Post-streptococcal glomerulonephritis

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]

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.

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

There is no established system for the classification of post-streptococcal glomerulonephritis.

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.

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.

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.

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.

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.

There is insufficient evidence to recommend routine screening for post-streptococcal glomerulonephritis.

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.

The antistreptolysin O (ASO) positive is the gold standard test for the diagnosis of post-streptococcal glomerulonephritis.

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.

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 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.

There are no ECG findings associated with post-streptococcal glomerulonephritis.

There are no x-ray findings associated with post-streptococcal glomerulonephritis.

There are no echocardiography/ultrasound findings associated with post-streptococcal glomerulonephritis.

There are no CT scan findings associated with post-streptococcal glomerulonephritis.

There are no MRI findings associated with post-streptococcal glomerulonephritis.

There are no other imaging findings associated with post-streptococcal glomerulonephritis.

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.

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.

Surgical intervention is not recommended for the management of post-streptococcal glomerulonephritis.

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.

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.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

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.

• In 1812, Wells showed that a latent period was required for edema and red urine seem to be present.^[1]
• 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 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, based on his clinical observations during his pediatric residency training. His theory was outlined and sent to the Academy of Sciences in Vienna and was read in the Academy in 1908.^[2]
• In 1941, Seegal and Earle determined the nephritogenic properties of streptococcal strains and differentiated streptococcal strains based on their nephritogenic vs. rheumatic complication.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

There is no established system for the classification of post-streptococcal glomerulonephritis.

There is no established system for the classification of post-streptococcal glomerulonephritis.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

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.

• It is thought that post-streptococcal glomerulonephritis (PSGN) is caused by nephritogenic strains of group A beta-hemolytic streptococcus (GAS)
• Other strains of Group A streptococci which cause PSGN include:
  • Group A streptococci M protein types 47, 49, 55, 2, 60
  • Group A streptococci M types 1, 2, 4, 3, 25, 49, and 12
• Two antigens isolated from nephritogenic streptococci are commonly implicated are:^[1][2]
  • Streptococcal pyrogenic exotoxin B
  • Nephritis-associated plasmin receptor

The mechanism which leads to immunologic injury to the glomerulus are:^[3]

• There is deposition of immune complexes with streptococcal antigenic components
• Immune complexes are deposited in glomerular basement membrane and antibodies bind to the GBM
• Further antigen reacts with antibodies bind to GBM and cross glomerular membranes

• On gross pathology, following features are seen:
  • Kidney are enlarged and pale in color

On microscopic histopathological analysis:

• Glomeruli are enlarged and hypercellular due to the deposition of neutrophils and macrophages
• There is a proliferation of mesangial and endothelial cells
• There is a swelling of endothelial cells and presence of inflammatory cells obstructs capillary lumina
• There is an accumulation of mononuclear leukocytic infiltrate and edema in the interstitium

Immunofluorescence findings

• During the early phase of post-infectious glomerulonephritis, there is the starry sky appearance due to deposition of C3 and IgG in the capillary walls and mesangial areas
• In later stages, there is a predominance of C3 deposition in mesangium^[4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

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.

Common causes of post-streptococcal glomerulonephritis include:^[1][2][3]

• Infection with group A streptococci
• Others strain of streptococci include:^[4]
  • Streptococci M types 47, 49, 55, 2, 60, and 57 causes pyodermatitis
  • Streptococci M types 1, 2, 4, 3, 25, 49, and 12 causes throat infection

Less common causes of post-streptococcal glomerulonephritis include:^[5]

• Group C such as S. zooepidemicus
• Group G streptococcal infections

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2] Manpreet Kaur, MD [3]

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.

Post-streptococcal glomerulonephritis should be differentiate from other causes of glomerular disease. 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. The following table differentiates between various types of glumerular diseases:

Glomerular diseases	Disease		History and Symtoms									Laboratory Findings		Pathology
			History	Systemic symptoms	Hemeturia	Proteinuria	Hypertension	Pitting edema	Oliguria	Nephrotic features	Nephritic features	Hyperlipidemia and hypercholesterolemia	Auto-antibodies, Complements	Light microscope	Electron microscope	Immunoflourescence pattern
Acute Nephritic Syndromes	Poststreptococcal Glomerulonephritis[1][2][3]		Streptococcal skin infections Streptococcal pharyngitis 2-3 weeks after infection	Fever Fatigue Skin rash	+/-	+	+/-	+/-	+/-	+/-	+/-	+/-	Anti-dsDNA antibodies Anti-C1q antibodies Antineutrophil cytoplasmic antibodies (ANCA)	Hypercellular and inflamed glomeruli	Sub-epithelial immune complex deposits Obliteration of epithelial cell foot processes	Immune complex GN Granular deposit
	Renal disease due to Subacute Bacterial Endocarditis, or cardiac shunt (Atrioventricular)[4][5]		History of infective endocarditis mostly due to S. aureus Cardiac shunt	Fever Fatigue Weight loss	+/-	+	+/-	+/-	+/-	+/-	+/-	+/-	ANCA (myeloperoxidase) positive in 1/3 Activation of the alternative complement pathway (Decreased C3, C4) Positive RF Positive anti-GBM autoantibodies	Crescentic GN is the most common pathological features Diffuse membranoproliferative glomerulonephritis features Focal proliferative GN Mesangial proliferative GN	Mesangial deposits, Subendothelial deposits Subepithelial “humps,” in minority of cases	Pauci-immune GN
	Lupus Nephritis[6]		History of SLE features	Lupus criteria: Malar rash Arthritis Arthralgia Anemia Easy bruising	+/-	+	+/-	+/-	+/-	+/-	+/-	+/-	Anti-C1q antibodies Anti-dsDNA	Differs based on the disease classification	Differs based on the disease classification	Differs based on the disease classification, mostly immune complex GN Granular deposit
	Antiglomerular Basement Membrane Disease (Goodpasture’s syndrome)[7][8]		Young adults	Dry cough Hemoptysis Malaise  Fever and chills Arthralgia  Fatigue Lethargy Pallor Anorexia Easy bruising	+	+	+	+	+	+	–	–	ANCA (myeloperoxidase) Positive anti-GBM autoantibodies	Hypercellular and inflamed glomeruli (Crescent formation)	Diffuse thickening of the glomerular basement membrane with absence of sub-epithelial and sub-endothelial deposits	Immune complex GN Linear deposit
	IgA Nephropathy[9][10]		Young children History of mucosal infections (e.g. gastroenteritis) and upper respiratory tract infection 2-3 days after infection (synpharyngitic)	Low grade fever Flank pain	+	+/-	+	+/-	+	–	+	–	Immune complex deposition	Crescent formation	Mesangial proliferation	Immune complex GN, granular deposite
	Disease		History	Systemic symptoms	Hemeturia	Proteinuria	Hypertension	Pitting edema	Oliguria	Nephrotic features	Nephritic features	Hyperlipidemia and hypercholesterolemia	Auto-antibodies, Complements	Light microscope	Electron microscope	Immunoflourescence pattern
	ANCA Small-Vessel Vasculitis[11][12]	Granulomatosis with Polyangiitis (Wegener’s)[13][14][15]	Middle age male	Constitutional symptoms Dyspnea Purpura Arthralgias Neurologic dysfunction Sinusitis Otitis media Epistaxis.	+	+	+	+/-	+	–	+	–	ANCA	Necrotizing and crescentic glomerulonephritis	Subendothelial edema Microthrombosis Degranulation of neutrophils	Pauci-immune GN
		Microscopic Polyangiitis[16]	+/-	Constitutional symptoms Dyspnea Purpura Arthralgias Neurologic dysfunction	+	+	+	+	+	+		–	P-ANCA	Hypercellular and inflamed glomeruli (Crescent formation)	Hypercellular and inflamed glomeruli (Crescent formation)	Pauci-immune GN
		Churg-Strauss Syndrome[17]	+/-	Asthma Sinusitis Myalgia  Arthralgia Purpura Arrythmias Peripheral neuropathy	+	+	+	+	+	+		–	C-ANCA	Hypercellular and inflamed glomeruli (Crescent formation)	Hypercellular and inflamed glomeruli (Crescent formation)	Pauci-immune GN
	Membranoproliferative Glomerulonephritis[18][19]		Idiopathic Hepatitis B and C (Type 1) C3 nepritic factor (Type2)	Hematuria Oliguria Periorbital edema Hypertension	+	+	+	+/-	+	+	–	–	–	Thick glomerular basement membrane (Tram-track appearance)	Mesangial proliferation Leukocyte infiltration	Immune complex GN Granular deposite
	Henoch-Schönlein purpura [20]		Most common in young male, following upper respiratory infections	Skin manifestations- Palpable purpura on buttocks Gastrointestinal manifestations- Abdominal pain Melena Bloody diarrhea Hematemesis Joints manifestations- Arthralgia	+	+	+	+/-	+	+	–	–	–	Diffuse mesangial IgA deposits often associated with mesangial hypercellularity	Diffuse mesangial IgA deposits often associated with mesangial hypercellularity	Immune complex GN, granular deposite
	Disease		History	Systemic symptoms	Hemeturia	Proteinuria	Hypertension	Pitting edema	Oliguria	Nephrotic features	Nephritic features	Hyperlipidemia and hypercholesterolemia	Auto-antibodies, Complements	Light microscope	Electron microscope	Immunoflourescence pattern
	Cryoglobulinemia[21]		Patients having cryoglobulinemia may have positive history of: Hepatitis C infection Hepatitis B infection Leg ulcers Recurrent thrombosis	Pulmonary symptoms: Difficulty breathing Cough Cutaneous symptoms: Purpura  Skin ulcer Gastrointestinal symptoms: Abdominal pain General symptoms: Fever Arthralgia, Myalgia Fatigue Blurring/loss of vision Diplopia Confusion	+/-	+	+/-	+	+/-	+/-	+/-	+/-	+/-	Membranoproliferative glomerulonephritis	Mesangial and subendothelial deposits	Prominent IgM and C3
Nephrotic Syndrome	Minimal Change Disease[22][23]		Young children Recent infection and immunization Atopy Hodgkin lymphoma Thrombosis (due to urinary loss of antithrombin-III)		–	+	–	+	+/-	+	–	+		Normal	Fusion of podocytes	–
	Focal Segmental Glomerulosclerosis[24][25][26]		Idiopathic HIV Heroine use Sickle cell disease Interferon Severe obesity Mixed cryoglobulinemia (Hepatitis C)		–	+	–	+	+/-	+	–	+		Focal (some glomeruli) and segmental (only part of glomerulus)	Effacement of podocytes	–
	Membranous Glomerulonephritis[27][28]		Idiopathic Hepatitis B and C Solid tumors Systemic lupus erythematosus Drugs (NSAIDS, pencilamine, gold, captopril)		–	+	–	+	+/-	+	–	+	Immune complex deposition	Thick glomerular basement membrane	Sub-epithelial immune complex depositis with ‘spike and dome’ appearance	Immune complex GN, granular deposite
	Diabetic Nephropathy[29][30][31][32][33][34][35][36][37][38]		For more information on diabetes click here.		–	+	–	+	+/-	+	–	+		Diffuse mesangial matrix expansion (nodular glomerulosclerosis) Increased mesangial hypercellularity Prominent glomerular basement membranes Thick basement membrane without any deposit	Nodular glomerulosclerosis	–
	Disease		History	Systemic symptoms	Hemeturia	Proteinuria	Hypertension	Pitting edema	Oliguria	Nephrotic features	Nephritic features	Hyperlipidemia and hypercholesterolemia	Auto-antibodies, Complements	Light microscope	Electron microscope	Immunoflourescence pattern
	Glomerular Deposition Diseases	Light Chain Deposition Disease[39]	Occurs in the setting of high tumor burden	–	–	+	–	+	+/-	+	–	+	–	Light-chain deposits	Granular deposits on electron microscopy	Detection of light chain deposits using anti–light chain antibody
		Renal Amyloidosis[40][41][42][43]	For the secondary causes of amloidosis: Tuberculosis Familial Mediterranean fever Rheumatoid arthritis Multiple myeloma	Dyspnea Lethargy Weight loss Bleeding tendency	–	+	–	+	+/-	+	–	+	–	Diffuse glomerular deposition of amorphous hyaline material (nodular pattern), in mesangium (weakly staining with periodic acid-Schiff (PAS)	Nodular deposit	AA amyloidosis type: negative for immunoglobulins and complement AL amyloidosis type: Positive for lambda or kappa light chains
		Fibrillary-Immunotactoid Glomerulopathy[44]	Malignancy Monoclonal gammopathy Autoimmune disease	–	+/-	+	+/-	+/-	+/-	+	+/-	+/-	–	Diffuse sclerosing glomerulonephritis Diffuse proliferative glomerulonephritis Membranoproliferative glomerulonephritis Mesangioproliferative/sclerosing disease Membranous glomerulonephritis	Large fibrillar deposits in the mesangium randomly Glomerular capillary walls different from amloidosis No staining with Congo red or thioflavine-T or with antibodies to a specific type	Positive for immunoglobulin G (IgG), C3 Kappa and lambda (ie, polyclonal) light chains
		Fabry’s Disease[45][46][47]	Family history suggestive of the disorder	Anhidrosis or decreased sweating Fatigue Angiokeratomas Burning pain of the extremities Corneal opacities. Dysphagia Abdominal pain Steatorrhea Delayed puberty Raynaud’s phenomenon Hearing loss Telangiectasis Ataxia	–	+	–	+	+/-	+	–	+	–	Vacuolization of visceral glomerular epithelial cells (podocytes) and distal tubular epithelial cells Glycolipid accumulation	Myeloid or zebra bodies: Gb3 deposition within enlarged secondary lysosomes as lamellated membrane structures Inclusions, composed of concentric layers (onion skin appearance)	–
Basement Membrane Syndrome	Alport’s Syndrome[48][49][50][51][52][53]		Positive family history	Auditary: Early Tinnitus Vertigo High-frequency progressive bilateral hearing loss Occular problems: Refractory Error Arcus Glaucoma Band Keratopathy Lenticonus Spherophakia Cataracts	–	+	–	+	+/-	+	–	+	–	Early stage: unremarkable Late stages: glomerulosclerosis, interstitial fibrosis, and interstitial foam cells (due to prolonged proteinuria).	Within glomerular basement membrane (GBM): longitudinal splitting of the lamina densa	Absence of staining of the alpha-3, alpha-4, and alpha-5 (IV) chains in the glomerular basement membrane Minimal binding to a glomerulus in indirect immunofluorescence microscopy with anti-glomerular basement membrane antibodies
	Disease		History	Systemic symptoms	Hemeturia	Proteinuria	Hypertension	Pitting edema	Oliguria	Nephrotic features	Nephritic features	Hyperlipidemia and hypercholesterolemia	Auto-antibodies, Complements	Light microscope	Electron microscope	Immunoflourescence pattern
	Thin Basement Membrane Disease[54][55]		Positive family history Gross hematuria following upper respiratory tract infection	–	–	+	-/+	–	-/+	–	-/+	–	–	–	Diffuse thinning of the glomerular basement membranes (GBM)	–
	Nail-Patella Syndrome[56][57]		Positive family history	Poorly developed fingernails, toe nails, and patellae (kneecaps). Elbow deformities Abnormally shaped pelvis bone (hip bone) Knee may be small, deformed or absent	+	+	–	–	–	–	–	–	–	Mostly unremarkable changes Secondary FSGS Late stages: Global glomerulosclerosis, Tubulointerstitial fibrosis	Glomerular basement membranes (GBMs): Focal or diffuse irregular thickening with electron-lucent areas (moth-eaten appearance) containing type III collagen bundles. Similar collagen fibrils can be seen in mesangial matrix. Podocytes: Segmental effacement of foot processes.	Immunofluorescence studies are typically negative. Nonspecific IgM and C3 deposition may be seen in sclerotic glomeruli.
Glomerular-Vascular Syndromes	Hypertensive Nephrosclerosis[58]		Chronic hypertension	Hypertensive retinal changes. High jugular venous pressure Rales from pulmonary edema on auscultation .Signs of left ventricular hypertrophy Left ventricular heave Shifting of apex towards the left S3 and gallop rhythm Loud S2 Ascites Paralysis from stroke secondary to hypertension Inferior limb edema	+/-	+/-	+	+/-	+/-	+/-	–	+/-	–	Interstitial fibrosis and atrophy Medial thickening and intimal fibrosis of medium-sized and larger vessels Arteriolar thickening, and hyalinosis Chronic stages: Global sclerosis Focal segmental sclerosis
	Cholesterol Emboli[59]		Atherosclerotic cardiovascular disease Anticoagulation therapy Cardiopulmonary resuscitation Hypertension Aortic aneurysm Hypercholesterolemia Smoking history Male sex Age over 55 years Vascular procedures Invasive angiography Aortic aneurysm rupture or surgery Vascular surgery	Depends on the organ involved	+/-	+/-	+	+/-	+/-	+/-	–	+/-	–	Atheroemboli are seen in interlobular and arcuate arteries, as lance-shaped clefts, due to dissolution of cholesterol crystals Acute lesions: Atheroemboli are surrounded by red blood cells, fibrin, and leukocytes, with multinucleated giant cell reactions Chronic lesions: Cholesterol clefts are surrounded by intimal fibrosis Vessel recanalization of chronic lesions can occur. Global and segmental sclerosis of glomeruli may be present.	Extensive foot process effacement can be seen	Not specific changes
	Disease		History	Systemic symptoms	Hemeturia	Proteinuria	Hypertension	Pitting edema	Oliguria	Nephrotic features	Nephritic features	Hyperlipidemia and hypercholesterolemia	Auto-antibodies, Complements	Light microscope	Electron microscope	Immunoflourescence pattern
	Sickle Cell Disease[60]		Positive family history	Pain and/or bone pain Dactylitis Blurry vision Persistent and painful erection Numbness Tingling Motor skill loss Speech deficits Gait disturbance Leg ulceration Jaundice	+/-	+/-	+/-	–	–	–	–	–	–	Glomerular hypertrophy Hemosiderin deposits Focal areas of hemorrhage or necrosis Chronic stage: interstitial inflammation, edema, fibrosis, tubular atrophy, and papillary infarcts Glomerular enlargement and focal segmental glomerulosclerosis (FSGS)
	Thrombotic Microangiopathies[61]		Click for more information on Thrombotic Microangiopathies.		+	+/-	+	+/-	+/-	+/-	–	–	–	Acute stage: Inravasculr fibrin thrombi Chronic stage: Endocapillary hypercellularity. Intimal proliferation of arterioles	Swollen glomerular endothelial cells with loss of fenestrations Chronic stage: interposed cells with new GBM matrix material deposition.	Thrombi stain positive for fibrinogen
	Antiphospholipid Antibody Syndrome [62][63][64]		Thrombosis Miscarriage  History of nephropathy History of hematologic abnormalities Nonthrombotic neurologic symptoms, such as migraine headaches Pulmonary hypertension	Fatigue Fever Weight loss Venous thrombosis Arterial thrombosis Thrombocytopenia Recurrent fetal loss	+	+/-	+	+/-	+/-	+/-	–	–	–	Acute stage: Inravasculr fibrin thrombi Chronic stage: Endocapillary hypercellularity. Intimal proliferation of arterioles	Swollen glomerular endothelial cells with loss of fenestrations Chronic stage: interposed cells with new GBM matrix material deposition.	Thrombi stain positive for fibrinogen

Some infectious diseases such as HIV, HBV, HCV, syphilis, leprosy, malaria, and schistosomiasis may cause glomerular diseases.

References

1. ↑ GERMUTH FG (1953). “A comparative histologic and immunologic study in rabbits of induced hypersensitivity of the serum sickness type”. J Exp Med. 97 (2): 257–82. PMC 2136196. PMID 13022878.CS1 maint: PMC format (link)
2. ↑ Germuth FG, Senterfit LB, Dreesman GR (1972). “Immune complex disease. V. The nature of the circulating complexes associated with glomerular alterations in the chronic BSA-rabbit system”. Johns Hopkins Med J. 130 (6): 344–57. PMID 5031005.CS1 maint: Multiple names: authors list (link)
3. ↑ Radhakrishnan J, Cattran DC (2012). “The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines–application to the individual patient”. Kidney Int. 82 (8): 840–56. doi:10.1038/ki.2012.280. PMID 22895519.
4. ↑ Neugarten J, Baldwin DS (August 1984). “Glomerulonephritis in bacterial endocarditis”. Am. J. Med. 77 (2): 297–304. PMID 6380288.
5. ↑ Arze RS, Rashid H, Morley R, Ward MK, Kerr DN (January 1983). “Shunt nephritis: report of two cases and review of the literature”. Clin. Nephrol. 19 (1): 48–53. PMID 6831779.
6. ↑ Weening JJ, D’Agati VD, Schwartz MM, Seshan SV, Alpers CE, Appel GB, Balow JE, Bruijn JA, Cook T, Ferrario F, Fogo AB, Ginzler EM, Hebert L, Hill G, Hill P, Jennette JC, Kong NC, Lesavre P, Lockshin M, Looi LM, Makino H, Moura LA, Nagata M (February 2004). “The classification of glomerulonephritis in systemic lupus erythematosus revisited”. Kidney Int. 65 (2): 521–30. doi:10.1111/j.1523-1755.2004.00443.x. PMID 14717922.
7. ↑ Bolton WK (November 1996). “Goodpasture’s syndrome”. Kidney Int. 50 (5): 1753–66. PMID 8914046.
8. ↑ Mathew TH, Hobbs JB, Kalowski S, Sutherland PW, Kincaid-Smith P (February 1975). “Goodpasture’s syndrome: normal renal diagnostic findings”. Ann. Intern. Med. 82 (2): 215–8. PMID 1090223.
9. ↑ Suzuki H, Kiryluk K, Novak J, Moldoveanu Z, Herr AB, Renfrow MB, Wyatt RJ, Scolari F, Mestecky J, Gharavi AG, Julian BA (October 2011). “The pathophysiology of IgA nephropathy”. J. Am. Soc. Nephrol. 22 (10): 1795–803. doi:10.1681/ASN.2011050464. PMC 3892742. PMID 21949093.
10. ↑ Wyatt RJ, Julian BA (June 2013). “IgA nephropathy”. N. Engl. J. Med. 368 (25): 2402–14. doi:10.1056/NEJMra1206793. PMID 23782179.
11. ↑ Higgins RM, Goldsmith DJ, Connolly J, Scoble JE, Hendry BM, Ackrill P, Venning MC (January 1996). “Vasculitis and rapidly progressive glomerulonephritis in the elderly”. Postgrad Med J. 72 (843): 41–4. PMC 2398323. PMID 8746284.
12. ↑ Jennette JC (March 2003). “Rapidly progressive crescentic glomerulonephritis”. Kidney Int. 63 (3): 1164–77. doi:10.1046/j.1523-1755.2003.00843.x. PMID 12631105.
13. ↑ Renaudineau Y, Le Meur Y (October 2008). “Renal involvement in Wegener’s granulomatosis”. Clin Rev Allergy Immunol. 35 (1–2): 22–9. doi:10.1007/s12016-007-8066-6. PMID 18172777.
14. ↑ Weiss MA, Crissman JD (October 1984). “Renal biopsy findings in Wegener’s granulomatosis: segmental necrotizing glomerulonephritis with glomerular thrombosis”. Hum. Pathol. 15 (10): 943–56. PMID 6384024.
15. ↑ Pagnoux C (March 2008). “[Wegener’s granulomatosis and microscopic polyangiitis]”. Rev Prat (in French). 58 (5): 522–32. PMID 18524109.CS1 maint: Unrecognized language (link)
16. ↑ Chung SA, Seo P (August 2010). “Microscopic polyangiitis”. Rheum. Dis. Clin. North Am. 36 (3): 545–58. doi:10.1016/j.rdc.2010.04.003. PMC 2917831. PMID 20688249.
17. ↑ Sinico RA, Di Toma L, Maggiore U, Tosoni C, Bottero P, Sabadini E, Giammarresi G, Tumiati B, Gregorini G, Pesci A, Monti S, Balestrieri G, Garini G, Vecchio F, Buzio C (May 2006). “Renal involvement in Churg-Strauss syndrome”. Am. J. Kidney Dis. 47 (5): 770–9. doi:10.1053/j.ajkd.2006.01.026. PMID 16632015.
18. ↑ Alchi B, Jayne D (August 2010). “Membranoproliferative glomerulonephritis”. Pediatr. Nephrol. 25 (8): 1409–18. doi:10.1007/s00467-009-1322-7. PMC 2887509. PMID 19908070.
19. ↑ Davis AE, Schneeberger EE, Grupe WE, McCluskey RT (May 1978). “Membranoproliferative glomerulonephritis (MPGN type I) and dense deposit disease (DDD) in children”. Clin. Nephrol. 9 (5): 184–93. PMID 657595.
20. ↑ Jennette JC, Falk RJ (July 1994). “The pathology of vasculitis involving the kidney”. Am. J. Kidney Dis. 24 (1): 130–41. PMID 8023818.
21. ↑ Fogo AB, Lusco MA, Najafian B, Alpers CE (February 2016). “AJKD Atlas of Renal Pathology: Cryoglobulinemic Glomerulonephritis”. Am. J. Kidney Dis. 67 (2): e5–7. doi:10.1053/j.ajkd.2015.12.007. PMID 26802335.
22. ↑ Saha TC, Singh H (November 2006). “Minimal change disease: a review”. South. Med. J. 99 (11): 1264–70. doi:10.1097/01.smj.0000243183.87381.c2. PMID 17195422.
23. ↑ Saleem MA, Kobayashi Y (2016). “Cell biology and genetics of minimal change disease”. F1000Res. 5. doi:10.12688/f1000research.7300.1. PMC 4821284. PMID 27092244.
24. ↑ Rosenberg AZ, Kopp JB (March 2017). “Focal Segmental Glomerulosclerosis”. Clin J Am Soc Nephrol. 12 (3): 502–517. doi:10.2215/CJN.05960616. PMC 5338705. PMID 28242845.
25. ↑ Jefferson JA, Shankland SJ (September 2014). “The pathogenesis of focal segmental glomerulosclerosis”. Adv Chronic Kidney Dis. 21 (5): 408–16. doi:10.1053/j.ackd.2014.05.009. PMC 4149756. PMID 25168829.
26. ↑ Gephardt GN, Tubbs RR, Popowniak KL, McMahon JT (October 1986). “Focal and segmental glomerulosclerosis. Immunohistologic study of 20 renal biopsy specimens”. Arch. Pathol. Lab. Med. 110 (10): 902–5. PMID 2429634.
27. ↑ Lai WL, Yeh TH, Chen PM, Chan CK, Chiang WC, Chen YM, Wu KD, Tsai TJ (February 2015). “Membranous nephropathy: a review on the pathogenesis, diagnosis, and treatment”. J. Formos. Med. Assoc. 114 (2): 102–11. doi:10.1016/j.jfma.2014.11.002. PMID 25558821.
28. ↑ Wasserstein AG (April 1997). “Membranous glomerulonephritis”. J. Am. Soc. Nephrol. 8 (4): 664–74. PMID 10495797.
29. ↑ Drummond K, Mauer M, International Diabetic Nephropathy Study Group (2002). “The early natural history of nephropathy in type 1 diabetes: II. Early renal structural changes in type 1 diabetes”. Diabetes. 51 (5): 1580–7. PMID 11978659.CS1 maint: Multiple names: authors list (link)
30. ↑ Hørlyck A, Gundersen HJ, Osterby R (1986). “The cortical distribution pattern of diabetic glomerulopathy”. Diabetologia. 29 (3): 146–50. PMID 3699305.CS1 maint: Multiple names: authors list (link)
31. ↑ Alpers CE, Hudkins KL (2011). “Mouse models of diabetic nephropathy”. Curr Opin Nephrol Hypertens. 20 (3): 278–84. doi:10.1097/MNH.0b013e3283451901. PMC 3658822. PMID 21422926.CS1 maint: PMC format (link)
32. ↑ Kimmelstiel P, Wilson C (1936). “Intercapillary Lesions in the Glomeruli of the Kidney”. Am J Pathol. 12 (1): 83–98.7. PMC 1911022. PMID 19970254.CS1 maint: PMC format (link)
33. ↑ Alpers CE, Biava CG (1989). “Idiopathic lobular glomerulonephritis (nodular mesangial sclerosis): a distinct diagnostic entity”. Clin Nephrol. 32 (2): 68–74. PMID 2766585.
34. ↑ Toyoda M, Najafian B, Kim Y, Caramori ML, Mauer M (2007). “Podocyte detachment and reduced glomerular capillary endothelial fenestration in human type 1 diabetic nephropathy”. Diabetes. 56 (8): 2155–60. doi:10.2337/db07-0019. PMID 17536064.CS1 maint: Multiple names: authors list (link)
35. ↑ Najafian B, Crosson JT, Kim Y, Mauer M (2006). “Glomerulotubular junction abnormalities are associated with proteinuria in type 1 diabetes”. J Am Soc Nephrol. 17 (4 Suppl 2): S53–60. doi:10.1681/ASN.2005121342. PMID 16565248.CS1 maint: Multiple names: authors list (link)
36. ↑ Najafian B, Kim Y, Crosson JT, Mauer M (2003). “Atubular glomeruli and glomerulotubular junction abnormalities in diabetic nephropathy”. J Am Soc Nephrol. 14 (4): 908–17. PMID 12660325.CS1 maint: Multiple names: authors list (link)
37. ↑ Najafian B, Alpers CE, Fogo AB (2011). “Pathology of human diabetic nephropathy”. Contrib Nephrol. 170: 36–47. doi:10.1159/000324942. PMID 21659756.CS1 maint: Multiple names: authors list (link)
38. ↑ Najafian B, Alpers CE, Fogo AB (2011). “Pathology of human diabetic nephropathy”. Contrib Nephrol. 170: 36–47. doi:10.1159/000324942. PMID 21659756.CS1 maint: Multiple names: authors list (link)
39. ↑ Hutchison CA, Cockwell P, Stringer S, Bradwell A, Cook M, Gertz MA, Dispenzieri A, Winters JL, Kumar S, Rajkumar SV, Kyle RA, Leung N (June 2011). “Early reduction of serum-free light chains associates with renal recovery in myeloma kidney”. J. Am. Soc. Nephrol. 22 (6): 1129–36. doi:10.1681/ASN.2010080857. PMC 3103732. PMID 21511832.
40. ↑ Baker KR, Rice L (2012). “The amyloidoses: clinical features, diagnosis and treatment”. Methodist Debakey Cardiovasc J. 8 (3): 3–7. PMC 3487569. PMID 23227278.
41. ↑ Gillmore JD, Hawkins PN (October 2013). “Pathophysiology and treatment of systemic amyloidosis”. Nat Rev Nephrol. 9 (10): 574–86. doi:10.1038/nrneph.2013.171. PMID 23979488.
42. ↑ Jerzykowska S, Cymerys M, Gil LA, Balcerzak A, Pupek-Musialik D, Komarnicki MA (2014). “Primary systemic amyloidosis as a real diagnostic challenge – case study”. Cent Eur J Immunol. 39 (1): 61–6. doi:10.5114/ceji.2014.42126. PMC 4439975. PMID 26155101.
43. ↑ Pepys MB (2006). “Amyloidosis”. Annu. Rev. Med. 57: 223–41. doi:10.1146/annurev.med.57.121304.131243. PMID 16409147.
44. ↑ Korbet SM, Schwartz MM, Lewis EJ (March 1991). “Immunotactoid glomerulopathy”. Am. J. Kidney Dis. 17 (3): 247–57. PMID 1996564.
45. ↑ Alroy J, Sabnis S, Kopp JB (June 2002). “Renal pathology in Fabry disease”. J. Am. Soc. Nephrol. 13 Suppl 2: S134–8. PMID 12068025.
46. ↑ Meikle PJ, Hopwood JJ, Clague AE, Carey WF (1999). “Prevalence of lysosomal storage disorders”. JAMA : the Journal of the American Medical Association. 281 (3): 249–54. PMID 9918480. Unknown parameter |month= ignored (help)CS1 maint: Multiple names: authors list (link)
47. ↑ Branton MH, Schiffmann R, Sabnis SG; et al. (2002). “Natural history of Fabry renal disease: influence of alpha-galactosidase A activity and genetic mutations on clinical course”. Medicine. 81 (2): 122–38. PMID 11889412. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
48. ↑ McCarthy PA, Maino DM (2000). “Alport syndrome: a review”. Clin Eye Vis Care. 12 (3–4): 139–150. PMID 11137428.
49. ↑ Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN; et al. (1993). “Hereditary nephritis (Alport’s syndrome)–clinical profile and inheritance in 28 kindreds”. Nephrol Dial Transplant. 8 (8): 690–5. PMID 8414153.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
50. ↑ Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN; et al. (1993). “Hereditary nephritis (Alport’s syndrome)–clinical profile and inheritance in 28 kindreds”. Nephrol Dial Transplant. 8 (8): 690–5. PMID 8414153.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
51. ↑ McCarthy PA, Maino DM (2000). “Alport syndrome: a review”. Clin Eye Vis Care. 12 (3–4): 139–150. PMID 11137428.
52. ↑ Amari F, Segawa K, Ando F (1994). “Lens coloboma and Alport-like glomerulonephritis”. Eur J Ophthalmol. 4 (3): 181–3. PMID 7819734.CS1 maint: Multiple names: authors list (link)
53. ↑ Govan JA (1983). “Ocular manifestations of Alport’s syndrome: a hereditary disorder of basement membranes?”. Br J Ophthalmol. 67 (8): 493–503. PMC 1040106. PMID 6871140.CS1 maint: PMC format (link)
54. ↑ Savige J, Rana K, Tonna S, Buzza M, Dagher H, Wang YY (2003). “Thin basement membrane nephropathy”. Kidney Int. 64 (4): 1169–78. doi:10.1046/j.1523-1755.2003.00234.x. PMID 12969134. Unknown parameter |month= ignored (help)CS1 maint: Multiple names: authors list (link)
55. ↑ Hou P, Chen Y, Ding J, Li G, Zhang H (2007). “A novel mutation of COL4A3 presents a different contribution to Alport syndrome and thin basement membrane nephropathy”. Am. J. Nephrol. 27 (5): 538–44. doi:10.1159/000107666. PMID 17726307.CS1 maint: Multiple names: authors list (link)
56. ↑ Najafian B, Smith K, Lusco MA, Alpers CE, Fogo AB (October 2017). “AJKD Atlas of Renal Pathology: Nail-Patella Syndrome-Associated Nephropathy”. Am. J. Kidney Dis. 70 (4): e19–e20. doi:10.1053/j.ajkd.2017.08.001. PMID 28941488.
57. ↑ Guidera KJ, Satterwhite Y, Ogden JA, Pugh L, Ganey T (1991). “Nail patella syndrome: a review of 44 orthopaedic patients”. J Pediatr Orthop. 11 (6): 737–42. PMID 1960197.
58. ↑ Hughson MD, Puelles VG, Hoy WE, Douglas-Denton RN, Mott SA, Bertram JF (July 2014). “Hypertension, glomerular hypertrophy and nephrosclerosis: the effect of race”. Nephrol. Dial. Transplant. 29 (7): 1399–409. doi:10.1093/ndt/gft480. PMC 4071048. PMID 24327566.
59. ↑ Lusco MA, Najafian B, Alpers CE, Fogo AB (April 2016). “AJKD Atlas of Renal Pathology: Cholesterol Emboli”. Am. J. Kidney Dis. 67 (4): e23–4. doi:10.1053/j.ajkd.2016.02.034. PMID 27012950.
60. ↑ Wesson DE (June 2002). “The initiation and progression of sickle cell nephropathy”. Kidney Int. 61 (6): 2277–86. doi:10.1046/j.1523-1755.2002.00363.x. PMID 12028473.
61. ↑ Lusco MA, Fogo AB, Najafian B, Alpers CE (December 2016). “AJKD Atlas of Renal Pathology: Thrombotic Microangiopathy”. Am. J. Kidney Dis. 68 (6): e33–e34. doi:10.1053/j.ajkd.2016.10.006. PMID 27884283.
62. ↑ Jayakody Arachchillage D, Greaves M (2014). “The chequered history of the antiphospholipid syndrome”. Br J Haematol. 165 (5): 609–17. doi:10.1111/bjh.12848. PMID 24684307.
63. ↑ Jayakody Arachchillage D, Greaves M (2014). “The chequered history of the antiphospholipid syndrome”. Br J Haematol. 165 (5): 609–17. doi:10.1111/bjh.12848. PMID 24684307.
64. ↑ Popa A, Voinea L, Pop M, Stana D, Dascalu AM, Alexandrescu C; et al. (2008). “[Primary antiphospholipid syndrome]”. Oftalmologia. 52 (1): 13–7. PMID 18714484.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

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.

• The incidence of post-streptococcal glomerulonephritis is approximately 9.5 to 28.5 per 100,000 individuals worldwide.^[1]

• The case-fatality rate of post-streptococcal glomerulonephritis is approximately 2 percent in India and 0.08 percent in Turkey.^[2]

• 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.

• There is no racial predilection to post-streptococcal glomerulonephritis.

• Men are more commonly affected by post-streptococcal glomerulonephritis than women.

• The majority of post-streptococcal glomerulonephritis cases are reported in developing countries.^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

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 streptoccocal.

• Common risk factors in the development of post-streptococcal glomerulonephritis include:
  • Streptococcal throat infection
  • Impetigo

• Less common risk factors in the development of post-streptococcal glomerulonephritis include:
  • Household infection with the nephritogenic strain of group A streptococcal

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

There is insufficient evidence to recommend routine screening for post-streptococcal glomerulonephritis.

There is insufficient evidence to recommend routine screening for post-streptococcal glomerulonephritis.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

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.

• 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.
• If left untreated, patients with post-streptococcal glomerulonephritis may progress to develop renal failure.^[1]

Common complications of post-streptococcal glomerulonephritis include:^[2][3][4]

• Severe nephritis
• Renal failure
• Atypical hemolytic uremic syndrome
• Refractory hypoxic respiratory failure
• Seizures

• Prognosis is generally excellent.^[5][6]
• Some people develop recurrent proteinuria and renal dysfunction 10 to 40 years after the presentation.^[7]
• Age and presence of comorbidities are the most important prognostic factors for PSGN.
• Children have an excellent prognosis with a <1% rate of azotemia, and a 3-10% rate of non-nephrotic range proteinuria, microhematuria, and hypertension.
• The prognosis of PSGN in children might vary depending on individual co-morbidities, such as diabetes, obesity, and low birth weight.^[5]
• Elderly patients with PSGN who often have co-morbidities have a comparatively much poorer prognosis with a 60% rate of azotemia, 40% rate of congestive heart failure, and 20% rate of nephrotic syndrome.^[8][9]

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