Azotemia is characterized by high levels of nitrogenous waste products, such as BUN and creatinine, in the blood. It is caused by decreased kidney function, which results in the inability of the renal system to filter these waste products effectively. Azotemia is a common feature of both acute and chronic kidney injury.
It is significant in acute kidney injury, which has three subtypes: prerenal, intrinsic, and post-renal azotemia. If left untreated, azotemia can lead to more serious health problems, such as end-stage renal disease. The term azotemia is often used interchangeably with uremia, which refers specifically to the presence of high levels of urea in the blood.
Epidemiology
Azotemia is a common condition that leads to a significant number of hospital admissions and a higher risk of death. Despite its prevalence, many aspects of its natural history are poorly understood. The incidence and prevalence of azotemia can vary depending on the underlying cause of the condition.
A global study conducted in 2014 collected data on the burden of azotemia across 72 countries and found that the 7-day mortality rate was between 10-12% in both high- and low-income countries. The study also identified key risk factors for azotemia, including dehydration, shock, infection, sepsis, cardiac disease, and nephrotoxic medications.
Anatomy
Pathophysiology
Azotemia is characterized by an elevation of nitrogen-containing waste products in the blood, specifically blood urea nitrogen (BUN) and creatinine. This can occur as a result of decreased kidney function or an increase in the production of these waste products. Some common causes of azotemia include kidney disease, dehydration, urinary tract obstruction, and certain medications. In advanced cases, it can lead to uremia characterized by a build-up of waste products in the blood that can lead to nausea, vomiting, and even coma or death if left untreated.
The kidneys receive a significant portion of the body’s blood flow, making them highly sensitive to any reduction in perfusion and oxygenation. Prolonged or severe decrease in blood flow or hypoxia to the kidneys can lead to cellular damage and dysfunction in the vasculature, glomeruli, and tubules. This is reflected in a decrease in the glomerular filtration rate (GFR).
However, the GFR is not always a reliable indicator of the underlying condition, as renal dysfunction can be complex and involve multiple processes. Some of the most common findings in acute kidney injury (AKI) include ischemia, apoptosis, tubular necrosis, detachment of renal epithelial cells from basement membranes, loss of brush border in proximal tubules, tubular casts, interstitial edema, and peritubular capillary congestion.
Etiology
Prerenal azotemia is caused by decreased blood flow to the kidneys, often due to underlying conditions such as shock, dehydration, hemorrhage, overuse of diuretics, burns, and low-oncotic pressure states like congestive heart failure or liver failure.
Intrinsic azotemia is caused by damage to the structures of the kidney, such as the glomeruli, renal tubules and interstitium, and renal vasculature, which can be caused by conditions such as vasculitis, toxins, drugs, infections, and hypoperfusion.
Post-renal azotemia is caused by issues in the ureters and bladder, often resulting from obstructions such as recurrent urinary tract infections, nephrolithiasis, hydronephrosis, and benign prostatic hyperplasia.
Genetics
Prognostic Factors
The prognosis of azotemia depends on the underlying cause. In some cases, such as acute kidney injury, the condition may be reversible with proper treatment. However, in cases of chronic kidney disease, the damage to the kidneys may be irreversible and progressive, leading to end-stage kidney disease. The patient may require dialysis or a kidney transplant to survive these cases.
Clinical History
Clinical History
It is important to determine the cause of acute or chronic azotemia to initiate appropriate treatment and prevent progression. To evaluate volume status, signs of dehydration, such as dry mucous membranes and skin tenting, can help. Additionally, edema, mainly if it is non-pitting, hepatojugular reflux, and pulmonary crackles, should be assessed.
Other signs include ascites and indications of infection such as fever, chills, diaphoresis, cough, congestion, nausea, vomiting, diarrhea, dysuria, frequency, pyuria, and hematuria. Patients with intrarenal azotemia may have symptoms such as nocturia, polyuria, proteinuria, shock, and edema and have a history of underlying conditions such as diabetes, hypertension, SLE, and infections like HBV, HCV, syphilis, multiple myeloma, and HIV.
It is important to consider the patient’s medication history for any nephrotoxic drugs, chemical exposure, and any history of IV drug abuse, which increases the risk for infections. Patients with postrenal azotemia may have a history of symptoms such as renal colic, dysuria, frequency, hesitancy, urgency incontinence, and underlying conditions such as pelvic malignancy or irradiation or benign prostatic hypertrophy.
Physical Examination
Physical Examination
Prerenal findings in acute kidney injury can include sepsis or shock, burns, bleeding, dehydration, and a history of diarrhea and vomiting. These symptoms may present as skin tenting, worsening third spacing from intravascular depletion, and signs of fluid accumulation such as pitting edema and ascites. Additionally, there may be hypotension. Intra-renal findings in AKI include a history of nephrotoxic medication use, contrast exposure, and poorly controlled hypertension or diabetes mellitus.
Post-renal findings in AKI can include flank pain, which may be a concern for pyelonephritis, colicky pain, which may be a concern for nephrolithiasis, boggy prostate, urinary hesitancy, anuria, which may be a concern for benign prostatic hyperplasia, smoking history, which may be a concern for bladder cancer, and spinal cord trauma, which may be a concern for neurogenic bladder. In suspected prerenal azotemia, signs of dehydration such as tachycardia, orthostatic hypotension, dry mucous membranes, skin turgor, and loss of axillary sweat are present. They should also look for signs of congestive heart failure and hepatic insufficiency.
In suspected intrarenal azotemia hypertension and its end-organ effects, such as hypertensive retinopathy, left ventricular hypertrophy, rash, joint swelling or tenderness, needle tracks, hearing abnormality, palpable kidneys, abdominal bruits, pericardial rub, and asterixis are noted. The presence of uremic pericarditis requires immediate dialysis. In suspected postrenal azotemia, healthcare professionals should look for a palpable bladder that is dull to percussion and the presence of a rectal or pelvic mass on digital examination.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnosis
Ketoacidosis
Chronic Kidney Disease
Chronic Glomerulonephritis
Hyperalimentation
Tubulointerstitial Nephritis
States of protein catabolism
Uremia
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
In managing azotemia, the primary goal is to address the underlying condition. For prerenal causes, treatment may involve IV fluid hydration and vasopressor support to improve blood flow to the kidneys. In cases of intrinsic renal disease, discontinuing harmful substances, hydrating, and controlling blood pressure and diabetes can help preserve kidney function. Obstruction in the urinary tract should be relieved and monitored through urine output. A minimum of 0.5 mL/kg per hour is considered normal and a sign of stable kidney function. Diuretic-induced volume depletion, especially in the elderly, is characterized by dehydration, hyponatremia, and occasionally hypokalemia.
Treatment typically involves normal saline infusion and correction of hypokalemia. Decreased cardiac output, on the other hand, requires optimizing cardiac performance through diuretics, ACE inhibitors, beta-blockers, nitrates, positive inotropic agents, and specific therapy for the cause of impaired cardiac function. ACE inhibitors may be contraindicated in cases of hyperkalemia, and in such cases, the combination of nitrates and hydralazine can be used as an alternative.
Patients with decreased cardiac output also tend to have risk factors for macrovascular disease, and the diagnosis of ischemic nephropathy or atheroembolic disease should be considered when renal function worsens despite optimizing cardiac function. Reduced effective arterial volume due to systemic shunting can result from sepsis or liver failure, leading to severe edema, hyponatremia, and hypoalbuminemia, making management difficult. Treatment includes effective management of sepsis with antibiotics and hypotension with dopamine and norepinephrine.
Crystalloid replacement can be attempted, but it often leads to more edema. Salt-poor albumin infusion may be attempted in severely hypoalbuminemia patients, but there is no conclusive evidence of its benefits. Adequate nutrition and effective treatment of sepsis can improve oncotic pressure, decrease systemic shunting, and improve renal perfusion, urinary output, and edema. In cases of hepatorenal syndrome, the average survival is 1-2 weeks, but early liver transplantation can lead to recovery of kidney function. In some cases, renal function may be advanced, requiring replacement therapy.
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Azotemia is characterized by high levels of nitrogenous waste products, such as BUN and creatinine, in the blood. It is caused by decreased kidney function, which results in the inability of the renal system to filter these waste products effectively. Azotemia is a common feature of both acute and chronic kidney injury.
It is significant in acute kidney injury, which has three subtypes: prerenal, intrinsic, and post-renal azotemia. If left untreated, azotemia can lead to more serious health problems, such as end-stage renal disease. The term azotemia is often used interchangeably with uremia, which refers specifically to the presence of high levels of urea in the blood.
Azotemia is a common condition that leads to a significant number of hospital admissions and a higher risk of death. Despite its prevalence, many aspects of its natural history are poorly understood. The incidence and prevalence of azotemia can vary depending on the underlying cause of the condition.
A global study conducted in 2014 collected data on the burden of azotemia across 72 countries and found that the 7-day mortality rate was between 10-12% in both high- and low-income countries. The study also identified key risk factors for azotemia, including dehydration, shock, infection, sepsis, cardiac disease, and nephrotoxic medications.
Azotemia is characterized by an elevation of nitrogen-containing waste products in the blood, specifically blood urea nitrogen (BUN) and creatinine. This can occur as a result of decreased kidney function or an increase in the production of these waste products. Some common causes of azotemia include kidney disease, dehydration, urinary tract obstruction, and certain medications. In advanced cases, it can lead to uremia characterized by a build-up of waste products in the blood that can lead to nausea, vomiting, and even coma or death if left untreated.
The kidneys receive a significant portion of the body’s blood flow, making them highly sensitive to any reduction in perfusion and oxygenation. Prolonged or severe decrease in blood flow or hypoxia to the kidneys can lead to cellular damage and dysfunction in the vasculature, glomeruli, and tubules. This is reflected in a decrease in the glomerular filtration rate (GFR).
However, the GFR is not always a reliable indicator of the underlying condition, as renal dysfunction can be complex and involve multiple processes. Some of the most common findings in acute kidney injury (AKI) include ischemia, apoptosis, tubular necrosis, detachment of renal epithelial cells from basement membranes, loss of brush border in proximal tubules, tubular casts, interstitial edema, and peritubular capillary congestion.
Prerenal azotemia is caused by decreased blood flow to the kidneys, often due to underlying conditions such as shock, dehydration, hemorrhage, overuse of diuretics, burns, and low-oncotic pressure states like congestive heart failure or liver failure.
Intrinsic azotemia is caused by damage to the structures of the kidney, such as the glomeruli, renal tubules and interstitium, and renal vasculature, which can be caused by conditions such as vasculitis, toxins, drugs, infections, and hypoperfusion.
Post-renal azotemia is caused by issues in the ureters and bladder, often resulting from obstructions such as recurrent urinary tract infections, nephrolithiasis, hydronephrosis, and benign prostatic hyperplasia.
The prognosis of azotemia depends on the underlying cause. In some cases, such as acute kidney injury, the condition may be reversible with proper treatment. However, in cases of chronic kidney disease, the damage to the kidneys may be irreversible and progressive, leading to end-stage kidney disease. The patient may require dialysis or a kidney transplant to survive these cases.
Clinical History
It is important to determine the cause of acute or chronic azotemia to initiate appropriate treatment and prevent progression. To evaluate volume status, signs of dehydration, such as dry mucous membranes and skin tenting, can help. Additionally, edema, mainly if it is non-pitting, hepatojugular reflux, and pulmonary crackles, should be assessed.
Other signs include ascites and indications of infection such as fever, chills, diaphoresis, cough, congestion, nausea, vomiting, diarrhea, dysuria, frequency, pyuria, and hematuria. Patients with intrarenal azotemia may have symptoms such as nocturia, polyuria, proteinuria, shock, and edema and have a history of underlying conditions such as diabetes, hypertension, SLE, and infections like HBV, HCV, syphilis, multiple myeloma, and HIV.
It is important to consider the patient’s medication history for any nephrotoxic drugs, chemical exposure, and any history of IV drug abuse, which increases the risk for infections. Patients with postrenal azotemia may have a history of symptoms such as renal colic, dysuria, frequency, hesitancy, urgency incontinence, and underlying conditions such as pelvic malignancy or irradiation or benign prostatic hypertrophy.
Physical Examination
Prerenal findings in acute kidney injury can include sepsis or shock, burns, bleeding, dehydration, and a history of diarrhea and vomiting. These symptoms may present as skin tenting, worsening third spacing from intravascular depletion, and signs of fluid accumulation such as pitting edema and ascites. Additionally, there may be hypotension. Intra-renal findings in AKI include a history of nephrotoxic medication use, contrast exposure, and poorly controlled hypertension or diabetes mellitus.
Post-renal findings in AKI can include flank pain, which may be a concern for pyelonephritis, colicky pain, which may be a concern for nephrolithiasis, boggy prostate, urinary hesitancy, anuria, which may be a concern for benign prostatic hyperplasia, smoking history, which may be a concern for bladder cancer, and spinal cord trauma, which may be a concern for neurogenic bladder. In suspected prerenal azotemia, signs of dehydration such as tachycardia, orthostatic hypotension, dry mucous membranes, skin turgor, and loss of axillary sweat are present. They should also look for signs of congestive heart failure and hepatic insufficiency.
In suspected intrarenal azotemia hypertension and its end-organ effects, such as hypertensive retinopathy, left ventricular hypertrophy, rash, joint swelling or tenderness, needle tracks, hearing abnormality, palpable kidneys, abdominal bruits, pericardial rub, and asterixis are noted. The presence of uremic pericarditis requires immediate dialysis. In suspected postrenal azotemia, healthcare professionals should look for a palpable bladder that is dull to percussion and the presence of a rectal or pelvic mass on digital examination.
Differential Diagnosis
Ketoacidosis
Chronic Kidney Disease
Chronic Glomerulonephritis
Hyperalimentation
Tubulointerstitial Nephritis
States of protein catabolism
Uremia
In managing azotemia, the primary goal is to address the underlying condition. For prerenal causes, treatment may involve IV fluid hydration and vasopressor support to improve blood flow to the kidneys. In cases of intrinsic renal disease, discontinuing harmful substances, hydrating, and controlling blood pressure and diabetes can help preserve kidney function. Obstruction in the urinary tract should be relieved and monitored through urine output. A minimum of 0.5 mL/kg per hour is considered normal and a sign of stable kidney function. Diuretic-induced volume depletion, especially in the elderly, is characterized by dehydration, hyponatremia, and occasionally hypokalemia.
Treatment typically involves normal saline infusion and correction of hypokalemia. Decreased cardiac output, on the other hand, requires optimizing cardiac performance through diuretics, ACE inhibitors, beta-blockers, nitrates, positive inotropic agents, and specific therapy for the cause of impaired cardiac function. ACE inhibitors may be contraindicated in cases of hyperkalemia, and in such cases, the combination of nitrates and hydralazine can be used as an alternative.
Patients with decreased cardiac output also tend to have risk factors for macrovascular disease, and the diagnosis of ischemic nephropathy or atheroembolic disease should be considered when renal function worsens despite optimizing cardiac function. Reduced effective arterial volume due to systemic shunting can result from sepsis or liver failure, leading to severe edema, hyponatremia, and hypoalbuminemia, making management difficult. Treatment includes effective management of sepsis with antibiotics and hypotension with dopamine and norepinephrine.
Crystalloid replacement can be attempted, but it often leads to more edema. Salt-poor albumin infusion may be attempted in severely hypoalbuminemia patients, but there is no conclusive evidence of its benefits. Adequate nutrition and effective treatment of sepsis can improve oncotic pressure, decrease systemic shunting, and improve renal perfusion, urinary output, and edema. In cases of hepatorenal syndrome, the average survival is 1-2 weeks, but early liver transplantation can lead to recovery of kidney function. In some cases, renal function may be advanced, requiring replacement therapy.
medtigo
Azotemia
Updated :
September 6, 2023
Azotemia is characterized by high levels of nitrogenous waste products, such as BUN and creatinine, in the blood. It is caused by decreased kidney function, which results in the inability of the renal system to filter these waste products effectively. Azotemia is a common feature of both acute and chronic kidney injury.
It is significant in acute kidney injury, which has three subtypes: prerenal, intrinsic, and post-renal azotemia. If left untreated, azotemia can lead to more serious health problems, such as end-stage renal disease. The term azotemia is often used interchangeably with uremia, which refers specifically to the presence of high levels of urea in the blood.
Azotemia is a common condition that leads to a significant number of hospital admissions and a higher risk of death. Despite its prevalence, many aspects of its natural history are poorly understood. The incidence and prevalence of azotemia can vary depending on the underlying cause of the condition.
A global study conducted in 2014 collected data on the burden of azotemia across 72 countries and found that the 7-day mortality rate was between 10-12% in both high- and low-income countries. The study also identified key risk factors for azotemia, including dehydration, shock, infection, sepsis, cardiac disease, and nephrotoxic medications.
Azotemia is characterized by an elevation of nitrogen-containing waste products in the blood, specifically blood urea nitrogen (BUN) and creatinine. This can occur as a result of decreased kidney function or an increase in the production of these waste products. Some common causes of azotemia include kidney disease, dehydration, urinary tract obstruction, and certain medications. In advanced cases, it can lead to uremia characterized by a build-up of waste products in the blood that can lead to nausea, vomiting, and even coma or death if left untreated.
The kidneys receive a significant portion of the body’s blood flow, making them highly sensitive to any reduction in perfusion and oxygenation. Prolonged or severe decrease in blood flow or hypoxia to the kidneys can lead to cellular damage and dysfunction in the vasculature, glomeruli, and tubules. This is reflected in a decrease in the glomerular filtration rate (GFR).
However, the GFR is not always a reliable indicator of the underlying condition, as renal dysfunction can be complex and involve multiple processes. Some of the most common findings in acute kidney injury (AKI) include ischemia, apoptosis, tubular necrosis, detachment of renal epithelial cells from basement membranes, loss of brush border in proximal tubules, tubular casts, interstitial edema, and peritubular capillary congestion.
Prerenal azotemia is caused by decreased blood flow to the kidneys, often due to underlying conditions such as shock, dehydration, hemorrhage, overuse of diuretics, burns, and low-oncotic pressure states like congestive heart failure or liver failure.
Intrinsic azotemia is caused by damage to the structures of the kidney, such as the glomeruli, renal tubules and interstitium, and renal vasculature, which can be caused by conditions such as vasculitis, toxins, drugs, infections, and hypoperfusion.
Post-renal azotemia is caused by issues in the ureters and bladder, often resulting from obstructions such as recurrent urinary tract infections, nephrolithiasis, hydronephrosis, and benign prostatic hyperplasia.
The prognosis of azotemia depends on the underlying cause. In some cases, such as acute kidney injury, the condition may be reversible with proper treatment. However, in cases of chronic kidney disease, the damage to the kidneys may be irreversible and progressive, leading to end-stage kidney disease. The patient may require dialysis or a kidney transplant to survive these cases.
Clinical History
It is important to determine the cause of acute or chronic azotemia to initiate appropriate treatment and prevent progression. To evaluate volume status, signs of dehydration, such as dry mucous membranes and skin tenting, can help. Additionally, edema, mainly if it is non-pitting, hepatojugular reflux, and pulmonary crackles, should be assessed.
Other signs include ascites and indications of infection such as fever, chills, diaphoresis, cough, congestion, nausea, vomiting, diarrhea, dysuria, frequency, pyuria, and hematuria. Patients with intrarenal azotemia may have symptoms such as nocturia, polyuria, proteinuria, shock, and edema and have a history of underlying conditions such as diabetes, hypertension, SLE, and infections like HBV, HCV, syphilis, multiple myeloma, and HIV.
It is important to consider the patient’s medication history for any nephrotoxic drugs, chemical exposure, and any history of IV drug abuse, which increases the risk for infections. Patients with postrenal azotemia may have a history of symptoms such as renal colic, dysuria, frequency, hesitancy, urgency incontinence, and underlying conditions such as pelvic malignancy or irradiation or benign prostatic hypertrophy.
Physical Examination
Prerenal findings in acute kidney injury can include sepsis or shock, burns, bleeding, dehydration, and a history of diarrhea and vomiting. These symptoms may present as skin tenting, worsening third spacing from intravascular depletion, and signs of fluid accumulation such as pitting edema and ascites. Additionally, there may be hypotension. Intra-renal findings in AKI include a history of nephrotoxic medication use, contrast exposure, and poorly controlled hypertension or diabetes mellitus.
Post-renal findings in AKI can include flank pain, which may be a concern for pyelonephritis, colicky pain, which may be a concern for nephrolithiasis, boggy prostate, urinary hesitancy, anuria, which may be a concern for benign prostatic hyperplasia, smoking history, which may be a concern for bladder cancer, and spinal cord trauma, which may be a concern for neurogenic bladder. In suspected prerenal azotemia, signs of dehydration such as tachycardia, orthostatic hypotension, dry mucous membranes, skin turgor, and loss of axillary sweat are present. They should also look for signs of congestive heart failure and hepatic insufficiency.
In suspected intrarenal azotemia hypertension and its end-organ effects, such as hypertensive retinopathy, left ventricular hypertrophy, rash, joint swelling or tenderness, needle tracks, hearing abnormality, palpable kidneys, abdominal bruits, pericardial rub, and asterixis are noted. The presence of uremic pericarditis requires immediate dialysis. In suspected postrenal azotemia, healthcare professionals should look for a palpable bladder that is dull to percussion and the presence of a rectal or pelvic mass on digital examination.
Differential Diagnosis
Ketoacidosis
Chronic Kidney Disease
Chronic Glomerulonephritis
Hyperalimentation
Tubulointerstitial Nephritis
States of protein catabolism
Uremia
In managing azotemia, the primary goal is to address the underlying condition. For prerenal causes, treatment may involve IV fluid hydration and vasopressor support to improve blood flow to the kidneys. In cases of intrinsic renal disease, discontinuing harmful substances, hydrating, and controlling blood pressure and diabetes can help preserve kidney function. Obstruction in the urinary tract should be relieved and monitored through urine output. A minimum of 0.5 mL/kg per hour is considered normal and a sign of stable kidney function. Diuretic-induced volume depletion, especially in the elderly, is characterized by dehydration, hyponatremia, and occasionally hypokalemia.
Treatment typically involves normal saline infusion and correction of hypokalemia. Decreased cardiac output, on the other hand, requires optimizing cardiac performance through diuretics, ACE inhibitors, beta-blockers, nitrates, positive inotropic agents, and specific therapy for the cause of impaired cardiac function. ACE inhibitors may be contraindicated in cases of hyperkalemia, and in such cases, the combination of nitrates and hydralazine can be used as an alternative.
Patients with decreased cardiac output also tend to have risk factors for macrovascular disease, and the diagnosis of ischemic nephropathy or atheroembolic disease should be considered when renal function worsens despite optimizing cardiac function. Reduced effective arterial volume due to systemic shunting can result from sepsis or liver failure, leading to severe edema, hyponatremia, and hypoalbuminemia, making management difficult. Treatment includes effective management of sepsis with antibiotics and hypotension with dopamine and norepinephrine.
Crystalloid replacement can be attempted, but it often leads to more edema. Salt-poor albumin infusion may be attempted in severely hypoalbuminemia patients, but there is no conclusive evidence of its benefits. Adequate nutrition and effective treatment of sepsis can improve oncotic pressure, decrease systemic shunting, and improve renal perfusion, urinary output, and edema. In cases of hepatorenal syndrome, the average survival is 1-2 weeks, but early liver transplantation can lead to recovery of kidney function. In some cases, renal function may be advanced, requiring replacement therapy.
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