Contrast-induced nephropathy (CIN) is a severe outcome that can occur after undergoing angiographic procedures involving the injection of contrast media (CM). It ranks as the third leading cause of hospital-acquired acute renal damage, accounting for approximately 12% of such cases. CIN is diagnosed when there is a noticeable increase in serum creatinine levels.
Currently, it is understood as a decline in renal function characterized by either a 25% increase in serum creatinine levels from baseline or a rise of 0.5 mg/dL in absolute serum creatinine within 48-72 hours after receiving an intravenous contrast medium. This contrast is crucial in performing invasive cardiac procedures such as coronary angiography and interventional procedures.
However, the growing use of contrast media in these procedures, especially in patients with pre-existing conditions such as chronic kidney disease, diabetes, hypertension, and kidney failure, has led to an increase in CIN cases. This sudden change in kidney function is a frequent side effect of coronary angiography and percutaneous coronary intervention, primarily due to contrast-induced acute kidney injury or contrast-induced nephropathy.
Epidemiology
The occurrence of diabetes and chronic kidney disease is on the rise, and these are major risk factors for acute kidney injury that may arise from percutaneous coronary interventions and cardiac catheterization. The incidence of contrast-induced nephropathy ranges up to 30%, depending on the definition used. Most cases are reversible within a span of 2 to 4 weeks. The requirement for renal replacement therapy is uncommon, occurring in just 1% to 4% of cases, and out of these, fewer than 50% require long-term treatment.
The general population is estimated to have an incidence rate of over 2% for contrast-induced nephropathy. However, in groups with high-risk factors for kidney disease, the incidence can be as high as 20% to 30%. The risk can be reduced by using low osmolar contrast media. It is the third leading cause of iatrogenic acute kidney injury and is primarily caused by hypoperfusion of the kidneys leading to prerenal injury or acute tubular necrosis.
The number and type of risk factors present significantly influence the incidence of renal impairment. The incidence rate may also vary depending on the procedure, with diagnostic investigations having an incidence rate of 1.6-2.3% and coronary interventions having an overall incidence rate of 14.5%. Patients over 60 are reported to have an incidence rate of 8% to 16%. Additionally, patients with acute myocardial infarction undergoing coronary intervention have been shown to have an increased risk of developing CIN if they are 75 years or older.
Anatomy
Pathophysiology
The exact mechanisms behind contrast-induced nephropathy are not fully understood. However, it is believed to involve a combination of factors such as hypoxia, ischemia, vasoconstriction, and toxic effects on the renal tubular cells. Certain medications and changes in blood flow can increase the risk of CIN, especially when the contrast is administered through an artery rather than a vein. For example, metformin use can lead to lactic acidosis in the presence of kidney dysfunction or injury.
The FDA advises stopping metformin before and after a contrast media procedure. Other causes of CIN include air bubbles from catheters that obstruct the renal microvasculature and cholesterol atheroembolism, which can result in laboratory abnormalities such as eosinophilia and acute kidney injury. Contrast media can cause constriction of blood vessels through its direct impact on smooth muscle and by producing metabolites like endothelin and adenosine.
It also interferes with water reabsorption, leading to increased interstitial pressure, decreased glomerular filtration rate, and compression of blood vessels in the kidney. This exacerbates hypoxia and vasoconstriction in the kidneys, especially in patients who are already dehydrated. Additionally, contrast media can raise blood viscosity and decrease red blood cell flexibility, resulting in blockages and reducing blood flow, causing ischemia and activation of harmful reactive oxygen species that damage the tubular cells at a cellular level.
Etiology
Contrast-induced nephropathy is a condition that affects the kidneys and is caused by exposure to contrast media. It is most frequently seen in individuals with pre-existing chronic kidney disease, with an incidence of 8% for those with an estimated glomerular filtration rate of 45 to 60 mL/min/1.73m2, 13% for individuals with eGFR of 30 to 45 mL/min/1.73m2, and 27% for those with a GFR less than 30 mL/min/1.73m2.
Other factors that increase the risk of developing contrast-induced nephropathy include advanced age, heart failure, diabetes, female gender, hypertension, peripheral vascular disease, and a low left ventricular ejection fraction. Exposure to contrast media can harm different parts of the kidney and cause damage through several mechanisms, including a direct cytotoxic effect on the proximal tubules, increased production of reactive oxygen species, reduced blood flow in the kidney, and increased renal vasoconstriction.
Genetics
Prognostic Factors
A patient’s prognosis following the administration of contrast depends on various factors, including underlying medical conditions and the patient’s baseline renal function. Depending on the scoring system, there may be a chance of developing Contrast-Induced Nephropathy.
This condition is usually temporary and resolves within a week to two weeks. Although some residual renal impairment may persist in a small percentage of patients, it typically affects fewer than one-third of those who develop CIN.
Clinical History
Clinical History
Contrast-induced nephropathy is a type of acute kidney injury first documented by Bartel et al. in the 1950s. This condition is associated with a fatal outcome. It occurs when a patient experiences a sudden and temporary increase in creatine levels after receiving an intravenous injection of contrast medium during a diagnostic or therapeutic procedure, such as percutaneous coronary intervention. The incidence of CIN is reported to be around 15% in patients undergoing these types of procedures.
Patients who develop CIN typically have a preceding history of contrast administration, usually within 24-48 hours before presenting symptoms. The onset of CIN is usually non-oliguric in nature. It’s important to note that CIN can be prevented with proper screening and risk assessment before administering a contrast medium. This can include evaluating a patient’s creatinine levels and determining if there is a history of kidney disease or if the patient is taking certain medications that can affect kidney function.
Physical Examination
Physical Examination
Contrast-induced nephropathy is a condition where there is an increase in serum creatinine levels after exposure to contrast media. The traditional definition states that there must be a rise of at least 0.5 mg/dL or a 25% increase from the baseline level within 48 to 72 hours after the exposure. However, the Kidney Disease Improving Global Outcome (KDIGO) definition is more comprehensive.
According to KDIGO, stage 1 of contrast-induced nephropathy is defined as a rapid rise in creatinine levels to greater than 0.3 mg/dL within 48 hours or a relative increase of 50% or more from baseline in 7 days or less or a reduction in urine output to less than 0.5 ml/kg/hr for 6 to 12 hours. The severity of the condition is further staged based on the levels of creatinine, urine output, and the need for renal replacement therapy.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnosis
Acute renal failure
Acute tubular necrosis
Embolic renal disease
Interstitial nephritis
Renal artery stenosis
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Reducing the risk of contrast-induced nephropathy is an important consideration prior to undergoing a procedure that involves the use of contrast agents. The most common strategy for minimizing this risk is implementing a periprocedural hydration protocol for patients with chronic kidney disease. This involves initiating an intravenous (IV) fluid infusion with 0.9% normal saline at a rate of 1 ml/kg/hr for 6 to 12 hours before and continuing the infusion after the procedure.
Sometimes, a sliding scale IV hydration protocol based on left ventricular end-diastolic pressure is also used. Another strategy to reduce the risk of contrast-induced nephropathy is bicarbonate. Sodium bicarbonate, when infused at a rate of 3 mL/kg/hour an hour before the procedure and continued at a rate of 1 mL/kg/hour for six hours, can help alkalinize the renal tubular fluid, which slows down the Harber-Weiss reaction and helps scavenge reactive oxygen species from NO.
There is some debate surrounding the exact duration of the bicarbonate infusion, but some studies have shown that hydration with sodium bicarbonate is more effective than normal saline alone. Pre-treating patients with high-intensity statins prior to contrast use is also a reasonable approach. A meta-analysis observed that pre-treatment with rosuvastatin could significantly reduce the incidence of contrast-induced nephropathy. However, this strategy may not be effective for patients already suffering from chronic kidney disease who are undergoing elective cardiac catheterization.
Contrast-induced nephropathy (CIN) is a severe outcome that can occur after undergoing angiographic procedures involving the injection of contrast media (CM). It ranks as the third leading cause of hospital-acquired acute renal damage, accounting for approximately 12% of such cases. CIN is diagnosed when there is a noticeable increase in serum creatinine levels.
Currently, it is understood as a decline in renal function characterized by either a 25% increase in serum creatinine levels from baseline or a rise of 0.5 mg/dL in absolute serum creatinine within 48-72 hours after receiving an intravenous contrast medium. This contrast is crucial in performing invasive cardiac procedures such as coronary angiography and interventional procedures.
However, the growing use of contrast media in these procedures, especially in patients with pre-existing conditions such as chronic kidney disease, diabetes, hypertension, and kidney failure, has led to an increase in CIN cases. This sudden change in kidney function is a frequent side effect of coronary angiography and percutaneous coronary intervention, primarily due to contrast-induced acute kidney injury or contrast-induced nephropathy.
The occurrence of diabetes and chronic kidney disease is on the rise, and these are major risk factors for acute kidney injury that may arise from percutaneous coronary interventions and cardiac catheterization. The incidence of contrast-induced nephropathy ranges up to 30%, depending on the definition used. Most cases are reversible within a span of 2 to 4 weeks. The requirement for renal replacement therapy is uncommon, occurring in just 1% to 4% of cases, and out of these, fewer than 50% require long-term treatment.
The general population is estimated to have an incidence rate of over 2% for contrast-induced nephropathy. However, in groups with high-risk factors for kidney disease, the incidence can be as high as 20% to 30%. The risk can be reduced by using low osmolar contrast media. It is the third leading cause of iatrogenic acute kidney injury and is primarily caused by hypoperfusion of the kidneys leading to prerenal injury or acute tubular necrosis.
The number and type of risk factors present significantly influence the incidence of renal impairment. The incidence rate may also vary depending on the procedure, with diagnostic investigations having an incidence rate of 1.6-2.3% and coronary interventions having an overall incidence rate of 14.5%. Patients over 60 are reported to have an incidence rate of 8% to 16%. Additionally, patients with acute myocardial infarction undergoing coronary intervention have been shown to have an increased risk of developing CIN if they are 75 years or older.
The exact mechanisms behind contrast-induced nephropathy are not fully understood. However, it is believed to involve a combination of factors such as hypoxia, ischemia, vasoconstriction, and toxic effects on the renal tubular cells. Certain medications and changes in blood flow can increase the risk of CIN, especially when the contrast is administered through an artery rather than a vein. For example, metformin use can lead to lactic acidosis in the presence of kidney dysfunction or injury.
The FDA advises stopping metformin before and after a contrast media procedure. Other causes of CIN include air bubbles from catheters that obstruct the renal microvasculature and cholesterol atheroembolism, which can result in laboratory abnormalities such as eosinophilia and acute kidney injury. Contrast media can cause constriction of blood vessels through its direct impact on smooth muscle and by producing metabolites like endothelin and adenosine.
It also interferes with water reabsorption, leading to increased interstitial pressure, decreased glomerular filtration rate, and compression of blood vessels in the kidney. This exacerbates hypoxia and vasoconstriction in the kidneys, especially in patients who are already dehydrated. Additionally, contrast media can raise blood viscosity and decrease red blood cell flexibility, resulting in blockages and reducing blood flow, causing ischemia and activation of harmful reactive oxygen species that damage the tubular cells at a cellular level.
Contrast-induced nephropathy is a condition that affects the kidneys and is caused by exposure to contrast media. It is most frequently seen in individuals with pre-existing chronic kidney disease, with an incidence of 8% for those with an estimated glomerular filtration rate of 45 to 60 mL/min/1.73m2, 13% for individuals with eGFR of 30 to 45 mL/min/1.73m2, and 27% for those with a GFR less than 30 mL/min/1.73m2.
Other factors that increase the risk of developing contrast-induced nephropathy include advanced age, heart failure, diabetes, female gender, hypertension, peripheral vascular disease, and a low left ventricular ejection fraction. Exposure to contrast media can harm different parts of the kidney and cause damage through several mechanisms, including a direct cytotoxic effect on the proximal tubules, increased production of reactive oxygen species, reduced blood flow in the kidney, and increased renal vasoconstriction.
A patient’s prognosis following the administration of contrast depends on various factors, including underlying medical conditions and the patient’s baseline renal function. Depending on the scoring system, there may be a chance of developing Contrast-Induced Nephropathy.
This condition is usually temporary and resolves within a week to two weeks. Although some residual renal impairment may persist in a small percentage of patients, it typically affects fewer than one-third of those who develop CIN.
Clinical History
Contrast-induced nephropathy is a type of acute kidney injury first documented by Bartel et al. in the 1950s. This condition is associated with a fatal outcome. It occurs when a patient experiences a sudden and temporary increase in creatine levels after receiving an intravenous injection of contrast medium during a diagnostic or therapeutic procedure, such as percutaneous coronary intervention. The incidence of CIN is reported to be around 15% in patients undergoing these types of procedures.
Patients who develop CIN typically have a preceding history of contrast administration, usually within 24-48 hours before presenting symptoms. The onset of CIN is usually non-oliguric in nature. It’s important to note that CIN can be prevented with proper screening and risk assessment before administering a contrast medium. This can include evaluating a patient’s creatinine levels and determining if there is a history of kidney disease or if the patient is taking certain medications that can affect kidney function.
Physical Examination
Contrast-induced nephropathy is a condition where there is an increase in serum creatinine levels after exposure to contrast media. The traditional definition states that there must be a rise of at least 0.5 mg/dL or a 25% increase from the baseline level within 48 to 72 hours after the exposure. However, the Kidney Disease Improving Global Outcome (KDIGO) definition is more comprehensive.
According to KDIGO, stage 1 of contrast-induced nephropathy is defined as a rapid rise in creatinine levels to greater than 0.3 mg/dL within 48 hours or a relative increase of 50% or more from baseline in 7 days or less or a reduction in urine output to less than 0.5 ml/kg/hr for 6 to 12 hours. The severity of the condition is further staged based on the levels of creatinine, urine output, and the need for renal replacement therapy.
Differential Diagnosis
Acute renal failure
Acute tubular necrosis
Embolic renal disease
Interstitial nephritis
Renal artery stenosis
Reducing the risk of contrast-induced nephropathy is an important consideration prior to undergoing a procedure that involves the use of contrast agents. The most common strategy for minimizing this risk is implementing a periprocedural hydration protocol for patients with chronic kidney disease. This involves initiating an intravenous (IV) fluid infusion with 0.9% normal saline at a rate of 1 ml/kg/hr for 6 to 12 hours before and continuing the infusion after the procedure.
Sometimes, a sliding scale IV hydration protocol based on left ventricular end-diastolic pressure is also used. Another strategy to reduce the risk of contrast-induced nephropathy is bicarbonate. Sodium bicarbonate, when infused at a rate of 3 mL/kg/hour an hour before the procedure and continued at a rate of 1 mL/kg/hour for six hours, can help alkalinize the renal tubular fluid, which slows down the Harber-Weiss reaction and helps scavenge reactive oxygen species from NO.
There is some debate surrounding the exact duration of the bicarbonate infusion, but some studies have shown that hydration with sodium bicarbonate is more effective than normal saline alone. Pre-treating patients with high-intensity statins prior to contrast use is also a reasonable approach. A meta-analysis observed that pre-treatment with rosuvastatin could significantly reduce the incidence of contrast-induced nephropathy. However, this strategy may not be effective for patients already suffering from chronic kidney disease who are undergoing elective cardiac catheterization.
Contrast-induced nephropathy (CIN) is a severe outcome that can occur after undergoing angiographic procedures involving the injection of contrast media (CM). It ranks as the third leading cause of hospital-acquired acute renal damage, accounting for approximately 12% of such cases. CIN is diagnosed when there is a noticeable increase in serum creatinine levels.
Currently, it is understood as a decline in renal function characterized by either a 25% increase in serum creatinine levels from baseline or a rise of 0.5 mg/dL in absolute serum creatinine within 48-72 hours after receiving an intravenous contrast medium. This contrast is crucial in performing invasive cardiac procedures such as coronary angiography and interventional procedures.
However, the growing use of contrast media in these procedures, especially in patients with pre-existing conditions such as chronic kidney disease, diabetes, hypertension, and kidney failure, has led to an increase in CIN cases. This sudden change in kidney function is a frequent side effect of coronary angiography and percutaneous coronary intervention, primarily due to contrast-induced acute kidney injury or contrast-induced nephropathy.
The occurrence of diabetes and chronic kidney disease is on the rise, and these are major risk factors for acute kidney injury that may arise from percutaneous coronary interventions and cardiac catheterization. The incidence of contrast-induced nephropathy ranges up to 30%, depending on the definition used. Most cases are reversible within a span of 2 to 4 weeks. The requirement for renal replacement therapy is uncommon, occurring in just 1% to 4% of cases, and out of these, fewer than 50% require long-term treatment.
The general population is estimated to have an incidence rate of over 2% for contrast-induced nephropathy. However, in groups with high-risk factors for kidney disease, the incidence can be as high as 20% to 30%. The risk can be reduced by using low osmolar contrast media. It is the third leading cause of iatrogenic acute kidney injury and is primarily caused by hypoperfusion of the kidneys leading to prerenal injury or acute tubular necrosis.
The number and type of risk factors present significantly influence the incidence of renal impairment. The incidence rate may also vary depending on the procedure, with diagnostic investigations having an incidence rate of 1.6-2.3% and coronary interventions having an overall incidence rate of 14.5%. Patients over 60 are reported to have an incidence rate of 8% to 16%. Additionally, patients with acute myocardial infarction undergoing coronary intervention have been shown to have an increased risk of developing CIN if they are 75 years or older.
The exact mechanisms behind contrast-induced nephropathy are not fully understood. However, it is believed to involve a combination of factors such as hypoxia, ischemia, vasoconstriction, and toxic effects on the renal tubular cells. Certain medications and changes in blood flow can increase the risk of CIN, especially when the contrast is administered through an artery rather than a vein. For example, metformin use can lead to lactic acidosis in the presence of kidney dysfunction or injury.
The FDA advises stopping metformin before and after a contrast media procedure. Other causes of CIN include air bubbles from catheters that obstruct the renal microvasculature and cholesterol atheroembolism, which can result in laboratory abnormalities such as eosinophilia and acute kidney injury. Contrast media can cause constriction of blood vessels through its direct impact on smooth muscle and by producing metabolites like endothelin and adenosine.
It also interferes with water reabsorption, leading to increased interstitial pressure, decreased glomerular filtration rate, and compression of blood vessels in the kidney. This exacerbates hypoxia and vasoconstriction in the kidneys, especially in patients who are already dehydrated. Additionally, contrast media can raise blood viscosity and decrease red blood cell flexibility, resulting in blockages and reducing blood flow, causing ischemia and activation of harmful reactive oxygen species that damage the tubular cells at a cellular level.
Contrast-induced nephropathy is a condition that affects the kidneys and is caused by exposure to contrast media. It is most frequently seen in individuals with pre-existing chronic kidney disease, with an incidence of 8% for those with an estimated glomerular filtration rate of 45 to 60 mL/min/1.73m2, 13% for individuals with eGFR of 30 to 45 mL/min/1.73m2, and 27% for those with a GFR less than 30 mL/min/1.73m2.
Other factors that increase the risk of developing contrast-induced nephropathy include advanced age, heart failure, diabetes, female gender, hypertension, peripheral vascular disease, and a low left ventricular ejection fraction. Exposure to contrast media can harm different parts of the kidney and cause damage through several mechanisms, including a direct cytotoxic effect on the proximal tubules, increased production of reactive oxygen species, reduced blood flow in the kidney, and increased renal vasoconstriction.
A patient’s prognosis following the administration of contrast depends on various factors, including underlying medical conditions and the patient’s baseline renal function. Depending on the scoring system, there may be a chance of developing Contrast-Induced Nephropathy.
This condition is usually temporary and resolves within a week to two weeks. Although some residual renal impairment may persist in a small percentage of patients, it typically affects fewer than one-third of those who develop CIN.
Clinical History
Contrast-induced nephropathy is a type of acute kidney injury first documented by Bartel et al. in the 1950s. This condition is associated with a fatal outcome. It occurs when a patient experiences a sudden and temporary increase in creatine levels after receiving an intravenous injection of contrast medium during a diagnostic or therapeutic procedure, such as percutaneous coronary intervention. The incidence of CIN is reported to be around 15% in patients undergoing these types of procedures.
Patients who develop CIN typically have a preceding history of contrast administration, usually within 24-48 hours before presenting symptoms. The onset of CIN is usually non-oliguric in nature. It’s important to note that CIN can be prevented with proper screening and risk assessment before administering a contrast medium. This can include evaluating a patient’s creatinine levels and determining if there is a history of kidney disease or if the patient is taking certain medications that can affect kidney function.
Physical Examination
Contrast-induced nephropathy is a condition where there is an increase in serum creatinine levels after exposure to contrast media. The traditional definition states that there must be a rise of at least 0.5 mg/dL or a 25% increase from the baseline level within 48 to 72 hours after the exposure. However, the Kidney Disease Improving Global Outcome (KDIGO) definition is more comprehensive.
According to KDIGO, stage 1 of contrast-induced nephropathy is defined as a rapid rise in creatinine levels to greater than 0.3 mg/dL within 48 hours or a relative increase of 50% or more from baseline in 7 days or less or a reduction in urine output to less than 0.5 ml/kg/hr for 6 to 12 hours. The severity of the condition is further staged based on the levels of creatinine, urine output, and the need for renal replacement therapy.
Differential Diagnosis
Acute renal failure
Acute tubular necrosis
Embolic renal disease
Interstitial nephritis
Renal artery stenosis
Reducing the risk of contrast-induced nephropathy is an important consideration prior to undergoing a procedure that involves the use of contrast agents. The most common strategy for minimizing this risk is implementing a periprocedural hydration protocol for patients with chronic kidney disease. This involves initiating an intravenous (IV) fluid infusion with 0.9% normal saline at a rate of 1 ml/kg/hr for 6 to 12 hours before and continuing the infusion after the procedure.
Sometimes, a sliding scale IV hydration protocol based on left ventricular end-diastolic pressure is also used. Another strategy to reduce the risk of contrast-induced nephropathy is bicarbonate. Sodium bicarbonate, when infused at a rate of 3 mL/kg/hour an hour before the procedure and continued at a rate of 1 mL/kg/hour for six hours, can help alkalinize the renal tubular fluid, which slows down the Harber-Weiss reaction and helps scavenge reactive oxygen species from NO.
There is some debate surrounding the exact duration of the bicarbonate infusion, but some studies have shown that hydration with sodium bicarbonate is more effective than normal saline alone. Pre-treating patients with high-intensity statins prior to contrast use is also a reasonable approach. A meta-analysis observed that pre-treatment with rosuvastatin could significantly reduce the incidence of contrast-induced nephropathy. However, this strategy may not be effective for patients already suffering from chronic kidney disease who are undergoing elective cardiac catheterization.
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