AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Acute glomerulonephritis is characterized by the sudden appearance of hematuria, proteinuria and red blood cell casts in the urine, edema, and hypertension with or without oliguria. It can follow streptococcal infections. This illness was first recognized as a complication of the convalescence period of scarlet fever in the 18th century. A link between hemolytic streptococci and acute glomerulonephritis was recognized in the 20th century.

Although the incidence of poststreptococcal glomerulonephritis has declined in the United States, it continues to have high incidence in other parts of the world, especially in areas with tropical climates where skin infections are common.

Pathophysiology

Poststreptococcal glomerulonephritis follows infection with only certain strains of streptococci designated as nephritogenic. The offending organisms are virtually always group A streptococci. Acute poststreptococcal glomerulonephritis (APSGN) follows pyodermatitis with streptococci M types 47, 49, 55, 2, 60, and 57 and throat infection with streptococci M types 1, 2, 4, 3, 25, 49, and 12.

Although many morphologic, clinical, and serologic features suggest that APSGN is an immune complex disorder, the precise nature of the antigen-antibody interaction is undefined. ASPGN is believed to be an immune-mediated disease, in which an immune complex containing a streptococcal antigen is deposited in the affected glomeruli. The size of glomerular basement membrane (GBM) pores and the molecular size of the streptococcus-Ig complex are also important determinants. The molecular size of the streptococcus-Ig complex is about 15 nm (10 nm for streptococcus group A and 5 nm for immunoglobulin). The GBM pore sizes in children and adults are 2-3 nm and 4-4.5 nm, respectively. Therefore, the immune complex molecule can be more easily rodded into the glomerulus in children than in adults and, thus, may explain the increased frequency of ASPGN in children compared to that in adults.

The 2 antigens isolated from nephritogenic streptococci are under investigation in APSGN. These include the cationic cysteine protease exotoxin B and glyceraldehyde phosphate dehydrogenase (also known as presorbing antigen or PA-Ag). These fractions have an affinity for glomeruli and have been shown to induce specific, long-lasting antibody responses in biopsy specimens from patients with APSGN. The relevance of exotoxin B and glyceraldehyde phosphate dehydrogenase was recently evaluated in the same renal biopsy and serum samples of patients with well-defined APSGN. Glomerular deposits of and antibody response to exotoxin B was more consistently present in APSGN than deposits of and antibody response to glyceraldehyde phosphate dehydrogenase.

Antibodies to exotoxin B and PA-Ag are elevated in the majority of patients with APSGN. Intravenous injections of PA-Ag produce acute glomerulonephritis in animals. Antibodies to PA-Ag are found in 30 of 31 patients with APSGN but are low or absent in those with uncomplicated streptococcal infection or in patients with rheumatic fever.

PA-Ag is also known to activate the alternate pathway of the complement cascade, which happens to be preferentially activated in persons with APSGN. The observation that some patients may only have C3 deposition may relate to this mechanism.

In addition to streptococcal antigens, rheumatoid factor, cryoglobulins, and antineutrophil cytoplasmic serum antibodies are present in some of these patients. The pathogenic significance of this autoimmune response is not defined.

Frequency

International

APSGN can occur sporadically or epidemically.

• Incidence seems to be decreasing in the United States and Europe, but sporadic cases of the disease continue to be reported from all over the world. The prevalence of nephritis varies considerably among persons with sporadic infections with nephritogenic streptococci. The reason for this variability is not known.
• Epidemic poststreptococcal glomerulonephritis occurs mainly in developing countries in areas such as Africa, the West Indies, and the Middle East. Reasons for this changing epidemiology relate to the nutritional status of the community, the more liberal use of antibiotic prophylaxis, and, possibly, the change in the nephritogenic potential of streptococci. Among epidemic infections with nephritogenic streptococci, the apparent clinical attack rate is 10-12%.

Mortality/Morbidity

Early death is extremely rare in children (<1%) but is significantly more common in adults (25%). This is secondary to congestive heart failure and azotemia.

• Congestive heart failure is more common in adults (43%) than in children (<5%).
• Nephrotic-range proteinuria is more common in adults (20%) than in children (4-10%).
• Approximately 83% of adults have azotemia, compared to 25-40% of children.

Race

No racial predilection is recognized.

Sex

Clinical cases of APSGN are twice as common in males compared to females. If subclinical disease is considered, both sexes are affected equally. The familial incidence rate is nearly 40%, but no genetic marker has been identified.

Age

This condition typically affects children aged 2-12 years. A large series reported that 5% are younger than 2 years and 10% are older than 40 years.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

A history suggestive of preceding streptococcal infection may include a preceding infective episode such as pharyngitis, tonsillitis, or pyoderma. This is the sine qua non for the diagnosis of APSGN.

• Latent period
• • A latent period always occurs between the streptococcal infection and the onset of signs and symptoms of acute glomerulonephritis.
  • In general, the latent period is 1-2 weeks after a throat infection and 3-6 weeks after a skin infection.
  • The onset of signs and symptoms at the same time as pharyngitis (also called synpharyngitic nephritis) is more likely to be immunoglobulin A (IgA) nephropathy rather than APSGN.
• Dark urine (brown-, tea-, or cola-colored)
• • This is often the first clinical symptom.
  • Dark urine is caused by hemolysis of red blood cells that have penetrated the glomerular basement membrane and have passed into the tubular system.
• Periorbital edema
• • The onset of puffiness of the face or eyelids is sudden. It is usually prominent upon awakening and, if the patient is active, tends to subside at the end of the day.
  • In some cases, generalized edema and other features of circulatory congestion, such as dyspnea, may be present.
  • Edema is a result of a defect in renal excretion of salt and water.
  • The severity of edema is often disproportionate to the degree of renal impairment.
• Nonspecific symptoms
• • These can include general malaise, weakness, and anorexia and are present in 50% of patients.
  • Approximately 15% of patients complain of nausea and vomiting.

Physical

• Acute nephritic syndrome
• • Acute nephritic syndrome presenting as edema, hematuria, and hypertension with or without oliguria is the most frequent presentation of APSGN.
  • Approximately 95% of clinical cases have at least 2 manifestations, and 40% have the full-blown acute nephritic syndrome.
• Edema
• • Edema is present in 80-90% of cases, and it is the presenting complaint in 60% of cases.
  • Compromised intraglomerular blood flow due to glomerular hypercellularity results in progressive encroachment on the cross-sectional area of the glomerular capillaries.
  • This leads to reduced blood flow that manifests as low fractional excretion of sodium and concentrated urine. This salt and water retention leads to edema.
• Hypertension
• • Hypertension occurs in 60-80% of cases and is more common among elderly individuals.
  • In 50% of cases, the hypertension can be severe; however, more often it is transient, with normalization of blood pressure upon restoration of the glomerular filtration rate, loss of edema, and normalization of plasma volume.
  • If hypertension persists, it is more indicative of the progression to a more chronic stage or that the disease is not poststreptococcal glomerulonephritis.
  • Hypertension is thought to be the result of excessive salt and water retention.
  • Despite excessive sodium retention, the plasma levels of atrial natriuretic peptide are increased. In this condition, this suggests that the kidneys are unresponsive to atrial natriuretic peptide.
  • Plasma renin activity is usually low, and studies by Parra et al have shown that an inhibition of angiotensin-converting enzyme could be an effective short-term treatment for this low-renin hypertension.
  • Hypertensive encephalopathy occurs in no more than 5-10% of patients. Usually, clinical improvement occurs without any neurological sequelae.
• Oliguria
• • This is present in 10-50% of cases, and, in 15%, urine output is less than 200 mL.
  • Oliguria is indicative of the severe crescentic form of the disease.
  • It is often transient, with diuresis occurring within 1-2 weeks.
• Hematuria
• • This is present universally.
  • In 30% of cases, gross hematuria is present.
• Left ventricular dysfunction
  • Left ventricular dysfunction with or without hypertension or pericardial effusion may be present during the acute congestive and convalescent phases.
  • In rare cases, persons with APSGN can show signs of pulmonary hemorrhage.

Causes

• Poststreptococcal glomerulonephritis follows infection with only certain strains of streptococci designated as nephritogenic.
• The offending organisms are virtually always group A streptococci.
• APSGN follows pyodermatitis with streptococci M types 47, 49, 55, 2, 60, and 57 and throat infection with streptococci M types 1, 2, 4, 3, 25, 49, and 12.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Bacterial endocarditis
Essential cryoglobulinemia
IgA nephropathy
Microscopic polyarteritis
Shunt nephritis
Visceral abscess

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Evidence of preceding streptococcal infection
• • Antibody titers to extracellular products of streptococci are positive in more than 95% of patients with pharyngitis and 80% of patients with skin infections.
  • The antistreptolysin (ASO), antinicotinamide adenine dinucleotidase (anti-NAD), antihyaluronidase (AHase), and anti–DNAse B are commonly positive after pharyngitis, and anti–DNAse B and AHase titers are more often positive following skin infections.
  • ASO titers are frequently used to document streptococcal infection, but a more sensitive test is the streptozyme test, which tests antibodies to ASO, anti–DNAse B, AHase, and anti-NAD.
  • Recent studies suggest that the relatively unavailable antizymogen titer test is superior to both anti–DNAse B and ASO titers.
  • Antizymogen titers that are 2 dilutions higher than the mean in healthy controls are reported to have a sensitivity of 88% and a specificity of 85% in the diagnosis of streptococcal infection in patients with glomerulonephritis.
  • High antibody titers to glyceraldehyde phosphate dehydrogenase are also found in persons with APSGN.
  • In general, the antibody titers are elevated at 1 week, peak at 1 month, and fall toward preinfection levels after several months.
• Elevated BUN and creatinine values
• • This reflects the decrease in the glomerular filtration rate that occurs in the acute phase.
  • The elevations are usually transient.
  • Their failure to normalize within several weeks or months indicates that the patient may not have a true APSGN and suggests seeking an alternative diagnosis.
  • Patients who have the crescentic form of glomerulonephritis have rapid deterioration and, often, incomplete recovery of renal function.
• Serologic findings
• • Low serum complement levels indicative of an antigen-antibody interaction are a universal finding in the acute phase of APSGN.
  • Most patients have marked depression of serum hemolytic component CH50 and serum concentrations of C3.
  • The activation of the alternative pathway of the complement system is thought to be responsible for the hypocomplementemia.
  • In some patients, the levels of C2 and C4 may also be decreased, but to a lesser extent, suggesting that both classic and alternate pathways of the complement system are activated.
  • In most uncomplicated cases, the complement levels return to normal in 6-8 weeks. Prolonged hypocomplementemia suggests an alternative diagnosis.
  • Occasionally, low complement levels persist for 3 months.
  • The level of reduction of serum complement levels does not have any prognostic significance.
  • Circulating immune complexes and cryoglobulins are found in 60% of cases, and rheumatoid factor is found in 43% of cases.
• Urinalysis
  • Results are always abnormal.
  • Hematuria and proteinuria are present in all cases.
  • Urine sediment has red blood cells, red blood cell casts, white blood cells, granular casts, and, rarely, white blood cell casts.
  • Dysmorphic red blood cells indicative of glomerular hematuria can usually be detected by performing phase-contrast microscopy.
  • Red blood cell casts are best detected in first, early-morning urine specimens examined by the physician immediately after the patient voids.
  • Hematuria usually resolves within 3-6 months but may persist as long as 18 months.
  • Microscopic hematuria may be present in patients in whom the disease has otherwise clinically resolved.
  • Proteinuria may be mild or so severe that it causes nephrotic syndrome.
  • Approximately 5-10% of patients with APSGN have nephrotic-range proteinuria.
  • Proteinuria usually disappears in 6 months. A mild increase in urinary protein excretion is present in 15% at 3 years and 2% at 10 years.
  • Patients with nephrotic-range proteinuria in the acute phase or persistent heavy proteinuria have a worse prognosis. This is often associated with an evolution to a garlandlike pattern of immune deposits as the disease progresses.

Imaging Studies

• Chest radiographs may show findings of congestive heart failure.
• Renal ultrasound images usually reveal normal-sized kidneys bilaterally.

Procedures

• APSGN is often a clinical diagnosis and requires the detection of glomerulonephritis and evidence of preceding streptococcal infection.
• Atypical features in the early phase that suggest the need for renal biopsy include the following:
• • Absence of the latent period between streptococcal infection and acute glomerulonephritis
  • Anuria
  • Rapidly deteriorating renal function
  • Normal serum complement levels
  • No rise in antistreptococcal antibodies
  • Extrarenal manifestations of systemic disease
  • No improvement or continued decrease in the glomerular filtration rate at 2 weeks
  • Persistence of hypertension beyond 2 weeks
• Atypical features in the recovery phase that mandate a renal biopsy include the following:
• • Failure of glomerular filtration rate to normalize by 4 weeks
  • Persistent hypocomplementemia beyond 6 weeks
  • Persistent microscopic hematuria beyond 18 months
  • Persistent proteinuria beyond 6 months

Histologic Findings

• Pathologic findings of changes in gross appearance
  • The kidneys are symmetrically enlarged to approximately 25-50% of normal.
  • They are pale in appearance, and the cut surfaces bulge because of interstitial edema.
  • The glomeruli may stand out as reddish or gray translucent dots.
  • The cut surfaces may have tiny red speckles caused by red blood cells in the lumen of the Bowman space and tubules.
• Light microscopy
  • The most striking finding is hypercellularity of the glomeruli. All glomeruli are affected (diffuse) and usually to an approximately equal degree. The glomerular tufts are larger than normal, and the cells are more numerous.
  • The cell types typically present include endothelial and mesangial cells and migrant inflammatory cells, which include polymorphonuclear leukocytes and monocytes.
  • Polymorphonuclear leukocytes are present in large numbers, hence the term exudative glomerulonephritis.
  • Necrosis in the glomerular tuft is not typically found.
  • The individual lobules are wider than usual and may have a clubbed appearance.
  • Generally, the glomerular capillary walls are not thick.
  • In some patients, crescent formation may be found, but usually, only a small percentage of glomeruli are affected by crescents.
  • The tubules are normal in the majority of cases.
  • When proteinuria is present, hyaline droplets (protein reabsorption droplets) may be present in the proximal convoluted tubules.
  • In patients with severe exudative glomerulonephritis, polymorphonuclear leukocytes may be present in the lumen.
  • The degree of interstitial involvement is variable. The interstitial areas show edema and infiltration with polymorphonuclear leukocytes and mononuclear cells. The arteries and arterioles are normal.
• Immunofluorescence
  • In biopsy samples taken in the first 2-3 weeks of illness, deposits of immunoglobulin G and C3 in a diffuse granular pattern are present along the glomerular capillary wall and mesangium.
  • Immunoglobulin M may be present in small amounts. Significant amounts of IgA suggest an alternative diagnosis.
  • Sorger et al have described 3 different patterns of immunofluorescence called the garland pattern, the starry sky pattern, and the mesangial pattern.
  • The starry sky pattern is an irregular, finely granular pattern with small deposits often situated on the glomerular basement membrane overlying the mesangium. This pattern is often seen in the early phase of the disease.
  • The starry sky pattern may turn into the mesangial pattern, which is characterized by granular deposition of C3 with or without immunoglobulin G. It seems to be most closely related to a resolving pattern.
  • In approximately 25% of patients, the deposits are large and densely packed and aggregate into a ropelike or garlandlike pattern. These correspond to the humps on the subepithelial side of the glomerular capillary wall seen with electron microscopy. These types of deposits may persist for months and may be associated with the persistence of proteinuria and the development of glomerulosclerosis.
• Electron microscopy
  • Many of the ultrastructural changes confirm the findings from light microscopy evaluations.
  • The number of endothelial, mesangial, and infiltrating inflammatory cells is increased.
  • The glomerular basement membrane is usually normal in thickness and contour, although occasionally patchy thickening may be noted.
  • The most consistent and classic diagnostic finding is the presence of glomerular subepithelial electron-dense immune-type deposits, often referred to as humps. The deposits are discrete and are commonly found on the part of the glomerular basement membrane overlying the mesangium.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

Symptomatic therapy is recommended for patients with APSGN, and it should be based on the clinical severity of the illness. The major goal is to control edema and blood pressure.

• During the acute phase of the disease, restrict salt and water.
• • If significant edema or hypertension develops, administer diuretics.
  • Loop diuretics increase urinary output and consequently improve cardiovascular congestion and hypertension.
• For hypertension not controlled by diuretics, usually calcium channel blockers or angiotensin-converting enzyme inhibitors are useful. For malignant hypertension, intravenous nitroprusside or other parenteral agents are used.
• Indications for dialysis include life-threatening hyperkalemia and clinical manifestations of uremia.
• Restricting physical activity is appropriate in the first few days of the illness but is unnecessary once the patient feels well.
• Steroids, immunosuppressive agents, and plasmapheresis are not generally indicated.
• A renal biopsy is indicated for patients with rapidly progressive renal failure. If the biopsy findings show evidence of crescentic glomerulonephritis with more than 30% of the glomeruli involved, a short course of intravenous pulse steroid therapy is recommended (500 mg to 1 g/1.73 m² of methylprednisone qd for 3-5 d). However, no controlled clinical trials have evaluated such therapy.
• Long-term treatment with steroids or immunosuppressives is not recommended.
• Specific therapy for streptococcal infection is an important part of the therapeutic regimen.
• • Treat patients, family members, and any close personal contacts who are infected.
  • Throat cultures should be performed on all these individuals. Treat with oral penicillin G (250 mg qid for 7-10 d) or with erythromycin (250 mg qid for 7-10 d) for patients allergic to penicillin.
  • This helps prevent nephritis in carriers and helps prevent the spread of nephritogenic strains to others.
• Patients with skin infections must practice good personal hygiene. This is essential.
• During epidemics, recommend that high-risk individuals, including close contacts and family members, receive empirical prophylactic treatment.

Surgical Care

Surgical care is not indicated.

Consultations

• Nutritionist or dietitian
• Nephrologist

Diet

• Low-salt diet - Two grams of sodium per day
• Fluid restriction - One liter per day

Activity

• Restricting physical activity is appropriate in the first few days of the illness but is not necessary once the patient feels well.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Therapy for patients with APSGN is symptomatic in nature and depends on the clinical severity of the illness. The major aims are to control the edema and blood pressure.

During the acute phase of the disease, salt and water should be restricted. If significant edema or hypertension develops, diuretics should be administered. Loop diuretics increase urinary output and consequently improve cardiovascular congestion and hypertension.

For hypertension not controlled by diuretics, calcium channel blockers or angiotensin-converting enzyme inhibitors are generally useful. For malignant hypertension, intravenous nitroprusside or other parenteral agents are used.

The indications for dialysis include life-threatening hyperkalemia and clinical manifestations of uremia. Steroids, immunosuppressive agents, and plasmapheresis are not generally indicated. In patients with rapidly progressive renal failure, a renal biopsy is indicated. If the biopsy findings show evidence of crescentic glomerulonephritis with more than 30% of the glomeruli involved, a short course of intravenous pulse steroid therapy is recommended (500 mg to 1 g/1.73 m² of methylprednisone qd for 3-5 d). However, no controlled clinical trials have evaluated such therapy. Long-term treatment with steroids or immunosuppressives is not recommended.

Drug Category: Diuretics

Used to control edema and circulatory congestion.

Drug Category: Calcium channel blockers

In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. Calcium channel blockers inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.

Drug Category: Angiotensin-converting enzyme inhibitors

Decrease aldosterone secretion.

Drug Category: Vasodilators

Used to treat hypertensive emergencies. Vasodilators reduce SVR, which, in turn, may allow forward flow, improving cardiac output.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• In the acute phase, admit for observation and treatment of hypertension and congestive heart failure.
• Admit for monitoring and to initiate dialysis (when indicated) if renal function progressively worsens.

Further Outpatient Care

• Monitor blood pressure every month for 6 months and then every 6 months thereafter.
• Monitor BUN and serum creatinine levels every 3 months after the acute phase for 1 year and then yearly after that.
• Check serum complement levels at 6-8 weeks to make sure they have returned to normal.
• Check urine for hematuria and proteinuria every 3-6 months.

In/Out Patient Meds

• Most patients do not require any medications after the acute phase.
• In the acute phase, diuretics may be needed to control edema and congestive heart failure.
• Antihypertensives may be needed in the chronic phase if the patient's blood pressure remains high.

Transfer

• Transfer may be necessary if renal biopsy facilities are not available and the diagnosis is in doubt or if rapidly progressive renal failure develops.
• Transfer may be necessary if azotemia worsens and dialysis facilities are not available on site.

Deterrence/Prevention

• The patient and any family member or close personal contact should have a throat culture.
• Treatment with penicillin G or erythromycin (if allergic to penicillin) helps prevent nephritis in carriers and helps prevent the spread of nephritogenic strains to others.
• Patients with skin infections must pay close attention to personal hygiene.
• Epidemics should prompt empirical prophylactic treatment for high-risk individuals (family and close personal contacts).

Complications

• Complications in the acute phase include the following:
• • Congestive heart failure
  • Azotemia
  • Early death secondary to congestive heart failure and azotemia
• Complications in the chronic phase include the following:
• • Nephrotic-range proteinuria
  • Chronic renal insufficiency and end-stage renal disease

Prognosis

• In children, the immediate prognosis is excellent.
• In elderly patients who have congestive heart failure or azotemia in the early phase, early mortality rates can be as high as 25%.
• The long-term prognosis is debatable.
• • Fewer than 1% of children have elevated serum creatinine values after 10-15 years of follow-up.
  • Adults who develop massive proteinuria often have the garlandlike pattern of immune deposits. Their prognosis is worse; approximately 25% progress to chronic renal failure.

Patient Education

• Patients with skin infections should know the importance of personal hygiene.
• In epidemics, all close personal contacts and family members should be told to seek medical attention for prophylactic treatment of streptococcal infections.
• For excellent patient education resources, visit eMedicine's Kidneys and Urinary System Center and Ear, Nose, and Throat Center. Also, see eMedicine's patient education articles Blood in the Urine and Strep Throat.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to follow up on the natural course of the disease
• • Make sure serum complement levels have returned to normal at 6-8 weeks.
  • Make sure hematuria and proteinuria resolve or improve and do not get worse.
• Failure to make the correct diagnosis
• • A risk of missing alternative diagnoses in atypical cases exists if a renal biopsy is not performed.
  • See Procedures for details on indications for renal biopsy.

Special Concerns

• Patients with subclinical nephritis outnumber those with overt nephritis by a ratio ranging from 4-10:1. Careful evaluation of abnormal urinalysis results may help reveal a diagnosis of poststreptococcal glomerulonephritis.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Batsford SR, Mezzano S, Mihatsch M, et al. Is the nephritogenic antigen in post-streptococcal glomerulonephritis pyrogenic exotoxin B (SPE B) or GAPDH?. Kidney Int. Sep 2005;68(3):1120-9.
• Dedeoglu IO, Springate JE, Waz WR, et al. Prolonged hypocomplementemia in poststreptococcal acute glomerulonephritis. Clin Nephrol. Nov 1996;46(5):302-5. [Medline].
• Deen WM, Bridges CR, Brenner BM. Biophysical basis of glomerular permselectivity. J Membr Biol. 1983;71(1-2):1-10.
• Dorrington KJ, Tanford C. Molecular size and conformation of immunoglobulins. Adv Immunol. 1970;12:333-81.
• Massry SG, Glassock RJ. Glomerulonephritis associated with infection. In: Massry SG, Glasscock RJ, eds. Textbook of Nephrology. 3rd ed. Baltimore, Md: Williams & Wilkins;. 1995: 698-703.
• Parra G, Rodriguez-Iturbe B, Batsford S, et al. Antibody to streptococcal zymogen in the serum of patients with acute glomerulonephritis: a multicentric study. Kidney Int. Aug 1998;54(2):509-17. [Medline].
• Rodriguez-Iturbe B. Postinfectious glomerulonephritis. Am J Kidney Dis. Jan 2000;35(1):XLVI-XLVIII. [Medline].
• Shrier RW, Gottschalk CW, eds. Diseases of the Kidney. Vol 2. 6th ed. Boston, Mass: Little, Brown & Company; 1997:. 1579- 84.
• Silva FG. Acute Postinfectious Glomerulonephritis and Glomerulonephritis Complicating Persistent Bacterial Infection. In: Jennette JC, Olson JL, Schwartz MM, eds. Heptinstall's Pathology of the Kidney. Vol 1. 5th ed. Philadelphia, Pa: Lippincott-Raven;. 1998: 389-455.
• Sorger K, Gessler U, Hubner FK, et al. Subtypes of acute postinfectious glomerulonephritis. Synopsis of clinical and pathological features. Clin Nephrol. Mar 1982;17(3):114-28. [Medline].
• Wiwanitkit V. Why is acute post-streptococcal glomerulonephritis more common in the pediatric population?. Clin Exp Nephrol. Jun 2006;10(2):164.

Article Last Updated: Dec 7, 2006