Post-streptococcal glomerulonephritis overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ayesha A. Khan, MD[2] Manpreet Kaur, MD [3]
Overview
Poststreptococcal glomerulonephritis (PSGN) is caused by preceding infection with nephritogenic strains of group A beta-hemolytic streptococcus. The intial clinical presentation of PSGN is usually asymptomatic then it progresses to microscopic hematuria, proteinuria , edema, hypertension, and symptoms of acute kidney injury. Common risk factors in the development of post-streptococcal glomerulonephritis include streptococcal throat infection and impetigo. Less common risk factors are household infection with the nephritogenic strain of group A streptococcal. Common complications of post-streptococcal glomerulonephritis include severe nephritis, renal failure , atypical hemolytic uremic syndrome , refractory hypoxic respiratory failure, and seizures. Prognosis is generally excellent but depends upon age and co-morbidities. Laboratory findings consistent with the diagnosis of streptococcal infection include antistreptolysin O (ASO) positive, antinicotinamide adenine dinucleotides positive, antihyaluronidase, and anti–DNAse B positive. Other abnormal laboratory findings include leukocytosis with neutrophilia, CRP is raised, increased levels of blood urea nitrogen (BUN) and serum creatinine levels are increased. On serologic testing, hypocomplementemia is usually found. On urinalysis, proteinuria, hematuria, and dysmorphic red cells are usually found. Effective measures for the primary prevention of post-streptococcal glomerulonephritis include improving hand hygiene, better housing, prevent overcrowding, treatment of an infected patient within 24 hours with antibiotics and prevent close contact. A 26-valent vaccine is recommended for children to prevent post-streptococcal glomerulonephritis. Effective measures for the secondary prevention of post-streptococcal glomerulonephritis include compliant with anti-hypertensive medication and follow up with the nephrologist.
Historical Perspective
Klebs and colleagues showed that the clinical findings were consistent with a form of glomerulonephritis that was associated with the period following scarlet fever. In 1812, Wells showed that a latent period was required for edema and red urine seem to be present. In 1905 and 1933, Reichel and Osman further elaborated on PSGN and revealed detailed findings and description of the disease, its prevalence, its clinical findings, and its outcome, respectively. In 1903 when Clemens von Pirquet hypothesized the presence of immune complexes that might be the culprit of PSGN. In 1941, Seegal and Earle determined the nephritogenic properties of streptococcal strains and differentiated streptococcal strains based on their nephritogenic vs. rheumatic complication. The mainstay of treatment is pharmacotherapy, however dietary therapy is useful for controlling edema and hypertension. Dietary therapy includes low salt, protein intake, and water restriction. If the streptococcal infection is still present, it should be treated with antibiotics. To control severe hypertension, labetalol is usually used, For mild to moderate hypertension, furosemide is used. For rapidly progressive crescentic acute post-streptococcal glomerulonephritis, methylprednisolone is preferred
Classification
There is no established system for the classification of post-streptococcal glomerulonephritis.
Pathophysiology
It is thought that post-streptococcal glomerulonephritis (PSGN) is caused by nephritogenic strains of group A beta-hemolytic streptococcus (GAS). The mechanism which leads to immunologic injury to the glomerulus include deposition of immune complexes with streptococcal antigenic components, then immune complexes are deposited in glomerular basement membrane and antibodies bind to the GBM. In-situ formation of immune complexes is a characteristic associated with cationic antigens that have a charge-facilitated penetration through the polyanionic glomerular basement membrane. The plasmin-binding capacity of streptococcal antigens favors immune complex deposition and inflammation. The typical pathological changes are endocapillary proliferation with varying degrees of leukocyte infiltration, and C3, IgG, and IgM immune deposits. Electron microscopy shows the hallmark lesion of subepithelial electron dense deposits (“humps”). The immediate prognosis is excellent in children, but adults have a significant early mortality, which partially results from cardiovascular disease.
Causes
Common causes of post-streptococcal glomerulonephritis include infection with group A streptococci. Others strain of streptococci which cause post-streptococcal glomerulonephritis include streptococci M types 47, 49, 55, 2, 60, and 57 causes pyodermatitis and streptococci M types 1, 2, 4, 3, 25, 49, and 12 causes throat infection. Less common causes of post-streptococcal glomerulonephritis include group C such as S. zooepidemicus and group G streptococcal infections.
Differentiating Xyz from Other Diseases
Post-streptococcal glomerulonephritis should be differentiate from other causes of glomerular disease such as nephritic syndrome, nephrotic syndrome, Fabry's disease, poststreptococcal glomerulonephritis, lupus nephritis, antiglomerular basement membrane disease (goodpasture's syndrome), Cryoglobulinemia, Henoch-Schönlein purpura, amyloidosis, pulmonary-renal syndromes (vasculitis), thin basement membrane disease, Alport's Syndrome, anti-GBM Disease, hypertensive nephrosclerosis, and subacute bacterial endocarditis. The various types of glomerular diseases may be differentiated from each other based on associations, presence of pitting edema, hemeturia, hypertension, hemoptysis, oliguria, peri-orbital edema, hyperlipidemia, type of antibodies, light and electron microscopic features.
Epidemiology and Demographics
The incidence of post-streptococcal glomerulonephritis is approximately 9.5 to 28.5 per 100,000 individuals worldwide. The case-fatality rate of post-streptococcal glomerulonephritis is approximately 2 percent in India and 0.08 percent in Turkey. It commonly affects children with age between 5 to 12 years. The incidence of post-streptococcal glomerulonephritis increases in older people age greater than 60 years. It commonly affects children with age between 5 to 12 years. Men are more commonly affected by post-streptococcal glomerulonephritis than women. The majority of post-streptococcal glomerulonephritis cases are reported in developing countries.
Risk Factors
Common risk factors in the development of post-streptococcal glomerulonephritis include streptococcal throat infection and impetigo. Less common risk factors are household infection with the nephritogenic strain of group A streptococcal.
Screening
There is insufficient evidence to recommend routine screening for post-streptococcal glomerulonephritis.
Natural History, Complications, and Prognosis
The symptoms of post-streptococcal glomerulonephritis typically develop one to three weeks after exposure to group A streptococcal throat infection and 3 to 6 weeks after group A streptococcal skin infection. Common complications of post-streptococcal glomerulonephritis include severe nephritis, renal failure , atypical hemolytic uremic syndrome , refractory hypoxic respiratory failure, and seizures. Prognosis is generally excellent but depends upon age and co-morbidities.
Diagnosis
Diagnostic Study of Choice
The antistreptolysin O (ASO) positive is the gold standard test for the diagnosis of post-streptococcal glomerulonephritis.
History and Symptoms
Patients with post-streptococcal glomerulonephritis may have a positive history of streptococcal throat infection and streptococcal skin infection. Common symptoms of post-streptococcal glomerulonephritis include dark urine, oliguria, periorbital edema and hypertension. Less common symptoms of post-streptococcal glomerulonephritis include general malaise, weakness, anorexia, nausea and vomiting.
Physical Examination
Patients with post-streptococcal glomerulonephritis usually appear lethargic. On physical examination, patients usually have high blood pressure, periorbital edema and edema of extremities.
Laboratory Findings
Laboratory findings consistent with the diagnosis of streptococcal infection include antistreptolysin O (ASO) positive, antinicotinamide adenine dinucleotides positive, antihyaluronidase, and anti–DNAse B positive. Other abnormal laboratory findings include leukocytosis with neutrophilia, CRP is raised, increased levels of blood urea nitrogen (BUN) and serum creatinine levels are increased. On serologic testing, hypocomplementemia is usually found. On urinalysis, proteinuria, hematuria, and dysmorphic red cells are usually found.
Electrocardiogram
There are no ECG findings associated with post-streptococcal glomerulonephritis.
X-ray
There are no x-ray findings associated with post-streptococcal glomerulonephritis.
Echocardiography and Ultrasound
There are no echocardiography/ultrasound findings associated with post-streptococcal glomerulonephritis.
CT scan
There are no CT scan findings associated with post-streptococcal glomerulonephritis.
MRI
There are no MRI findings associated with post-streptococcal glomerulonephritis.
Other Imaging Findings
There are no other imaging findings associated with post-streptococcal glomerulonephritis.
Other Diagnostic Studies
Renal biopsy is routinely not done to diagnose post-streptococcal glomerulonephritis. There are the indications for biopsy include persistent proteinuria of more than 6 months, persistent microscopic hematuria more than 18 months, decreasing GFR after 4 weeks, and persistent hypocomplementemia after 6 weeks.
Treatment
Medical Therapy
The mainstay of treatment is pharmacotherapy, however dietary therapy is useful for controlling edema and hypertension. Dietary therapy includes low salt, protein intake, and water restriction. If the streptococcal infection is still present, it should be treated with antibiotics. To control severe hypertension, labetalol is usually used, For mild to moderate hypertension, furosemide is used. For rapidly progressive crescentic acute post-streptococcal glomerulonephritis, methylprednisolone is preferred.
Surgery
Surgical intervention is not recommended for the management of post-streptococcal glomerulonephritis.
Primary Prevention
Effective measures for the primary prevention of post-streptococcal glomerulonephritis include improving hand hygiene, better housing, prevent overcrowding, treatment of an infected patient within 24 hours with antibiotics and prevent close contact. A 26-valent vaccine is recommended for children to prevent post-streptococcal glomerulonephritis.
Secondary Prevention
Post-streptococcal glomerulonephritis is resolved completely, however, effective measures for the secondary prevention of post-streptococcal glomerulonephritis include compliant with anti-hypertensive medication and follow up with the nephrologist.