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Glomerulonephritis

Glomerulonephritis is a primary or secondary autoimmune renal disease featuring inflammation of the glomeruli. It may be asymptomatic, or present with hematuria and/or proteinuria (blood resp. protein in the urine). There are many recognised types, divided in acute, subacute or chronic glomerulonephritis. Causes are infectious (bacterial, viral or parasitic pathogens), autoimmune or paraneoplastic. more...

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Medicines

Acute glomerulonephritis

Acute diffuse proliferative GN

Histopathology: the majority of glomeruli present hypercellularity due to proliferation of endothelial and mesangial cells, inflammatory infiltrate with neutrophils and with monocytes. The Bowman space is reduced (compressed). Tubules are not affected.

Rapidly progressive GN (Crescentic GN)

Histopathology: The majority of glomeruli present "crescents". Formation of crescents is initiated by passage of fibrin into the Bowman space as a result of increased permeability of glomerular basement membrane. Fibrin stimulates the proliferation of parietal cells of Bowman capsule, and an influx of monocytes. Rapid growing and fibrosis of crescents compresses the capillary loops and decreases the Bowman space which leads to renal failure within weeks or months.

Mesangial proliferative GN

This type is due to deposition of polymerised IgA1 in the mesangium, with a localised proliferation of tissue. It is consistent with IgA nephritis (Berger's disease) and usually presents with macroscopic hematuria.

Minimal change GN

This form of GN usually (though not exclusively) presents in children with nephrotic syndrome and massive proteinuria. It is controlled with steroids. As the name indicates, there are no changes on light microscopy.

Chronic glomerulonephritis

Chronic glomerulonephritis represents the end-stage of all glomerulonephritis with unfavorable evolution.

Histopathology: few glomeruli may still present changes which permit to discern the etiology of CGN. The majority of the glomeruli are affected. Depending on the stage of the disease, they may present different degrees of hyalinization (hyalinosclerosis - total replacement of glomeruli and Bowman's space with hyaline). The hyaline is an amorphous material, pink, homogenous, resulted from combination of plasma proteins, increased mesangial matrix and collagen. Totally hyalines glomeruli are atrophic (smaller), lacking capillaries, hence non-functional. Obstruction of blood flow will produce secondary tubular atrophy, interstitial fibrosis and thickening of the arterial wall by hyaline deposits. Functional nephrons have dilated tubules, often with hyaline casts in the lumens. In the interstitium is present an abundant inflammatory infiltrate (mostly with lymphocytes).

This general (glomerular, vascular and interstitial) affection constitutes the so-called "end stage kidney". In most cases, it is associated with systemic hypertension.

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Acute poststreptococcal glomerulonephritis
From Gale Encyclopedia of Medicine, 4/6/01 by Maureen Haggerty

Definition

Acute poststreptococcal glomerulonephritis (APSGN) is an inflammation of the kidney tubules (glomeruli) that filter waste products from the blood, following a streptococcal infection such as strep throat. APSGN is also called postinfectious glomerulonephritis.

Description

APSGN develops after certain streptococcal bacteria (group A beta-hemolytic streptococci) have infected the skin or throat. Antigens from the dead streptococci clump together with the antibodies that killed them. These clumps are trapped in the kidney tubules, cause the tubules to become inflamed, and impair that organs' ability to filter and eliminate body wastes. The onset of APSGN usually occurs one to six weeks (average two weeks) after the streptococcal infection.

APSGN is a relatively uncommon disease affecting about 1 of every 10,000 people, although four or five times that many may actually be affected by it but show no symptoms. APSGN is most prevalent among boys between the ages of 3 and 7, but it can occur at any age.

Causes & symptoms

Frequent sore throats and a history of streptococcal infection increase the risk of acquiring APSGN. Symptoms of APSGN include:

  • Fluid accumulation and tissue swelling (edema) initially in the face and around the eyes, later in the legs
  • Low urine output (oliguria)
  • Blood in the urine (hematuria)
  • Protein in the urine (proteinuria)
  • High blood pressure
  • Joint pain or stiffness.

Diagnosis

Diagnosis of APSGN is made by taking the patient's history, assessing his/her symptoms, and performing certain laboratory tests. Urinalysis usually shows blood and protein in the urine. Concentrations of urea and creatinine (two waste products normally filtered out of the blood by the kidneys) in the blood are often high, indicating impaired kidney function. A reliable, inexpensive blood test called the anti-streptolysin-O test can confirm that a patient has or has had a streptococcal infection. A throat culture may also show the presence of group A beta-hemolytic streptococci.

Treatment

Treatment of ASPGN is designed to relieve the symptoms and prevent complications. Some patients are advised to stay in bed until they feel better and to restrict fluid and salt intake. Antibiotics may be prescribed to kill any lingering streptococcal bacteria, if their presence is confirmed. Antihypertensives may be given to help control high blood pressure and diuretics may be used to reduce fluid retention and swelling. Kidney dialysis is rarely needed.

Prognosis

Most children (up to 95%) fully recover from APSGN in a matter of weeks or months. Most adults (up to 70%) also recover fully. In those who do not recover fully, chronic or progressive problems of kidney function may occur. Kidney failure may result in some patients.

Prevention

Receiving prompt treatment for streptococcal infections may prevent APSGN.

Key Terms

Streptococcus
A gram-positive, round or oval bacteria in the genus . Group A streptococci cause a number of human diseases including strep throat, impetigo, and ASPGN.

Further Reading

For Your Information

    Books

  • Fauci, Anthony S., et al, eds. Harrison's Principles of Internal Medicine. 14th ed. New York: McGraw-Hill, 1998.
  • Professional Guide to Diseases. 5th ed. Springhouse, PA: Springhouse Corp., 1995.

    Organizations

  • American Kidney Fund. 6110 Executive Boulevard, Rockville, MD 20852. (800) 638-8299.
  • National Kidney Foundation. 30 East 33rd Street, New York, NY 10016. (800) 622-9010.

Gale Encyclopedia of Medicine. Gale Research, 1999.

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