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Article: What is Poststreptococcal Glomerulonephritis and What Causes it?

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Article: What is Poststreptococcal Glomerulonephritis and What Causes it?

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Poststreptococcal Glomerulonephritis is a kidney disease that is caused by a bacterial infection. This disease is due to an inflammatory response and is known as a type III hypersensitivity reaction. It leads to the deterioration of the kidneys, causing complications such as hypotension, swelling, decreased urine output, and rust-colored urine. This disease is treated by supportive care and antibiotics (Rawla et al., 2022).

I have included this article because it includes a clear definition of the disease, Poststreptococcal Glomerulonephritis, and how it is caused. I know it is a credible source because it is backed up by research, is recent, and has been peer-reviewed. I liked that this source also defined and explained that PSGN is an inflammatory response and a type three hypersensitivity reaction. I feel that this source was very detailed as it also included the epidemiology, evaluation, and treatment of PSGN. This source also included complications and prognosis of PSGN. I feel that this resource provided an adequate overview of this disease.

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Continuing Education Activity

Poststreptococcal glomerulonephritis (PSGN) results from a bacterial infection that causes rapid deterioration of the kidney function due to an inflammatory response following streptococcal infection. PSGN most commonly presents in children 1 to 2 weeks after a streptococcal throat infection, or within 6 weeks following a streptococcal skin infection. When symptomatic, PSGN typically presents with features of the nephritic syndrome such as hematuria, oliguria, hypertension, and edema, though it can also present with significant proteinuria. This activity reviews the etiology, pathogenesis, evaluation, and management of PSGN and explains the role of the interprofessional team in evaluating and treating patients with this condition.

Objectives:

Identify the epidemiology, etiology, pathophysiology of poststreptococcal glomerulonephritis.

Review how to evaluate a patient for poststreptococcal glomerulonephritis.

Summarize the treatment and management options available for poststreptococcal glomerulonephritis.

Explain interprofessional team strategies for improving care coordination and communication to improve outcomes for patients affected by poststreptococcal glomerulonephritis.

Access free multiple choice questions on this topic.
Introduction

Poststreptococcal glomerulonephritis (PSGN) is characterized by rapid deterioration of kidney functions due to an inflammatory response (type III hypersensitivity reaction) following streptococcal infection. This condition results from specific strains of group A beta-hemolytic streptococci called nephrogenic streptococci. The disease affects the glomeruli and the small blood vessels of the kidneys. PSGN most frequently presents in children 1 to 2 weeks after a sore throat, or 6 weeks after a skin infection (impetigo).[1]

Though the incidence of PSGN has declined in developed countries, the incidence of non-streptococcal organisms is emerging. Nephritis-associated plasmin receptor (NAPlr) and streptococcal pyrogenic exotoxin B (SPeB) are the two common antigens associated with the pathogenesis of PSGN. They not only activate the alternate complement pathway, resulting in hypocomplementemia, but they also have an affinity towards the plasmin and glomerular proteins. The clinical presentation of PIGN can vary from no symptoms to renal failure requiring renal replacement therapy (RRT). [2]

When symptomatic, PSGN typically presents with features of the nephritic syndrome such as hematuria, oliguria, hypertension, and edema. Less commonly presentation can mimic nephrotic syndrome with significant proteinuria.

Etiology

Nephrogenic streptococci infection precedes PSGN, which initially affects skin or the oropharynx. More recently, PSGN is associated with skin infections (impetigo) more frequently than throat infections (pharyngitis).[3][4]

Group A Streptococcus (GAS) has been subtyped depending on the surface M protein and opacity factor, which are known to be nephrogenic and can cause PSGN. Other causes of post-infectious glomerulonephritis include bacterial infections including endocarditis, enterocolitis, pneumonia, and intraventricular shunt infections, viral (hepatitis B and C infections, human immunodeficiency virus, cytomegalovirus, Epstein Barr virus, parvovirus B19), fungal (coccidioidomycosis, histoplasmosis), and parasitic infections (malaria, leishmania, toxoplasmosis, and schistosomiasis).[5]

Poor hygiene, overcrowding, and low socioeconomic status are important risk factors for streptococci outbreaks, and this explains the higher incidence of PSGN in impoverished countries. Genetic factors are expected to predispose to the condition since almost 40% of patients with PSGN gave a positive family history. There is no specific gene found to cause PSGN.[5]

Epidemiology

Over the past three decades, PSGN incidence has significantly dropped in developed countries; such as the United States, UK, Central Europe, and Japan. The reason for this progress is the use of antibiotic prophylaxis and the improvement of hygienic states. In these developed countries, PSGN has become more frequently seen in adult patients who suffer from chronic debilitating diseases.[6]

Higher incidence of PSGN in developing countries- due to increased skin infections (pyoderma). Though the incidence in developed countries has gone down, it is still the most common cause of glomerulonephritis (GN) in children in the united states. [5]

PSGN is also the most common cause of kidney injury in children in the Middle East, Africa, Australia, and worldwide. The annual incidence of new cases of PSGN in developing countries ranges from 8.5 to 28.5 per 100000 individuals.[7] Around 97% of cases reported with PSGN live in underprivileged countries.

Clinically manifestations of PSGN are more common in males than in females with a ratio of 2:1. However; the incidence of subclinical PSGN is almost equal in both sexes. Racial factors were not found to play a role. The disease most frequently affects children between the age of 3 and 12 (with the peak incidence between 5 to 6 years), and seniors greater than 60 years old.

Pathophysiology

The disease is immunological; representing a type III hypersensitivity reaction. The exact mechanism by which PSGN occurs is not fully determined. The body responds to nephrogenic streptococcal infection by forming immune complexes containing the streptococcal antigen with a human antibody.[2] Some theories suggest that these immune complexes become deposited in kidney glomeruli reaching through the circulation. Others claim that the condition results from an "in situ" formation of the antigen-antibody complex within the kidney glomeruli. This "In situ immune complex formation" is either due to a reaction against streptococci antigens deposited in the glomerular basement membrane or, according to other theories, due to an antibody reaction against glomerular components that cross-react with streptococcal antigen due to molecular mimicry.[5]

The presence of immune complexes leads to the activation of the alternate complement pathway causing infiltration of the leukocytes, and proliferation of the mesangial cells in the glomerulus thus impairing the capillary perfusion and glomerular filtration rate (GFR). Reduction in GFR can lead to renal failure (oliguria or anuria), acid-base imbalance, electrolyte abnormalities, volume overload, edema, and hypertension.

Histopathology

Light microscopy- The glomeruli show hypercellularity (endothelial, mesangial, and inflammatory cells) which are non-specific.

Electron microscopy- The most characteristic finding is the presence of sub-epithelial humps; which are electron-dense deposits in the subepithelial space near the glomerular basement membrane.[8]

Immunofluorescence microscopy- Evidence of IgG and C3 deposits in the first 2 to 3 weeks of the disease.

History and Physical

Approximately 50% of children with PSGN are asymptomatic and are discovered accidentally during routine urine analysis. The classic triad of glomerulonephritis includes hematuria, edema, and hypertension. Typically, patients give a history of a recent streptococcal infection such as pharyngitis, tonsillitis, or impetigo. However; some patients develop PSGN without experiencing symptoms of respiratory tract infection or pyoderma, which can be a diagnostic challenge.[9]

The most common presenting symptom is gross hematuria as it occurs in 30 to 50% of cases with acute PSGN; patients often describe their urine as smoky, tea-colored, cola-colored, or rusty. The hematuria can be described as postpharyngitic (hematuria seen after weeks of infection).

Renal involvement is common and is transient with recovery in 1-2 weeks. Less than half of the patients experience oliguria. Depending on the severity of renal involvement, signs, and symptoms suggestive of anuric renal failure or life-threatening acid-base imbalance, electrolyte abnormalities (especially hyperkalemia), and fluid overload would require RRT. About 60-80% of the patients experience high blood pressure which typically resolves in 10 days. [5]

The incidence of edema is seen in about 65-90% of the cases. Puffiness of the eyelids (periorbital edema) is typical for the nephritic syndrome. It is most prominent in the morning and tends to resolve at the end of the day. Generalized edema is also a common feature. Moreover, in severe cases, patients might experience respiratory distress as a result of pulmonary edema. They may experience other non-specific symptoms like anorexia, malaise, nausea, vomiting, etc.

Evaluation

PSGN should be suspected in all children with hypertension and heart failure, even in the absence of hematuria or a history of a preceding sore throat or pyoderma.

Laboratory investigations are the most useful in PSGN assessment.

Evidence of a preceding streptococcal infection is determined by measuring anti-streptolysin titer (ASO), and anti-nicotinamide-adenine dinucleotidase (anti-NAD) which tend to rise following pharyngitis. Other antibodies such as anti-DNAse B and anti-hyaluronidase (AHase) are usually elevated after both pharyngitis and skin infections. ASO titer is the most frequently used test, while the most sensitive is the streptozyme test; which includes measuring the titers of all the antibodies mentioned above. ASO titers can be falsely low in patients treated with antibiotics for streptococcal infections.

Serum complement level (C3) is usually low due to its consumption in the inflammatory reaction. Mostly, the decrease in C3 concentration occurs before serum ASO has risen.[5] Complement levels usually return to normal levels in 6-8 weeks.

Progressive decline in the Renal function

When there is no latent period between the acute glomerulonephritis and streptococcal infection

If the complement levels are normal

When there is no rise in antistreptococcal antibodies

Urine analysis: shows macroscopic or microscopic hematuria, RBC casts, mild proteinuria. Only 5% of patients with PSGN have massive proteinuria that indicates nephrotic syndrome. White blood cell casts, hyaline, and cellular casts are usually present in the urine analysis.

Ultrasonography: Kidneys are enlarged only in a few patients.

The chest x-ray may show pulmonary congestion in patients with symptoms consistent with volume overload or heart failure.

Renal Function Tests: Blood urea nitrogen (BUN) and serum creatinine typically elevate during the acute phase. These values usually return to normal later.

In patients with heart failure and PSGN, NT-proBNP levels are elevated along with the findings of pulmonary congestion on the chest x-ray.

Renal biopsy is not recommended for diagnosing patients with PSGN and is performed only when other glomerular pathologies are suspected. Renal biopsy is indicated when:

Imaging Studies

Treatment / Management

PSGN is a self-limiting condition in most cases, and thus only symptomatic treatment is needed. Supportive treatment aims at controlling the complications of volume overload such as hypertension and edema, which are prominent during the acute phase of the disease.[5]

Pharmacological Therapy

Antimicrobials: Patients with evidence of a streptococcal infection should receive a course of antibiotic therapy, and they may not prevent the development of PSGN.

Diuretics: Loop diuretics (furosemide) are preferred over thiazides (hydrochlorothiazide or chlorthalidone). The efficacy of thiazide diuretics is very minimal when GFR < 30 ml/min.

Antihypertensive medications: Blood pressure can be managed by restricting salt and fluid intake along with diuretics are needed. In cases with uncontrolled blood pressure, the use of calcium channel blockers is recommended. The use of angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARBs) is recommended in patients with stable GFR and with near-normal potassium levels.

Salt and water restriction to treat the edema.

Bed rest and immobilization are recommendations in the first few days of the disease.

Throat cultures on the patient and family members are important.

All affected members need to be treated with penicillin or erythromycin.

Immunosuppressive therapy: There's no evidence that immune suppression is useful in patients with PSGN.[10]However, patients with progressive renal failure or the presence of crescents on the renal biopsy may warrant the use of corticosteroids.[11][11][11]

IgA Nephropathy: usually occurs after an upper respiratory tract or gastrointestinal infection, but it differs from PSGN in the shorter latency period it takes to appear after the episode of infection. It can also be described as synpharyngitic hematuria- hematuria and infection coincide.

Membranoproliferative glomerulonephritis: also presents with a nephritic picture and hypocomplementemia following respiratory tract infection. Complement levels take a longer time to return to normal than in PSGN or persistently low C3 levels.

Lupus nephritis: sometimes PSGN presents with a picture similar to lupus nephritis. Laboratory testing for antibodies specific to each of the diseases can help in the diagnosis. Positive ANA, ds-DNA, cytopenia, and multi-organ involvement.

Nephrotic syndrome: 2 4-hour urine protein excretion is more than 3.5 gram/day along with hypoalbuminemia, edema, hypogammaglobulinemia, and increased risk of thrombosis (due to loss of pro-coagulants).

Henoch Schonlein purpura (HSP): The typical presentation is palpable purpura, renal failure, gastrointestinal and musculoskeletal manifestations. Have normal complement levels.

Hemolytic uremic syndrome (HUS): Labs consistent with Hemolysis (schistocytes, LDH, reticulocyte count, indirect bilirubin), bloody diarrhea, thrombocytopenia, stool culture for Escherichia coil O157: H7

ANCA: Have normal complement levels.

Goodpasture disease: Involves lung and kidneys. Have anti-glomerular basement antibody and normal complement levels.

Dialysis

Dialysis is only performed to manage the acid-base balance, electrolyte abnormalities (especially hyperkalemia), and fluid management

General measures

Differential Diagnosis

Prognosis

PSGN has an excellent prognosis especially in children with complete recovery usually occurring within 6 to 8 weeks. In adults, around 50% of the patients continue to have reduced renal function, hypertension, or persistent proteinuria.[12][13]

Death in adults is often secondary to heart failure and renal dysfunction. Studies show that in the long term some patients may continue to have abnormalities in urine, proteinuria, and hypertension.

Mortality during the acute phase of glomerulonephritis has been estimated at around 2 and 12 percent. It has been assumed that the renal changes found in the majority of patients who survived the initial acute attack would be qualitatively similar to those noted in the fatal cases, although little direct evidence existed to support this view.[14]

Complications

During the acute phase, congestive heart failure and azotemia are likely complications that could be life-threatening. The delayed complications include chronic kidney disease and nephrotic syndrome.

Deterrence and Patient Education

Avoidance of overcrowding and personal hygiene are important measures that patients should undertake to decrease the risk of catching streptococcal infections.

Patients with throat or skin infections should seek medical advice and get the proper antibiotic therapy if they receive confirmation of a bacterial infection.

Enhancing Healthcare Team Outcomes

Managing a case of PSGN requires cooperation between internists, nephrologists, infectious disease consultants, pharmacists, and nursing staff, functioning as an interprofessional team, to provide excellent care for their patients. PSGN patient's fluid and salt intake, as well as urine output, should be carefully monitored by the team. The pharmacist should coordinate with the clinician to ensure that the patient is on no nephrotoxic medications and emphasize medication compliance if the patient has hypertension. The visiting nurse should encourage all close contacts and family members to undergo throat swabs to rule out an acute infection. The nurse should also weigh the patient to ensure that the edema is not worsening. Besides, renal function and potassium levels need to be closely monitored.

Consulting a nephrologist (or a pediatric nephrologist) must be sought in complicated cases. These patients need monitoring for fluid and electrolyte status at each visit. Close communication between interprofessional team members is vital to ensure good outcomes. [Level 5]

The prognosis in children is excellent but adults tend to have a protracted course with at least 30 to 50% developing renal dysfunction and hypertension.[15][16][Level 5]

References

1.

2.

3.

4.

5.

6.

Rodriguez-Iturbe B, Haas M. Post-Streptococcal Glomerulonephritis. In: Ferretti JJ, Stevens DL, Fischetti VA, editors. Streptococcus pyogenes : Basic Biology to Clinical Manifestations [Internet]. University of Oklahoma Health Sciences Center; Oklahoma City (OK): Feb 10, 2016. [ PubMed: 26866231 ]

7.

8.

9.

10.

11.

Yang TJ, Shah H, Olagunju A, Novak M, Difilippo W. Role of Steroids in Post-streptococcal Glomerulonephritis Without Crescents on Renal Biopsy. Cureus. 2018 Aug 15;10(8):e3150. [ PMC free article: PMC6191008 ] [ PubMed: 30345206 ]

12.

13.

14.

JENNINGS RB, EARLE DP. Post-streptococcal glomerulo-nephritis: histopathologic and clinical studies of the acute, subsiding acute and early chronic latent phases. J Clin Invest. 1961 Aug;40:1525-95. [ PMC free article: PMC292535 ] [ PubMed: 13789862 ]

15.

16.

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Poststreptococcal glomerulonephritis (PSGN) is characterized by rapid deterioration of kidney functions due to an inflammatory response (type III hypersensitivity reaction) following streptococcal infection. This condition results from specific strains of group A beta-hemolytic streptococci called nephrogenic streptococci. The disease affects the glomeruli and the small blood vessels of the kidneys.

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Common physiological risk factors for PSGN include: age, recent infection of strep throat, scarlet fever, and impetigo. PSGN tends to be more common in children than adults, putting pre-school children at risk (CDC, 2025).

I chose this article because it discusses common physical risk factors for PSGN. I also chose this specific resource because I know the CDC is a reputable resource. I like that it lists the factors directly, making the article organized and simple to follow. Another thing I like about this source is that it provides details about each risk factor. For example, if the risk factor is impetigo, the article explains that this risk is most common in young children. It continues to go into detail for other risk factors as well, like strep throat or scarlet fever.

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Learn about post-streptococcal glomerulonephritis: Symptoms, treatment, and more.

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PSGN begins when exposed to a Group A β-hemolytic Streptococci infection. Group A creates streptolysin and causes beta-hemolysis. The group A infection causes a type 3 hypersensitivity reaction, resulting in formed immune complexes. These complexes are made up of IgM or IgG and are swept into the bloodstream and glomeruli. They become trapped between epithelial cells in the GBM. This entrapment causes them to send an inflammatory response. This response causes RBCs to leak into the urine, causing Hematuria (Elsevier, n.d.).

I chose this video to describe the cellular pathophysiology of PSGN. I really like the videos made by Elsevier because they tend to put complicated topics into simpler terms. The video includes visual aids, which help to remember and implement the concepts being taught. The way Elsevier teaches type 3 hypersensitivity allows me to truly understand it and apply it in other situations. The video is very detailed and not too long, making it a great source. I also included this video as I know Elsevier is a well-known name and reputable source.

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Video: Poststreptococcal glomerulonephritis - Video Explanation! | Osmosis | Osmosis

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Video: Poststreptococcal glomerulonephritis: Symptoms, Causes, Videos & Quizzes | Learn Fast for Better Retention! | Osmosis

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This image shows how PSGN develops. The process involves the inflammatory response that comes right after exposure to a bacterial infection. This causes a decrease in kidney function due to the inflammation present in the glomeruli. After the inflammation has begun, RBCs leak into the urine, which is the cause of Hematuria (National Kidney Foundation, n.d.).

I included this image so that PSGN could be visualized and easily understood. I personally tend to understand concepts better when I can visualize them and look back at images in my mind pertaining to the topic. This picture does that by showing the inflammation that first takes place in the glomeruli and eventually leads to decreased kidney function. Something else I really like about this image is that it shows proteinuria and hematuria. This is important as these are symptoms caused by PSGN.

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This diagram shows the antibody complex binding to the surface and activating. It shows how the antigens travel and become trapped in the GBM. This entrapment involves inflammation as the response, which is where the red aura is shown. After this, the RBCs are excreted through urine, causing a red colored tint (Lecturio Medical, n.d.).

I included this diagram of the pathophysiology of PSGN. I like that this source shows how the antibodies bind to the antigen, causing activation. The image shows that after the complement activation occurs, inflammation begins in the glomeruli. This can be shown by the redness that appears by the antibody complex binding to the GBM. I like that this source allows the mechanism of PSGN to be easily followed and is simple to understand. I always feel that visual aids tend to help when learning complex processes like the PSGN diase mechanism.

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Article: PSGN Environmental and Genetic Risk Factors

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Article: PSGN Environmental and Genetic Risk Factors

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Environmental risk factors of PSGN include: overcrowding and poor hygiene, low socioeconomic status, tropical climates, and developing countries. Tropical climates have higher rates of impetigo, and developing countries have higher infection rates of strep.

Genetic risk factors of PSGN include: family history, 40% of patients report a family member with the same disease (Rawla et al., 2022).

I again used this source, but this time it was for risk factors. In this article, it is mentioned that PSGN has multiple risk factors. This article includes how genetic and environmental risk factors affect the disease rather than just the physical risk factors. This article mentions low socioeconomic status, overcrowding, and genetic predisposition as risk factors for PSGN. I like this journal article because it states the factors simply and is a reputable source.

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Continuing Education Activity

Poststreptococcal glomerulonephritis (PSGN) results from a bacterial infection that causes rapid deterioration of the kidney function due to an inflammatory response following streptococcal infection. PSGN most commonly presents in children 1 to 2 weeks after a streptococcal throat infection, or within 6 weeks following a streptococcal skin infection. When symptomatic, PSGN typically presents with features of the nephritic syndrome such as hematuria, oliguria, hypertension, and edema, though it can also present with significant proteinuria. This activity reviews the etiology, pathogenesis, evaluation, and management of PSGN and explains the role of the interprofessional team in evaluating and treating patients with this condition.

Objectives:

Identify the epidemiology, etiology, pathophysiology of poststreptococcal glomerulonephritis.

Review how to evaluate a patient for poststreptococcal glomerulonephritis.

Summarize the treatment and management options available for poststreptococcal glomerulonephritis.

Explain interprofessional team strategies for improving care coordination and communication to improve outcomes for patients affected by poststreptococcal glomerulonephritis.

Access free multiple choice questions on this topic.
Introduction

Poststreptococcal glomerulonephritis (PSGN) is characterized by rapid deterioration of kidney functions due to an inflammatory response (type III hypersensitivity reaction) following streptococcal infection. This condition results from specific strains of group A beta-hemolytic streptococci called nephrogenic streptococci. The disease affects the glomeruli and the small blood vessels of the kidneys. PSGN most frequently presents in children 1 to 2 weeks after a sore throat, or 6 weeks after a skin infection (impetigo).[1]

Though the incidence of PSGN has declined in developed countries, the incidence of non-streptococcal organisms is emerging. Nephritis-associated plasmin receptor (NAPlr) and streptococcal pyrogenic exotoxin B (SPeB) are the two common antigens associated with the pathogenesis of PSGN. They not only activate the alternate complement pathway, resulting in hypocomplementemia, but they also have an affinity towards the plasmin and glomerular proteins. The clinical presentation of PIGN can vary from no symptoms to renal failure requiring renal replacement therapy (RRT). [2]

When symptomatic, PSGN typically presents with features of the nephritic syndrome such as hematuria, oliguria, hypertension, and edema. Less commonly presentation can mimic nephrotic syndrome with significant proteinuria.

Etiology

Nephrogenic streptococci infection precedes PSGN, which initially affects skin or the oropharynx. More recently, PSGN is associated with skin infections (impetigo) more frequently than throat infections (pharyngitis).[3][4]

Group A Streptococcus (GAS) has been subtyped depending on the surface M protein and opacity factor, which are known to be nephrogenic and can cause PSGN. Other causes of post-infectious glomerulonephritis include bacterial infections including endocarditis, enterocolitis, pneumonia, and intraventricular shunt infections, viral (hepatitis B and C infections, human immunodeficiency virus, cytomegalovirus, Epstein Barr virus, parvovirus B19), fungal (coccidioidomycosis, histoplasmosis), and parasitic infections (malaria, leishmania, toxoplasmosis, and schistosomiasis).[5]

Poor hygiene, overcrowding, and low socioeconomic status are important risk factors for streptococci outbreaks, and this explains the higher incidence of PSGN in impoverished countries. Genetic factors are expected to predispose to the condition since almost 40% of patients with PSGN gave a positive family history. There is no specific gene found to cause PSGN.[5]

Epidemiology

Over the past three decades, PSGN incidence has significantly dropped in developed countries; such as the United States, UK, Central Europe, and Japan. The reason for this progress is the use of antibiotic prophylaxis and the improvement of hygienic states. In these developed countries, PSGN has become more frequently seen in adult patients who suffer from chronic debilitating diseases.[6]

Higher incidence of PSGN in developing countries- due to increased skin infections (pyoderma). Though the incidence in developed countries has gone down, it is still the most common cause of glomerulonephritis (GN) in children in the united states. [5]

PSGN is also the most common cause of kidney injury in children in the Middle East, Africa, Australia, and worldwide. The annual incidence of new cases of PSGN in developing countries ranges from 8.5 to 28.5 per 100000 individuals.[7] Around 97% of cases reported with PSGN live in underprivileged countries.

Clinically manifestations of PSGN are more common in males than in females with a ratio of 2:1. However; the incidence of subclinical PSGN is almost equal in both sexes. Racial factors were not found to play a role. The disease most frequently affects children between the age of 3 and 12 (with the peak incidence between 5 to 6 years), and seniors greater than 60 years old.

Pathophysiology

The disease is immunological; representing a type III hypersensitivity reaction. The exact mechanism by which PSGN occurs is not fully determined. The body responds to nephrogenic streptococcal infection by forming immune complexes containing the streptococcal antigen with a human antibody.[2] Some theories suggest that these immune complexes become deposited in kidney glomeruli reaching through the circulation. Others claim that the condition results from an "in situ" formation of the antigen-antibody complex within the kidney glomeruli. This "In situ immune complex formation" is either due to a reaction against streptococci antigens deposited in the glomerular basement membrane or, according to other theories, due to an antibody reaction against glomerular components that cross-react with streptococcal antigen due to molecular mimicry.[5]

The presence of immune complexes leads to the activation of the alternate complement pathway causing infiltration of the leukocytes, and proliferation of the mesangial cells in the glomerulus thus impairing the capillary perfusion and glomerular filtration rate (GFR). Reduction in GFR can lead to renal failure (oliguria or anuria), acid-base imbalance, electrolyte abnormalities, volume overload, edema, and hypertension.

Histopathology

Light microscopy- The glomeruli show hypercellularity (endothelial, mesangial, and inflammatory cells) which are non-specific.

Electron microscopy- The most characteristic finding is the presence of sub-epithelial humps; which are electron-dense deposits in the subepithelial space near the glomerular basement membrane.[8]

Immunofluorescence microscopy- Evidence of IgG and C3 deposits in the first 2 to 3 weeks of the disease.

History and Physical

Approximately 50% of children with PSGN are asymptomatic and are discovered accidentally during routine urine analysis. The classic triad of glomerulonephritis includes hematuria, edema, and hypertension. Typically, patients give a history of a recent streptococcal infection such as pharyngitis, tonsillitis, or impetigo. However; some patients develop PSGN without experiencing symptoms of respiratory tract infection or pyoderma, which can be a diagnostic challenge.[9]

The most common presenting symptom is gross hematuria as it occurs in 30 to 50% of cases with acute PSGN; patients often describe their urine as smoky, tea-colored, cola-colored, or rusty. The hematuria can be described as postpharyngitic (hematuria seen after weeks of infection).

Renal involvement is common and is transient with recovery in 1-2 weeks. Less than half of the patients experience oliguria. Depending on the severity of renal involvement, signs, and symptoms suggestive of anuric renal failure or life-threatening acid-base imbalance, electrolyte abnormalities (especially hyperkalemia), and fluid overload would require RRT. About 60-80% of the patients experience high blood pressure which typically resolves in 10 days. [5]

The incidence of edema is seen in about 65-90% of the cases. Puffiness of the eyelids (periorbital edema) is typical for the nephritic syndrome. It is most prominent in the morning and tends to resolve at the end of the day. Generalized edema is also a common feature. Moreover, in severe cases, patients might experience respiratory distress as a result of pulmonary edema. They may experience other non-specific symptoms like anorexia, malaise, nausea, vomiting, etc.

Evaluation

PSGN should be suspected in all children with hypertension and heart failure, even in the absence of hematuria or a history of a preceding sore throat or pyoderma.

Laboratory investigations are the most useful in PSGN assessment.

Evidence of a preceding streptococcal infection is determined by measuring anti-streptolysin titer (ASO), and anti-nicotinamide-adenine dinucleotidase (anti-NAD) which tend to rise following pharyngitis. Other antibodies such as anti-DNAse B and anti-hyaluronidase (AHase) are usually elevated after both pharyngitis and skin infections. ASO titer is the most frequently used test, while the most sensitive is the streptozyme test; which includes measuring the titers of all the antibodies mentioned above. ASO titers can be falsely low in patients treated with antibiotics for streptococcal infections.

Serum complement level (C3) is usually low due to its consumption in the inflammatory reaction. Mostly, the decrease in C3 concentration occurs before serum ASO has risen.[5] Complement levels usually return to normal levels in 6-8 weeks.

Progressive decline in the Renal function

When there is no latent period between the acute glomerulonephritis and streptococcal infection

If the complement levels are normal

When there is no rise in antistreptococcal antibodies

Urine analysis: shows macroscopic or microscopic hematuria, RBC casts, mild proteinuria. Only 5% of patients with PSGN have massive proteinuria that indicates nephrotic syndrome. White blood cell casts, hyaline, and cellular casts are usually present in the urine analysis.

Ultrasonography: Kidneys are enlarged only in a few patients.

The chest x-ray may show pulmonary congestion in patients with symptoms consistent with volume overload or heart failure.

Renal Function Tests: Blood urea nitrogen (BUN) and serum creatinine typically elevate during the acute phase. These values usually return to normal later.

In patients with heart failure and PSGN, NT-proBNP levels are elevated along with the findings of pulmonary congestion on the chest x-ray.

Renal biopsy is not recommended for diagnosing patients with PSGN and is performed only when other glomerular pathologies are suspected. Renal biopsy is indicated when:

Imaging Studies

Treatment / Management

PSGN is a self-limiting condition in most cases, and thus only symptomatic treatment is needed. Supportive treatment aims at controlling the complications of volume overload such as hypertension and edema, which are prominent during the acute phase of the disease.[5]

Pharmacological Therapy

Antimicrobials: Patients with evidence of a streptococcal infection should receive a course of antibiotic therapy, and they may not prevent the development of PSGN.

Diuretics: Loop diuretics (furosemide) are preferred over thiazides (hydrochlorothiazide or chlorthalidone). The efficacy of thiazide diuretics is very minimal when GFR < 30 ml/min.

Antihypertensive medications: Blood pressure can be managed by restricting salt and fluid intake along with diuretics are needed. In cases with uncontrolled blood pressure, the use of calcium channel blockers is recommended. The use of angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARBs) is recommended in patients with stable GFR and with near-normal potassium levels.

Salt and water restriction to treat the edema.

Bed rest and immobilization are recommendations in the first few days of the disease.

Throat cultures on the patient and family members are important.

All affected members need to be treated with penicillin or erythromycin.

Immunosuppressive therapy: There's no evidence that immune suppression is useful in patients with PSGN.[10]However, patients with progressive renal failure or the presence of crescents on the renal biopsy may warrant the use of corticosteroids.[11][11][11]

IgA Nephropathy: usually occurs after an upper respiratory tract or gastrointestinal infection, but it differs from PSGN in the shorter latency period it takes to appear after the episode of infection. It can also be described as synpharyngitic hematuria- hematuria and infection coincide.

Membranoproliferative glomerulonephritis: also presents with a nephritic picture and hypocomplementemia following respiratory tract infection. Complement levels take a longer time to return to normal than in PSGN or persistently low C3 levels.

Lupus nephritis: sometimes PSGN presents with a picture similar to lupus nephritis. Laboratory testing for antibodies specific to each of the diseases can help in the diagnosis. Positive ANA, ds-DNA, cytopenia, and multi-organ involvement.

Nephrotic syndrome: 2 4-hour urine protein excretion is more than 3.5 gram/day along with hypoalbuminemia, edema, hypogammaglobulinemia, and increased risk of thrombosis (due to loss of pro-coagulants).

Henoch Schonlein purpura (HSP): The typical presentation is palpable purpura, renal failure, gastrointestinal and musculoskeletal manifestations. Have normal complement levels.

Hemolytic uremic syndrome (HUS): Labs consistent with Hemolysis (schistocytes, LDH, reticulocyte count, indirect bilirubin), bloody diarrhea, thrombocytopenia, stool culture for Escherichia coil O157: H7

ANCA: Have normal complement levels.

Goodpasture disease: Involves lung and kidneys. Have anti-glomerular basement antibody and normal complement levels.

Dialysis

Dialysis is only performed to manage the acid-base balance, electrolyte abnormalities (especially hyperkalemia), and fluid management

General measures

Differential Diagnosis

Prognosis

PSGN has an excellent prognosis especially in children with complete recovery usually occurring within 6 to 8 weeks. In adults, around 50% of the patients continue to have reduced renal function, hypertension, or persistent proteinuria.[12][13]

Death in adults is often secondary to heart failure and renal dysfunction. Studies show that in the long term some patients may continue to have abnormalities in urine, proteinuria, and hypertension.

Mortality during the acute phase of glomerulonephritis has been estimated at around 2 and 12 percent. It has been assumed that the renal changes found in the majority of patients who survived the initial acute attack would be qualitatively similar to those noted in the fatal cases, although little direct evidence existed to support this view.[14]

Complications

During the acute phase, congestive heart failure and azotemia are likely complications that could be life-threatening. The delayed complications include chronic kidney disease and nephrotic syndrome.

Deterrence and Patient Education

Avoidance of overcrowding and personal hygiene are important measures that patients should undertake to decrease the risk of catching streptococcal infections.

Patients with throat or skin infections should seek medical advice and get the proper antibiotic therapy if they receive confirmation of a bacterial infection.

Enhancing Healthcare Team Outcomes

Managing a case of PSGN requires cooperation between internists, nephrologists, infectious disease consultants, pharmacists, and nursing staff, functioning as an interprofessional team, to provide excellent care for their patients. PSGN patient's fluid and salt intake, as well as urine output, should be carefully monitored by the team. The pharmacist should coordinate with the clinician to ensure that the patient is on no nephrotoxic medications and emphasize medication compliance if the patient has hypertension. The visiting nurse should encourage all close contacts and family members to undergo throat swabs to rule out an acute infection. The nurse should also weigh the patient to ensure that the edema is not worsening. Besides, renal function and potassium levels need to be closely monitored.

Consulting a nephrologist (or a pediatric nephrologist) must be sought in complicated cases. These patients need monitoring for fluid and electrolyte status at each visit. Close communication between interprofessional team members is vital to ensure good outcomes. [Level 5]

The prognosis in children is excellent but adults tend to have a protracted course with at least 30 to 50% developing renal dysfunction and hypertension.[15][16][Level 5]

References

1.

2.

3.

4.

5.

6.

Rodriguez-Iturbe B, Haas M. Post-Streptococcal Glomerulonephritis. In: Ferretti JJ, Stevens DL, Fischetti VA, editors. Streptococcus pyogenes : Basic Biology to Clinical Manifestations [Internet]. University of Oklahoma Health Sciences Center; Oklahoma City (OK): Feb 10, 2016. [ PubMed: 26866231 ]

7.

8.

9.

10.

11.

Yang TJ, Shah H, Olagunju A, Novak M, Difilippo W. Role of Steroids in Post-streptococcal Glomerulonephritis Without Crescents on Renal Biopsy. Cureus. 2018 Aug 15;10(8):e3150. [ PMC free article: PMC6191008 ] [ PubMed: 30345206 ]

12.

13.

14.

JENNINGS RB, EARLE DP. Post-streptococcal glomerulo-nephritis: histopathologic and clinical studies of the acute, subsiding acute and early chronic latent phases. J Clin Invest. 1961 Aug;40:1525-95. [ PMC free article: PMC292535 ] [ PubMed: 13789862 ]

15.

16.

# data[].attributes.attachment_link.description
Poststreptococcal glomerulonephritis (PSGN) is characterized by rapid deterioration of kidney functions due to an inflammatory response (type III hypersensitivity reaction) following streptococcal infection. This condition results from specific strains of group A beta-hemolytic streptococci called nephrogenic streptococci. The disease affects the glomeruli and the small blood vessels of the kidneys.

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Centers for Disease Control and Prevention. (2025, August 7). About post-streptococcal glomerulonephritis. Centers for Disease Control and Prevention. https://www.cdc.gov/group-a-strep/about/post-streptococcal-glomerulonephritis.html

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Elsevier. (n.d.). Poststreptococcal glomerulonephritis: Video, causes, & meaning | osmosis. Osmosis. https://www.osmosis.org/learn/Poststreptococcal_glomerulonephritis

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National Kidney Foundation. (n.d.). Postinfectious Glomerulonephritis. National Kidney Foundation. Retrieved from https://www.kidney.org/kidney-topics/post-infectious-glomerulonephritis-pign.

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Rawla, P., Padala, S. A., & Ludhwani, D. (2022, October 9). Poststreptococcal glomerulonephritis. StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK538255/

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Suspected pathophysiology of postinfectious glomerulonephritis: immune complex deposition in the glomerular basement membrane (GBM). (n.d.). Lecturio Medical. Retrieved from https://www.lecturio.com/concepts/poststreptococcal-glomerulonephritis/.

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Clinical Manifestations vary depending on severity (acute or chronic & the cause):

Hypertension

Oliguria (Reduced urine output)

Hematuria (Dark, reddish-brown urine)

Proteinuria (bubbly/foamy urine from excess protein in urine)

Fluid retention (edema) causes swelling in face, feet, hands & abdomen

Fatigue due to anemia (feeling tired from low blood iron levels)

Nausea/vomiting/fever

Muscle cramps

I included this source because it gives a clear, patient-friendly list of clinical manifestations in one place, so patients/families can quickly recognize signs/symptoms (blood in urine, swelling, high blood pressure) and know when to seek care.

Source:

Mayo Foundation for Medical Education and Research. (2024, February 24). Glomerulonephritis. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/glomerulonephritis/symptoms-causes/syc-20355705

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Glomerulonephritis - Symptoms and causes

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Learn about symptoms, causes and treatments for acute and chronic glomerulonephritis, a type of kidney inflammation.

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Treatment options usually involve treating the bacterial infection, treating symptoms, as well as monitoring & supporting kidney functions.

Treatment Options:

Decreasing swelling by reducing salt intake or by prescribing diuretics medications that increase the flow of urine

Medications to reduce blood pressure

Antibiotics to treat any strep bacteria left in the body

For severe kidney damage, dialysis may be needed to support the affected individual while the kidney recover

This short video quickly explains PSGN treatment: salt/fluid restriction, diuretics to increase urine and reduce swelling/BP, when to use antibiotics, and when dialysis is needed

Source:

Medical Centric. (2019, July 15). POST STREPTOCOCCAL GLOMERULONEPHRITIS, Causes, Signs and Symptoms, Diagnosis and Treatment. YouTube. https://www.youtube.com/watch?v=mDjPhHSE-5I

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POST STREPTOCOCCAL GLOMERULONEPHRITIS, Causes, Signs and Symptoms, Diagnosis and Treatment.

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The antigen-antibody complexes circulate and deposit in the glomeruli of the kidneys

The complement system is activated and triggers inflammation

After the neutrophils and other immune cells infiltrate and release enzymes and free radicals into the glomeruli, it causes swelling and damage to the glomerular capillary walls.

The injured glomeruli becomes leaky and allows protein and red blood cells to pass into the urine

This results in decreased filtration, edema hypertension, and dark cola-colored urine

I chose this source because it clearly describes the pathophysiology of Poststreptococcal Glomerulonephritis

# data[].attributes.attachment_link.description
Acute glomerulonephritis is characterized by the sudden appearance of hematuria, proteinuria, red blood cell casts in the urine, edema, and hypertension with or without oliguria. It can follow streptococcal infections.

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This is an overview of the hypersensitivity including pathophysiology, symptoms, etc.

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This photo shows the inflamed glomerulus vs a regular one.

It also shows the immune complex related to it

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Post-streptococcal Glomerulonephritis conforms to the traditional definition of a Type 3 hypersensitivity reaction. It involves immune complex formation, complement activation, and inflammatory tissue injury. One aspect that doesn’t completely conform is that it’s localized instead of systemic like the others. It mostly affects the glomeruli.

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VitalSource Bookshelf is the world's leading platform for distributing, accessing, consuming, and engaging with digital textbooks and course materials.

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This image includes the most common clinical manifestation of Poststreptococcal Glomerulonephritis, which is hematuria (dark, reddish-brown urine). This “cola-colored urine” happens because a small amount of blood from the kidneys is mixing into the urine, it’s not just from dehydration. If someone recently had strep throat or a skin infection and notices this color, it’s a cue to get a quick urine test and a blood pressure check. It important to be aware of this because spotting this early helps the care team treat swelling and high blood pressure sooner and protect the kidneys while they heal.

Source:

Heilman, J. (n.d.). What are the signs and symptoms of post-streptococcal glomerulonephritis? - storymd. Symtoms. https://storymd.com/journal/mrkgo35szw-post-streptococcal-glomerulonephritis/page/8z85nsxd358-what-are-the-signs-and-symptoms-of-post-streptococcal-glomerulonephritis