss of kidney function. Recovery of kidney function can be slow, and some patients may require dialysis or kidney transplantation.
Clinical History
When evaluating a patient for AKI, it is important to note their history of urine output and medications. Oliguria, or decreased urine output, is a strong indicator of AKI. Sudden anuria, or complete lack of urine output, can suggest several serious causes, such as acute urinary tract obstruction, acute glomerulonephritis (inflammation of the kidneys), or vascular catastrophe.
On the other hand, a gradually diminishing urine output may be caused by more chronic issues such as urethral stricture or bladder outlet obstruction caused by conditions such as prostate enlargement. Overall, monitoring urine output can provide valuable clues to determine the underlying cause of AKI.
Differentiating AKI from chronic kidney disease (CKD) is crucial, but it can be challenging. This is because CKD is a significant risk factor for AKI. A patient with a history of prolonged symptoms such as fatigue, weight loss, anorexia, nocturia, sleep disturbance, and pruritus is likely to suffer from chronic kidney disease.
However, AKI can also cause similar symptoms over a shorter period. Therefore, it is important to carefully consider the symptoms’ duration and nature when distinguishing between AKI and CKD.
Physical Examination
During an abdominal examination, certain findings can help identify obstruction at the bladder outlet as a possible cause of AKI. This obstruction can be caused by cancer or an enlarged prostate. The presence of tense ascites can also suggest elevated intra-abdominal pressure, which can impede renal venous return and lead to AKI. If an epigastric bruit is present, it may indicate renal vascular hypertension, increasing the risk of AKI.
Furthermore, on physical examination, specific cutaneous changes like livido reticularis, digital ischemia, butterfly rash, and palpable purpura could indicate systemic vasculitis. A maculopapular rash can indicate allergic interstitial nephritis, and track marks can indicate endocarditis, all possible causes of AKI.
Petechiae, purpura, ecchymosis, and livedo reticularis can also provide clues to AKI’s inflammatory and vascular causes. Infectious diseases can cause these cutaneous changes, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation DIC, and embolic phenomena, all potential causes of AKI. A thorough examination, including abdominal and physical examinations, can provide clues to the underlying cause of AKI.
Differential Diagnoses
Sickle cell anemia
Renal calculi
Dehydration
Heart failure
Diabetic ketoacidosis
Urinary tract infection
Protein overloading
Chronic renal failure
Gastrointestinal bleeding
Urinary obstruction
It is crucial to address the underlying causes of acute kidney injury as soon as kidney dysfunction is detected. The relationship between glomerular filtration rate and serum creatinine level is not linear, particularly in the early stages of the disease, so an abnormal increase in serum creatinine may only be evident when 50% of GFR is lost.
It is important to note that the current treatment for AKI is mainly supportive. The main goals of treatment are to maintain volume homeostasis and correct biochemical abnormalities, which can include measures such as correcting fluid overload with furosemide, correcting severe acidosis with bicarbonate administration, correcting hyperkalemia, and correcting hematologic abnormalities like anemia and uremic platelet dysfunction with transfusions or administration of desmopressin or estrogens.
https://www.ncbi.nlm.nih.gov/books/NBK441896/
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