Poststreptococcal glomerulonephritis is caused by an inflammatory reaction in the kidneys, leading to a rapid decline in kidney function. This condition occurs due to an overreaction of the immune system to a type of bacteria called group A beta-hemolytic streptococci, specifically nephrogenic strains. PSGN primarily affects the glomeruli and small blood vessels in the kidneys, leading to significant impairment in the organ’s ability to filter waste products and excess fluids from the blood.
Typically, PSGN develops in children about 1 to 2 weeks after experiencing a sore throat, although it can also occur up to 6 weeks after a skin infection called impetigo. The inflammatory response that causes PSGN is known as a type III hypersensitivity reaction, characterized by the accumulation of immune complexes in the kidneys’ glomeruli. Over time, these immune complexes cause damage to the kidneys, leading to a range of symptoms such as high blood pressure, proteinuria, and decreased urine output.
Epidemiology
Over the last thirty years, the incidence has substantially declined in developed countries, such as the United Kingdom, the United States, Japan, and Central Europe. This is due to the increased use of antibiotic prophylaxis and better hygienic practices. However, it is still commonly seen in adult patients suffering from chronic debilitating diseases in these countries.
Developing countries still have a higher incidence rate of PSGN due to an increased prevalence of skin infections, especially pyoderma. Despite the decrease in incidence, it remains the most common cause of glomerulonephritis in children in the United States and the most frequent cause of kidney injury in children in the Middle East, Australia, Africa, and globally.
The annual incidence rate of new cases in developing countries ranges from 28.5 per 100,000 individuals, and 97% of reported cases occur in underprivileged countries. PSGN is more frequently observed in males than in females clinically, with a ratio of 2:1. However, the incidence of subclinical PSGN is almost equal in both sexes. Racial factors have not been found to play a role in the incidence of the disease.
The age group most commonly affected is children aged between 3 and 12, with the highest incidence rate occurring between the ages of 5 and 6. PSGN is also more common in older adults over 60 years old. Overall, despite the decline in developed countries, it remains a significant public health concern, especially in developing countries, where it is associated with poor hygiene and inadequate access to healthcare.
Anatomy
Pathophysiology
Post-streptococcal glomerulonephritis (PSGN) is an immunological disease characterized by a type III hypersensitivity reaction. The exact mechanism by which it occurs is not fully understood. However, it is known that the body responds to a nephrogenic streptococcal infection by forming immune complexes containing streptococcal antigens and human antibodies. These immune complexes can then be deposited in the kidney glomeruli through the circulation or an in-situ formation within the glomeruli.
Several theories exist on how in situ immune complex formation occurs in PSGN. One theory suggests that the immune complexes are formed as a reaction against streptococcal antigens deposited in the glomerular basement membrane. Another theory proposes that immune complexes are formed due to an antibody reaction against glomerular components that cross-react with streptococcal antigens, possibly due to molecular mimicry.
The presence of immune complexes in the glomeruli leads to the activation of the alternate complement pathway, which causes infiltration of leukocytes and proliferation of mesangial cells. This can impair capillary perfusion and reduce the glomerular filtration rate. Reducing GFR can lead to renal failure, electrolyte abnormalities, acid-base imbalances, volume overload, edema, and hypertension.
Etiology
Nephrogenic streptococcal infection is often a precursor to post-streptococcal glomerulonephritis which initially affects the skin or oropharynx. In recent years, PSGN has been more commonly associated with skin infections like impetigo than throat infections like pharyngitis. Group A Streptococcus (GAS) has been subtyped based on the surface M protein and opacity factor, which are nephrogenic and can contribute to the development of PSGN.
In addition to GAS, other bacterial infections such as endocarditis, enterocolitis, pneumonia, and intraventricular shunt infections, as well as viral infections like hepatitis B and C, human immunodeficiency virus (HIV), Epstein Barr virus, cytomegalovirus and parvovirus B19, and even parasitic and fungal infections such as malaria, coccidioidomycosis, leishmania, histoplasmosis, toxoplasmosis, and schistosomiasis can also cause post-infectious glomerulonephritis.
Poor hygiene, overcrowding, and low socioeconomic status are significant risk factors for streptococcal outbreaks, which may explain the higher incidence of PSGN in impoverished countries. Additionally, genetic factors may predispose individuals to the condition, as almost 40% of patients with PSGN have a positive family history. While no specific gene has been identified as the sole cause of PSGN, research suggests that genetic factors may play a role in increasing the risk of developing the condition.
Genetics
Prognostic Factors
PSGN has a favorable prognosis, particularly in children, with complete recovery typically occurring within 6 to 8 weeks. However, in adults, approximately 50% of patients may experience hypertension, renal impairment, or persistent proteinuria. In adults, mortality is often due to renal dysfunction and heart failure.
Long-term studies indicate that some patients may continue to exhibit abnormalities in urine, proteinuria, and hypertension. During the acute phase of glomerulonephritis, mortality rates are up to 12%. While it was previously assumed that the renal changes observed in survivors of the initial acute attack would be similar to those found in fatal cases, there was limited direct evidence to support this hypothesis.
Clinical History
Clinical History
Approximately half of the children diagnosed with PSGN do not show symptoms and are discovered through routine urine analysis. The classic triad of glomerulonephritis includes edema, hematuria, and hypertension. Usually, patients report a recent streptococcal infection, such as tonsillitis, pharyngitis, or impetigo.
However, some patients may develop PSGN without experiencing respiratory tract infection or pyoderma symptoms, making diagnosis challenging. Renal involvement is common and typically resolves within one to two weeks.
Oliguria is experienced by less than half of the patients. In severe cases of renal involvement, symptoms such as anuria (a complete lack of urine output) or life-threatening acid-base imbalances, electrolyte abnormalities (especially hyperkalemia), and fluid overload may necessitate the use of RRT (renal replacement therapy). High blood pressure is experienced by 60-80% of patients and typically resolves within ten days.
Physical Examination
Physical Examination
Acute PSGN is often accompanied by a range of symptoms, the most common being gross hematuria. This is characterized by smoky, tea-colored, cola-colored, or rusty urine, which occurs in 30 to 50% of cases. The hematuria is typically postpharyngitic, which is seen several weeks after the initial infection.
Another common symptom of acute PSGN is edema, which occurs in approximately 65-90% of cases. This can present as periorbital edema, which causes puffiness of the eyelids and is typical of nephrotic syndrome. This symptom is most pronounced in the morning and tends to subside towards the end of the day. Generalized edema, affecting other parts of the body, is also common.
In severe cases, patients may experience respiratory distress due to pulmonary edema resulting from fluid accumulation in the lungs. Additionally, patients may experience non-specific symptoms, including nausea, vomiting, malaise, and anorexia. It is important to note that while these symptoms are characteristic of acute PSGN, they are not always present and may vary in severity from one individual to another.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnoses
Lupus nephritis
Nephrotic Syndrome
Henoch Schonlein purpura
Hemolytic uremic syndrome
Goodpasture disease
IgA Nephropathy
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Patients who show signs of a streptococcal infection should receive a antibiotic therapy as a first-line treatment. However, it is important to note that antibiotics may not necessarily prevent. It is recommended that loop diuretics such as furosemide be preferred over thiazides like chlorthalidone or hydrochlorothiazide in managing edema in patients with PSGN. This is because the efficacy of thiazide diuretics is significantly reduced when the GFR is less than 30 ml/min.
Blood pressure management in PSGN patients can be achieved by limiting salt and fluid intake and using diuretics. If blood pressure remains, uncontrolled, calcium channel blockers may be recommended. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are recommended for patients with stable GFR and near-normal potassium levels.
Dialysis is usually not necessary except in cases where it is required to manage the acid-base balance, electrolyte abnormalities, and fluid management. In the initial stages of the disease, general measures such as salt and water restriction, bed rest, and immobilization are often recommended to help alleviate symptoms of edema.
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Poststreptococcal glomerulonephritis is caused by an inflammatory reaction in the kidneys, leading to a rapid decline in kidney function. This condition occurs due to an overreaction of the immune system to a type of bacteria called group A beta-hemolytic streptococci, specifically nephrogenic strains. PSGN primarily affects the glomeruli and small blood vessels in the kidneys, leading to significant impairment in the organ’s ability to filter waste products and excess fluids from the blood.
Typically, PSGN develops in children about 1 to 2 weeks after experiencing a sore throat, although it can also occur up to 6 weeks after a skin infection called impetigo. The inflammatory response that causes PSGN is known as a type III hypersensitivity reaction, characterized by the accumulation of immune complexes in the kidneys’ glomeruli. Over time, these immune complexes cause damage to the kidneys, leading to a range of symptoms such as high blood pressure, proteinuria, and decreased urine output.
Over the last thirty years, the incidence has substantially declined in developed countries, such as the United Kingdom, the United States, Japan, and Central Europe. This is due to the increased use of antibiotic prophylaxis and better hygienic practices. However, it is still commonly seen in adult patients suffering from chronic debilitating diseases in these countries.
Developing countries still have a higher incidence rate of PSGN due to an increased prevalence of skin infections, especially pyoderma. Despite the decrease in incidence, it remains the most common cause of glomerulonephritis in children in the United States and the most frequent cause of kidney injury in children in the Middle East, Australia, Africa, and globally.
The annual incidence rate of new cases in developing countries ranges from 28.5 per 100,000 individuals, and 97% of reported cases occur in underprivileged countries. PSGN is more frequently observed in males than in females clinically, with a ratio of 2:1. However, the incidence of subclinical PSGN is almost equal in both sexes. Racial factors have not been found to play a role in the incidence of the disease.
The age group most commonly affected is children aged between 3 and 12, with the highest incidence rate occurring between the ages of 5 and 6. PSGN is also more common in older adults over 60 years old. Overall, despite the decline in developed countries, it remains a significant public health concern, especially in developing countries, where it is associated with poor hygiene and inadequate access to healthcare.
Post-streptococcal glomerulonephritis (PSGN) is an immunological disease characterized by a type III hypersensitivity reaction. The exact mechanism by which it occurs is not fully understood. However, it is known that the body responds to a nephrogenic streptococcal infection by forming immune complexes containing streptococcal antigens and human antibodies. These immune complexes can then be deposited in the kidney glomeruli through the circulation or an in-situ formation within the glomeruli.
Several theories exist on how in situ immune complex formation occurs in PSGN. One theory suggests that the immune complexes are formed as a reaction against streptococcal antigens deposited in the glomerular basement membrane. Another theory proposes that immune complexes are formed due to an antibody reaction against glomerular components that cross-react with streptococcal antigens, possibly due to molecular mimicry.
The presence of immune complexes in the glomeruli leads to the activation of the alternate complement pathway, which causes infiltration of leukocytes and proliferation of mesangial cells. This can impair capillary perfusion and reduce the glomerular filtration rate. Reducing GFR can lead to renal failure, electrolyte abnormalities, acid-base imbalances, volume overload, edema, and hypertension.
Nephrogenic streptococcal infection is often a precursor to post-streptococcal glomerulonephritis which initially affects the skin or oropharynx. In recent years, PSGN has been more commonly associated with skin infections like impetigo than throat infections like pharyngitis. Group A Streptococcus (GAS) has been subtyped based on the surface M protein and opacity factor, which are nephrogenic and can contribute to the development of PSGN.
In addition to GAS, other bacterial infections such as endocarditis, enterocolitis, pneumonia, and intraventricular shunt infections, as well as viral infections like hepatitis B and C, human immunodeficiency virus (HIV), Epstein Barr virus, cytomegalovirus and parvovirus B19, and even parasitic and fungal infections such as malaria, coccidioidomycosis, leishmania, histoplasmosis, toxoplasmosis, and schistosomiasis can also cause post-infectious glomerulonephritis.
Poor hygiene, overcrowding, and low socioeconomic status are significant risk factors for streptococcal outbreaks, which may explain the higher incidence of PSGN in impoverished countries. Additionally, genetic factors may predispose individuals to the condition, as almost 40% of patients with PSGN have a positive family history. While no specific gene has been identified as the sole cause of PSGN, research suggests that genetic factors may play a role in increasing the risk of developing the condition.
PSGN has a favorable prognosis, particularly in children, with complete recovery typically occurring within 6 to 8 weeks. However, in adults, approximately 50% of patients may experience hypertension, renal impairment, or persistent proteinuria. In adults, mortality is often due to renal dysfunction and heart failure.
Long-term studies indicate that some patients may continue to exhibit abnormalities in urine, proteinuria, and hypertension. During the acute phase of glomerulonephritis, mortality rates are up to 12%. While it was previously assumed that the renal changes observed in survivors of the initial acute attack would be similar to those found in fatal cases, there was limited direct evidence to support this hypothesis.
Clinical History
Approximately half of the children diagnosed with PSGN do not show symptoms and are discovered through routine urine analysis. The classic triad of glomerulonephritis includes edema, hematuria, and hypertension. Usually, patients report a recent streptococcal infection, such as tonsillitis, pharyngitis, or impetigo.
However, some patients may develop PSGN without experiencing respiratory tract infection or pyoderma symptoms, making diagnosis challenging. Renal involvement is common and typically resolves within one to two weeks.
Oliguria is experienced by less than half of the patients. In severe cases of renal involvement, symptoms such as anuria (a complete lack of urine output) or life-threatening acid-base imbalances, electrolyte abnormalities (especially hyperkalemia), and fluid overload may necessitate the use of RRT (renal replacement therapy). High blood pressure is experienced by 60-80% of patients and typically resolves within ten days.
Physical Examination
Acute PSGN is often accompanied by a range of symptoms, the most common being gross hematuria. This is characterized by smoky, tea-colored, cola-colored, or rusty urine, which occurs in 30 to 50% of cases. The hematuria is typically postpharyngitic, which is seen several weeks after the initial infection.
Another common symptom of acute PSGN is edema, which occurs in approximately 65-90% of cases. This can present as periorbital edema, which causes puffiness of the eyelids and is typical of nephrotic syndrome. This symptom is most pronounced in the morning and tends to subside towards the end of the day. Generalized edema, affecting other parts of the body, is also common.
In severe cases, patients may experience respiratory distress due to pulmonary edema resulting from fluid accumulation in the lungs. Additionally, patients may experience non-specific symptoms, including nausea, vomiting, malaise, and anorexia. It is important to note that while these symptoms are characteristic of acute PSGN, they are not always present and may vary in severity from one individual to another.
Differential Diagnoses
Lupus nephritis
Nephrotic Syndrome
Henoch Schonlein purpura
Hemolytic uremic syndrome
Goodpasture disease
IgA Nephropathy
Patients who show signs of a streptococcal infection should receive a antibiotic therapy as a first-line treatment. However, it is important to note that antibiotics may not necessarily prevent. It is recommended that loop diuretics such as furosemide be preferred over thiazides like chlorthalidone or hydrochlorothiazide in managing edema in patients with PSGN. This is because the efficacy of thiazide diuretics is significantly reduced when the GFR is less than 30 ml/min.
Blood pressure management in PSGN patients can be achieved by limiting salt and fluid intake and using diuretics. If blood pressure remains, uncontrolled, calcium channel blockers may be recommended. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are recommended for patients with stable GFR and near-normal potassium levels.
Dialysis is usually not necessary except in cases where it is required to manage the acid-base balance, electrolyte abnormalities, and fluid management. In the initial stages of the disease, general measures such as salt and water restriction, bed rest, and immobilization are often recommended to help alleviate symptoms of edema.
medtigo
Poststreptococcal Glomerulonephritis
Updated :
August 24, 2023
Poststreptococcal glomerulonephritis is caused by an inflammatory reaction in the kidneys, leading to a rapid decline in kidney function. This condition occurs due to an overreaction of the immune system to a type of bacteria called group A beta-hemolytic streptococci, specifically nephrogenic strains. PSGN primarily affects the glomeruli and small blood vessels in the kidneys, leading to significant impairment in the organ’s ability to filter waste products and excess fluids from the blood.
Typically, PSGN develops in children about 1 to 2 weeks after experiencing a sore throat, although it can also occur up to 6 weeks after a skin infection called impetigo. The inflammatory response that causes PSGN is known as a type III hypersensitivity reaction, characterized by the accumulation of immune complexes in the kidneys’ glomeruli. Over time, these immune complexes cause damage to the kidneys, leading to a range of symptoms such as high blood pressure, proteinuria, and decreased urine output.
Over the last thirty years, the incidence has substantially declined in developed countries, such as the United Kingdom, the United States, Japan, and Central Europe. This is due to the increased use of antibiotic prophylaxis and better hygienic practices. However, it is still commonly seen in adult patients suffering from chronic debilitating diseases in these countries.
Developing countries still have a higher incidence rate of PSGN due to an increased prevalence of skin infections, especially pyoderma. Despite the decrease in incidence, it remains the most common cause of glomerulonephritis in children in the United States and the most frequent cause of kidney injury in children in the Middle East, Australia, Africa, and globally.
The annual incidence rate of new cases in developing countries ranges from 28.5 per 100,000 individuals, and 97% of reported cases occur in underprivileged countries. PSGN is more frequently observed in males than in females clinically, with a ratio of 2:1. However, the incidence of subclinical PSGN is almost equal in both sexes. Racial factors have not been found to play a role in the incidence of the disease.
The age group most commonly affected is children aged between 3 and 12, with the highest incidence rate occurring between the ages of 5 and 6. PSGN is also more common in older adults over 60 years old. Overall, despite the decline in developed countries, it remains a significant public health concern, especially in developing countries, where it is associated with poor hygiene and inadequate access to healthcare.
Post-streptococcal glomerulonephritis (PSGN) is an immunological disease characterized by a type III hypersensitivity reaction. The exact mechanism by which it occurs is not fully understood. However, it is known that the body responds to a nephrogenic streptococcal infection by forming immune complexes containing streptococcal antigens and human antibodies. These immune complexes can then be deposited in the kidney glomeruli through the circulation or an in-situ formation within the glomeruli.
Several theories exist on how in situ immune complex formation occurs in PSGN. One theory suggests that the immune complexes are formed as a reaction against streptococcal antigens deposited in the glomerular basement membrane. Another theory proposes that immune complexes are formed due to an antibody reaction against glomerular components that cross-react with streptococcal antigens, possibly due to molecular mimicry.
The presence of immune complexes in the glomeruli leads to the activation of the alternate complement pathway, which causes infiltration of leukocytes and proliferation of mesangial cells. This can impair capillary perfusion and reduce the glomerular filtration rate. Reducing GFR can lead to renal failure, electrolyte abnormalities, acid-base imbalances, volume overload, edema, and hypertension.
Nephrogenic streptococcal infection is often a precursor to post-streptococcal glomerulonephritis which initially affects the skin or oropharynx. In recent years, PSGN has been more commonly associated with skin infections like impetigo than throat infections like pharyngitis. Group A Streptococcus (GAS) has been subtyped based on the surface M protein and opacity factor, which are nephrogenic and can contribute to the development of PSGN.
In addition to GAS, other bacterial infections such as endocarditis, enterocolitis, pneumonia, and intraventricular shunt infections, as well as viral infections like hepatitis B and C, human immunodeficiency virus (HIV), Epstein Barr virus, cytomegalovirus and parvovirus B19, and even parasitic and fungal infections such as malaria, coccidioidomycosis, leishmania, histoplasmosis, toxoplasmosis, and schistosomiasis can also cause post-infectious glomerulonephritis.
Poor hygiene, overcrowding, and low socioeconomic status are significant risk factors for streptococcal outbreaks, which may explain the higher incidence of PSGN in impoverished countries. Additionally, genetic factors may predispose individuals to the condition, as almost 40% of patients with PSGN have a positive family history. While no specific gene has been identified as the sole cause of PSGN, research suggests that genetic factors may play a role in increasing the risk of developing the condition.
PSGN has a favorable prognosis, particularly in children, with complete recovery typically occurring within 6 to 8 weeks. However, in adults, approximately 50% of patients may experience hypertension, renal impairment, or persistent proteinuria. In adults, mortality is often due to renal dysfunction and heart failure.
Long-term studies indicate that some patients may continue to exhibit abnormalities in urine, proteinuria, and hypertension. During the acute phase of glomerulonephritis, mortality rates are up to 12%. While it was previously assumed that the renal changes observed in survivors of the initial acute attack would be similar to those found in fatal cases, there was limited direct evidence to support this hypothesis.
Clinical History
Approximately half of the children diagnosed with PSGN do not show symptoms and are discovered through routine urine analysis. The classic triad of glomerulonephritis includes edema, hematuria, and hypertension. Usually, patients report a recent streptococcal infection, such as tonsillitis, pharyngitis, or impetigo.
However, some patients may develop PSGN without experiencing respiratory tract infection or pyoderma symptoms, making diagnosis challenging. Renal involvement is common and typically resolves within one to two weeks.
Oliguria is experienced by less than half of the patients. In severe cases of renal involvement, symptoms such as anuria (a complete lack of urine output) or life-threatening acid-base imbalances, electrolyte abnormalities (especially hyperkalemia), and fluid overload may necessitate the use of RRT (renal replacement therapy). High blood pressure is experienced by 60-80% of patients and typically resolves within ten days.
Physical Examination
Acute PSGN is often accompanied by a range of symptoms, the most common being gross hematuria. This is characterized by smoky, tea-colored, cola-colored, or rusty urine, which occurs in 30 to 50% of cases. The hematuria is typically postpharyngitic, which is seen several weeks after the initial infection.
Another common symptom of acute PSGN is edema, which occurs in approximately 65-90% of cases. This can present as periorbital edema, which causes puffiness of the eyelids and is typical of nephrotic syndrome. This symptom is most pronounced in the morning and tends to subside towards the end of the day. Generalized edema, affecting other parts of the body, is also common.
In severe cases, patients may experience respiratory distress due to pulmonary edema resulting from fluid accumulation in the lungs. Additionally, patients may experience non-specific symptoms, including nausea, vomiting, malaise, and anorexia. It is important to note that while these symptoms are characteristic of acute PSGN, they are not always present and may vary in severity from one individual to another.
Differential Diagnoses
Lupus nephritis
Nephrotic Syndrome
Henoch Schonlein purpura
Hemolytic uremic syndrome
Goodpasture disease
IgA Nephropathy
Patients who show signs of a streptococcal infection should receive a antibiotic therapy as a first-line treatment. However, it is important to note that antibiotics may not necessarily prevent. It is recommended that loop diuretics such as furosemide be preferred over thiazides like chlorthalidone or hydrochlorothiazide in managing edema in patients with PSGN. This is because the efficacy of thiazide diuretics is significantly reduced when the GFR is less than 30 ml/min.
Blood pressure management in PSGN patients can be achieved by limiting salt and fluid intake and using diuretics. If blood pressure remains, uncontrolled, calcium channel blockers may be recommended. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are recommended for patients with stable GFR and near-normal potassium levels.
Dialysis is usually not necessary except in cases where it is required to manage the acid-base balance, electrolyte abnormalities, and fluid management. In the initial stages of the disease, general measures such as salt and water restriction, bed rest, and immobilization are often recommended to help alleviate symptoms of edema.
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