Goodpasture syndrome is an anti-GBM (anti-glomerular basement membrane) illness that affects the kidneys and lungs and frequently manifests as glomerulonephritis & pulmonary bleeding. However, some medical professionals might use a number of words — such as anti-glomerular basement membrane illness, Goodpasture syndrome, & Goodpasture disease — interchangeably.
The most specific definition for this condition is an anti-GBM illness, which also includes pulmonary & renal involvement and anti-glomerular basement membrane autoantibodies. The illness spectrum can manifest traditionally or just as glomerulonephritis.
Ernest Goodpasture, who originally identified this condition in 1919, is honored by having his name attached to the eponym Goodpasture syndrome. The pathophysiology of Goodpasture syndrome was later better understood as a result of the finding of anti-GBM autoantibodies.
Epidemiology
A rare condition called Goodpasture syndrome. In European and Asian populations, the prevalence of anti-GBM illness ranges from 0.5 – 1.8 cases for every million annually. One to five percent of all glomerulonephritides is brought on by it. Additionally, it causes 10% to 20% of instances of crescentic glomerulonephritis.
Distribution by Gender, Race, & Age
Goodpasture syndrome may be more widespread in some ethnic groups, such as the Maori of New Zealand, however, it is more frequently encountered in White individuals than in the Black population. The age ranges for the syndrome are bimodal, falling between 20 & 30 and 60 & 70.
The condition seems to affect older women & younger men more frequently. Antineutrophilic cytoplasmic autoantibodies & anti-GBM autoantibodies are seen in a subgroup of individuals. Most guys in this category are between the ages of 60 and 70.
Anatomy
Pathophysiology
Systemic autoantibodies that target the glomerular basement membrane are the cause of Goodpasture syndrome. Antigen-antibody compounds that develop at the basal layer lead to crescentic glomerulonephritis. The basement membrane’s complement system is triggered by the antibodies, resulting in tissue damage. It is possible to visualize the attachment of antibodies as a linear immunoglobulin deposition along the basal cells. The characteristic glomerulonephritis appearance is brought on by the inflammatory reaction in that region.
The glomerulus and also the alveolar basal cells both share a common collagen target. Type 4 collagen, which can be represented as six distinct chains ranging from alpha 1 to alpha 6, is the major substance of the basal layer. Even though anti-glomerular outer membrane illness has circulating autoantibodies, pulmonary problems aren’t always present.
The likelihood of pulmonary signs appears to increase with initiating lung damage. The alveolar endothelial in a healthy person serves as a defense against the anti-basement membrane autoantibodies. However, if an insult causes the alveolar capillaries to become more permeable, it causes autoantibodies to trespass and attach to the basement membrane.
Alveolar-capillary transparency may be increased as a result of various factors, such as:
Bacteremia
Exposed to volatile organic compounds.
Tobacco smoking
Capillaries’ hydrostatic pressure has increased.
Infections of the upper respiratory tract
Endotoxemia
Increased inspired oxygen.
Patients with particular HLA (human leukocyte antigen) types are shown to be more sensitive to disease and have a poor prognosis, and there is strong evidence for hereditary involvement. HLA-DR15, DRB1*03, & DRB1*04 are more prevalent than usual, but DRB1*01 & DRB1*07 are less common. The DRB1*1501 gene and, to a lesser extent, the DRB1*1502 gene are strongly associated with Goodpasture syndrome.
However, among White people, the DRB1*1501 gene is found in one-third of individuals. Therefore, it is evident that the expression of the disorder requires certain extra elements, such as environmental or genetic. It is crucial to remember that HLA-B7 is more common and suggests a more severe case of anti-GBM nephritis. T cells are crucial in the onset and development of Goodpasture syndrome, despite the fact that it is thought to be an autoantibody-mediated disease.
Etiology
When a person has a genetic propensity for Goodpasture syndrome, environmental insults seem to be the cause. Anti-glomerular basement membrane antibody production has yet to be associated with a specific stimulus.
However, several HLA types (human leukocyte antigens), most notably HLA-DR15, have been linked to an elevated hereditary predisposition to Goodpasture syndrome. An initial injury to the pulmonary vasculature is required before these autoantibodies can be exposed to the alveolar microvascular. These environmental elements consist of:
Smoking
Illnesses like influenza A2
Cocaine inhalation
Exposure to organic solvents, hydrocarbons, or metal particles
Drugs that deplete lymphocytes, such as alemtuzumab
Shock wave lithotripsy outside the body
Genetics
Prognostic Factors
The outcome of Goodpasture syndrome has greatly improved with the emergence of aggressive therapy, including plasmapheresis, immunosuppressive, and corticosteroid drugs.
With these treatments, less than 30 percent of patients need long-term dialysis, and the five-year survival rate has surpassed 80%. But it has been discovered that cyclophosphamide delayed administration is connected to a catastrophic prognosis.
Clinical History
Clinical History
The clinical signs and symptoms of people with anti-glomerular basement membrane (anti-GBM) illness vary significantly. Between 60 and 80 percent of patients have pulmonary & renal illness that is clinically evident, 20 to 40 percent have the renal disease only, and less than 10 percent have a lung-only disease.
Among the symptoms are the following:
Constitutional signs, such as arthralgias, malaise, chills, and fever, may appear before or simultaneously with renal or pulmonary signs.
When the disease affects the lungs, hemoptysis is the first symptom to appear. There may be different levels of hemoptysis, and other patients may not have any at all. Additionally, coughing, dyspnea, and shortness of breath are pulmonary symptoms.
There could be a massive lung hemorrhage that causes respiratory distress.
Less than half of patients report having heart problems. Hematuria, edema, elevated blood pressure, &finally, uremia is examples of renal symptoms.
Chronic intrapulmonary hemorrhage may cause significant anemia.
Physical Examination
Physical examination
The following physical examination characteristics are seen in people with the anti-GBM disorder:
Edema
Rash
Hypertension (possible in 20% of cases)
Hepatosplenomegaly (possibly present)
Cyanosis
Tachypnea
Breathing crackles over the lungs’ bases
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnosis
In the differentials, all pulmonary-renal disorders that impact the kidney and lungs must be considered. These consist of:
Polyangiitis and granulomatosis (Wegener granulomatosis)
Microscopic polyangiitis
It might be challenging to identify Goodpasture syndrome from granulomatosis with polyangiitis because some patients with it also have positive ANCAs.
Some pulmonary-renal syndromes are also associated with IgA-mediated diseases, including:
Henoch-Schönlein purpura
IgA nephropathy
Additional differential diagnoses consist of:
Churg-Strauss syndrome
Pneumocystis jiroveci pneumoniae
Granulomatosis with polyangiitis
Community-acquired pneumoniae
Acute glomerulonephritis
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Patients with Goodpasture syndrome, which includes both glomerulonephritis & pulmonary bleeding, may already be in serious condition when they present. Standard indications frequently necessitate urgent hemodialysis, & intubation may be required in cases of respiratory impairment. As soon as the clinical circumstances permit, a renal biopsy should be performed when the clinician detects the diagnosis. Prednisone, daily plasmapheresis, and cyclophosphamide should be started in patients as soon as they are diagnosed in order to reduce overall fatality and increase kidney survival in particular.
The overall kidney prognosis is better if treatment can begin before the patient needs kidney replacement therapy. Regardless of their renal state, combination therapy should be initiated for all patients suffering from pulmonary signs. The risks of immunosuppressive & plasmapheresis medications may outweigh the advantages for individuals without pulmonary symptoms whose kidney recovery is highly unlikely (i.e., for those who came with an immediate need for dialysis during the initial 72 hours).
Given that the disease has yet to be well investigated in controlled studies, the decision to forego therapy in certain circumstances is still debatable. Who specifically in this group will respond and regain kidney function is still challenging to predict. Although there has been an average 8% improvement in renal function in this group, many doctors still choose to try more aggressive combination therapy at this point. Daily plasmapheresis is typically carried out until anti-glomerular outer membrane antibodies are undetectable, followed by three to six months of steroid & cyclophosphamide treatment until complete remission is obtained.
This can be assessed by running additional titers after plasmapheresis, and at any time, new signs emerge that might be a sign of recurrence. Overall, recurrence is still uncommon. Cyclophosphamide is first administered orally at a dose of 2 mg/kg that is modified to maintain a white cell count of about 5000. Acute, life-threatening alveolar hemorrhage is treated with 1g/day IV pulse therapy of methylprednisolone for 3 days, then a tapered dosage of 1 to 1.5 mg/kg orally. In several investigations, it was determined that rituximab played a part in the development of extremely low levels of anti-GBM autoantibodies.
Goodpasture syndrome is an anti-GBM (anti-glomerular basement membrane) illness that affects the kidneys and lungs and frequently manifests as glomerulonephritis & pulmonary bleeding. However, some medical professionals might use a number of words — such as anti-glomerular basement membrane illness, Goodpasture syndrome, & Goodpasture disease — interchangeably.
The most specific definition for this condition is an anti-GBM illness, which also includes pulmonary & renal involvement and anti-glomerular basement membrane autoantibodies. The illness spectrum can manifest traditionally or just as glomerulonephritis.
Ernest Goodpasture, who originally identified this condition in 1919, is honored by having his name attached to the eponym Goodpasture syndrome. The pathophysiology of Goodpasture syndrome was later better understood as a result of the finding of anti-GBM autoantibodies.
A rare condition called Goodpasture syndrome. In European and Asian populations, the prevalence of anti-GBM illness ranges from 0.5 – 1.8 cases for every million annually. One to five percent of all glomerulonephritides is brought on by it. Additionally, it causes 10% to 20% of instances of crescentic glomerulonephritis.
Distribution by Gender, Race, & Age
Goodpasture syndrome may be more widespread in some ethnic groups, such as the Maori of New Zealand, however, it is more frequently encountered in White individuals than in the Black population. The age ranges for the syndrome are bimodal, falling between 20 & 30 and 60 & 70.
The condition seems to affect older women & younger men more frequently. Antineutrophilic cytoplasmic autoantibodies & anti-GBM autoantibodies are seen in a subgroup of individuals. Most guys in this category are between the ages of 60 and 70.
Systemic autoantibodies that target the glomerular basement membrane are the cause of Goodpasture syndrome. Antigen-antibody compounds that develop at the basal layer lead to crescentic glomerulonephritis. The basement membrane’s complement system is triggered by the antibodies, resulting in tissue damage. It is possible to visualize the attachment of antibodies as a linear immunoglobulin deposition along the basal cells. The characteristic glomerulonephritis appearance is brought on by the inflammatory reaction in that region.
The glomerulus and also the alveolar basal cells both share a common collagen target. Type 4 collagen, which can be represented as six distinct chains ranging from alpha 1 to alpha 6, is the major substance of the basal layer. Even though anti-glomerular outer membrane illness has circulating autoantibodies, pulmonary problems aren’t always present.
The likelihood of pulmonary signs appears to increase with initiating lung damage. The alveolar endothelial in a healthy person serves as a defense against the anti-basement membrane autoantibodies. However, if an insult causes the alveolar capillaries to become more permeable, it causes autoantibodies to trespass and attach to the basement membrane.
Alveolar-capillary transparency may be increased as a result of various factors, such as:
Bacteremia
Exposed to volatile organic compounds.
Tobacco smoking
Capillaries’ hydrostatic pressure has increased.
Infections of the upper respiratory tract
Endotoxemia
Increased inspired oxygen.
Patients with particular HLA (human leukocyte antigen) types are shown to be more sensitive to disease and have a poor prognosis, and there is strong evidence for hereditary involvement. HLA-DR15, DRB1*03, & DRB1*04 are more prevalent than usual, but DRB1*01 & DRB1*07 are less common. The DRB1*1501 gene and, to a lesser extent, the DRB1*1502 gene are strongly associated with Goodpasture syndrome.
However, among White people, the DRB1*1501 gene is found in one-third of individuals. Therefore, it is evident that the expression of the disorder requires certain extra elements, such as environmental or genetic. It is crucial to remember that HLA-B7 is more common and suggests a more severe case of anti-GBM nephritis. T cells are crucial in the onset and development of Goodpasture syndrome, despite the fact that it is thought to be an autoantibody-mediated disease.
When a person has a genetic propensity for Goodpasture syndrome, environmental insults seem to be the cause. Anti-glomerular basement membrane antibody production has yet to be associated with a specific stimulus.
However, several HLA types (human leukocyte antigens), most notably HLA-DR15, have been linked to an elevated hereditary predisposition to Goodpasture syndrome. An initial injury to the pulmonary vasculature is required before these autoantibodies can be exposed to the alveolar microvascular. These environmental elements consist of:
Smoking
Illnesses like influenza A2
Cocaine inhalation
Exposure to organic solvents, hydrocarbons, or metal particles
Drugs that deplete lymphocytes, such as alemtuzumab
Shock wave lithotripsy outside the body
The outcome of Goodpasture syndrome has greatly improved with the emergence of aggressive therapy, including plasmapheresis, immunosuppressive, and corticosteroid drugs.
With these treatments, less than 30 percent of patients need long-term dialysis, and the five-year survival rate has surpassed 80%. But it has been discovered that cyclophosphamide delayed administration is connected to a catastrophic prognosis.
Clinical History
The clinical signs and symptoms of people with anti-glomerular basement membrane (anti-GBM) illness vary significantly. Between 60 and 80 percent of patients have pulmonary & renal illness that is clinically evident, 20 to 40 percent have the renal disease only, and less than 10 percent have a lung-only disease.
Among the symptoms are the following:
Constitutional signs, such as arthralgias, malaise, chills, and fever, may appear before or simultaneously with renal or pulmonary signs.
When the disease affects the lungs, hemoptysis is the first symptom to appear. There may be different levels of hemoptysis, and other patients may not have any at all. Additionally, coughing, dyspnea, and shortness of breath are pulmonary symptoms.
There could be a massive lung hemorrhage that causes respiratory distress.
Less than half of patients report having heart problems. Hematuria, edema, elevated blood pressure, &finally, uremia is examples of renal symptoms.
Chronic intrapulmonary hemorrhage may cause significant anemia.
Physical examination
The following physical examination characteristics are seen in people with the anti-GBM disorder:
Edema
Rash
Hypertension (possible in 20% of cases)
Hepatosplenomegaly (possibly present)
Cyanosis
Tachypnea
Breathing crackles over the lungs’ bases
Differential Diagnosis
In the differentials, all pulmonary-renal disorders that impact the kidney and lungs must be considered. These consist of:
Polyangiitis and granulomatosis (Wegener granulomatosis)
Microscopic polyangiitis
It might be challenging to identify Goodpasture syndrome from granulomatosis with polyangiitis because some patients with it also have positive ANCAs.
Some pulmonary-renal syndromes are also associated with IgA-mediated diseases, including:
Henoch-Schönlein purpura
IgA nephropathy
Additional differential diagnoses consist of:
Churg-Strauss syndrome
Pneumocystis jiroveci pneumoniae
Granulomatosis with polyangiitis
Community-acquired pneumoniae
Acute glomerulonephritis
Patients with Goodpasture syndrome, which includes both glomerulonephritis & pulmonary bleeding, may already be in serious condition when they present. Standard indications frequently necessitate urgent hemodialysis, & intubation may be required in cases of respiratory impairment. As soon as the clinical circumstances permit, a renal biopsy should be performed when the clinician detects the diagnosis. Prednisone, daily plasmapheresis, and cyclophosphamide should be started in patients as soon as they are diagnosed in order to reduce overall fatality and increase kidney survival in particular.
The overall kidney prognosis is better if treatment can begin before the patient needs kidney replacement therapy. Regardless of their renal state, combination therapy should be initiated for all patients suffering from pulmonary signs. The risks of immunosuppressive & plasmapheresis medications may outweigh the advantages for individuals without pulmonary symptoms whose kidney recovery is highly unlikely (i.e., for those who came with an immediate need for dialysis during the initial 72 hours).
Given that the disease has yet to be well investigated in controlled studies, the decision to forego therapy in certain circumstances is still debatable. Who specifically in this group will respond and regain kidney function is still challenging to predict. Although there has been an average 8% improvement in renal function in this group, many doctors still choose to try more aggressive combination therapy at this point. Daily plasmapheresis is typically carried out until anti-glomerular outer membrane antibodies are undetectable, followed by three to six months of steroid & cyclophosphamide treatment until complete remission is obtained.
This can be assessed by running additional titers after plasmapheresis, and at any time, new signs emerge that might be a sign of recurrence. Overall, recurrence is still uncommon. Cyclophosphamide is first administered orally at a dose of 2 mg/kg that is modified to maintain a white cell count of about 5000. Acute, life-threatening alveolar hemorrhage is treated with 1g/day IV pulse therapy of methylprednisolone for 3 days, then a tapered dosage of 1 to 1.5 mg/kg orally. In several investigations, it was determined that rituximab played a part in the development of extremely low levels of anti-GBM autoantibodies.
Goodpasture syndrome is an anti-GBM (anti-glomerular basement membrane) illness that affects the kidneys and lungs and frequently manifests as glomerulonephritis & pulmonary bleeding. However, some medical professionals might use a number of words — such as anti-glomerular basement membrane illness, Goodpasture syndrome, & Goodpasture disease — interchangeably.
The most specific definition for this condition is an anti-GBM illness, which also includes pulmonary & renal involvement and anti-glomerular basement membrane autoantibodies. The illness spectrum can manifest traditionally or just as glomerulonephritis.
Ernest Goodpasture, who originally identified this condition in 1919, is honored by having his name attached to the eponym Goodpasture syndrome. The pathophysiology of Goodpasture syndrome was later better understood as a result of the finding of anti-GBM autoantibodies.
A rare condition called Goodpasture syndrome. In European and Asian populations, the prevalence of anti-GBM illness ranges from 0.5 – 1.8 cases for every million annually. One to five percent of all glomerulonephritides is brought on by it. Additionally, it causes 10% to 20% of instances of crescentic glomerulonephritis.
Distribution by Gender, Race, & Age
Goodpasture syndrome may be more widespread in some ethnic groups, such as the Maori of New Zealand, however, it is more frequently encountered in White individuals than in the Black population. The age ranges for the syndrome are bimodal, falling between 20 & 30 and 60 & 70.
The condition seems to affect older women & younger men more frequently. Antineutrophilic cytoplasmic autoantibodies & anti-GBM autoantibodies are seen in a subgroup of individuals. Most guys in this category are between the ages of 60 and 70.
Systemic autoantibodies that target the glomerular basement membrane are the cause of Goodpasture syndrome. Antigen-antibody compounds that develop at the basal layer lead to crescentic glomerulonephritis. The basement membrane’s complement system is triggered by the antibodies, resulting in tissue damage. It is possible to visualize the attachment of antibodies as a linear immunoglobulin deposition along the basal cells. The characteristic glomerulonephritis appearance is brought on by the inflammatory reaction in that region.
The glomerulus and also the alveolar basal cells both share a common collagen target. Type 4 collagen, which can be represented as six distinct chains ranging from alpha 1 to alpha 6, is the major substance of the basal layer. Even though anti-glomerular outer membrane illness has circulating autoantibodies, pulmonary problems aren’t always present.
The likelihood of pulmonary signs appears to increase with initiating lung damage. The alveolar endothelial in a healthy person serves as a defense against the anti-basement membrane autoantibodies. However, if an insult causes the alveolar capillaries to become more permeable, it causes autoantibodies to trespass and attach to the basement membrane.
Alveolar-capillary transparency may be increased as a result of various factors, such as:
Bacteremia
Exposed to volatile organic compounds.
Tobacco smoking
Capillaries’ hydrostatic pressure has increased.
Infections of the upper respiratory tract
Endotoxemia
Increased inspired oxygen.
Patients with particular HLA (human leukocyte antigen) types are shown to be more sensitive to disease and have a poor prognosis, and there is strong evidence for hereditary involvement. HLA-DR15, DRB1*03, & DRB1*04 are more prevalent than usual, but DRB1*01 & DRB1*07 are less common. The DRB1*1501 gene and, to a lesser extent, the DRB1*1502 gene are strongly associated with Goodpasture syndrome.
However, among White people, the DRB1*1501 gene is found in one-third of individuals. Therefore, it is evident that the expression of the disorder requires certain extra elements, such as environmental or genetic. It is crucial to remember that HLA-B7 is more common and suggests a more severe case of anti-GBM nephritis. T cells are crucial in the onset and development of Goodpasture syndrome, despite the fact that it is thought to be an autoantibody-mediated disease.
When a person has a genetic propensity for Goodpasture syndrome, environmental insults seem to be the cause. Anti-glomerular basement membrane antibody production has yet to be associated with a specific stimulus.
However, several HLA types (human leukocyte antigens), most notably HLA-DR15, have been linked to an elevated hereditary predisposition to Goodpasture syndrome. An initial injury to the pulmonary vasculature is required before these autoantibodies can be exposed to the alveolar microvascular. These environmental elements consist of:
Smoking
Illnesses like influenza A2
Cocaine inhalation
Exposure to organic solvents, hydrocarbons, or metal particles
Drugs that deplete lymphocytes, such as alemtuzumab
Shock wave lithotripsy outside the body
The outcome of Goodpasture syndrome has greatly improved with the emergence of aggressive therapy, including plasmapheresis, immunosuppressive, and corticosteroid drugs.
With these treatments, less than 30 percent of patients need long-term dialysis, and the five-year survival rate has surpassed 80%. But it has been discovered that cyclophosphamide delayed administration is connected to a catastrophic prognosis.
Clinical History
The clinical signs and symptoms of people with anti-glomerular basement membrane (anti-GBM) illness vary significantly. Between 60 and 80 percent of patients have pulmonary & renal illness that is clinically evident, 20 to 40 percent have the renal disease only, and less than 10 percent have a lung-only disease.
Among the symptoms are the following:
Constitutional signs, such as arthralgias, malaise, chills, and fever, may appear before or simultaneously with renal or pulmonary signs.
When the disease affects the lungs, hemoptysis is the first symptom to appear. There may be different levels of hemoptysis, and other patients may not have any at all. Additionally, coughing, dyspnea, and shortness of breath are pulmonary symptoms.
There could be a massive lung hemorrhage that causes respiratory distress.
Less than half of patients report having heart problems. Hematuria, edema, elevated blood pressure, &finally, uremia is examples of renal symptoms.
Chronic intrapulmonary hemorrhage may cause significant anemia.
Physical examination
The following physical examination characteristics are seen in people with the anti-GBM disorder:
Edema
Rash
Hypertension (possible in 20% of cases)
Hepatosplenomegaly (possibly present)
Cyanosis
Tachypnea
Breathing crackles over the lungs’ bases
Differential Diagnosis
In the differentials, all pulmonary-renal disorders that impact the kidney and lungs must be considered. These consist of:
Polyangiitis and granulomatosis (Wegener granulomatosis)
Microscopic polyangiitis
It might be challenging to identify Goodpasture syndrome from granulomatosis with polyangiitis because some patients with it also have positive ANCAs.
Some pulmonary-renal syndromes are also associated with IgA-mediated diseases, including:
Henoch-Schönlein purpura
IgA nephropathy
Additional differential diagnoses consist of:
Churg-Strauss syndrome
Pneumocystis jiroveci pneumoniae
Granulomatosis with polyangiitis
Community-acquired pneumoniae
Acute glomerulonephritis
Patients with Goodpasture syndrome, which includes both glomerulonephritis & pulmonary bleeding, may already be in serious condition when they present. Standard indications frequently necessitate urgent hemodialysis, & intubation may be required in cases of respiratory impairment. As soon as the clinical circumstances permit, a renal biopsy should be performed when the clinician detects the diagnosis. Prednisone, daily plasmapheresis, and cyclophosphamide should be started in patients as soon as they are diagnosed in order to reduce overall fatality and increase kidney survival in particular.
The overall kidney prognosis is better if treatment can begin before the patient needs kidney replacement therapy. Regardless of their renal state, combination therapy should be initiated for all patients suffering from pulmonary signs. The risks of immunosuppressive & plasmapheresis medications may outweigh the advantages for individuals without pulmonary symptoms whose kidney recovery is highly unlikely (i.e., for those who came with an immediate need for dialysis during the initial 72 hours).
Given that the disease has yet to be well investigated in controlled studies, the decision to forego therapy in certain circumstances is still debatable. Who specifically in this group will respond and regain kidney function is still challenging to predict. Although there has been an average 8% improvement in renal function in this group, many doctors still choose to try more aggressive combination therapy at this point. Daily plasmapheresis is typically carried out until anti-glomerular outer membrane antibodies are undetectable, followed by three to six months of steroid & cyclophosphamide treatment until complete remission is obtained.
This can be assessed by running additional titers after plasmapheresis, and at any time, new signs emerge that might be a sign of recurrence. Overall, recurrence is still uncommon. Cyclophosphamide is first administered orally at a dose of 2 mg/kg that is modified to maintain a white cell count of about 5000. Acute, life-threatening alveolar hemorrhage is treated with 1g/day IV pulse therapy of methylprednisolone for 3 days, then a tapered dosage of 1 to 1.5 mg/kg orally. In several investigations, it was determined that rituximab played a part in the development of extremely low levels of anti-GBM autoantibodies.
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