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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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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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Glomerulonephritis
From Gale Encyclopedia of Medicine, 4/6/01 by Kathleen Dredge Wright

Definition

Acute glomerulonephritis is an inflammatory disease of both kidneys predominantly affecting children from ages 2-12. Chronic glomerulonephritis can develop over a period of 10-20 years and is most often associated with other systemic disease, including diabetes, malaria, hepatitis, or systemic lupus erythematosus.

Description

Acute glomerulonephritis is an inflammation of the glomeruli, bundles of tiny vessels inside the kidneys. The damaged glomeruli cannot effectively filter waste products and excess water from the bloodstream to make urine. The kidneys appear enlarged, fatty, and congested.

Causes & symptoms

Acute glomerulonephritis most often follows a streptococcal infection of the throat or skin. In children, it is most often associated with an upper respiratory infection, tonsillitis, or scarlet fever. Kidney symptoms usually begin two to three weeks after the initial infection. Exposure to certain paints, glue or other organic solvents may also be the causative agent. It is thought that the kidney is damaged with exposure to the toxins that are excreted into the urine.

Mild glomerulonephritis may produce no symptoms, and diagnosis is made with laboratory studies of the urine and blood. Individuals with more severe cases of the disease may exhibit:

  • Fatigue
  • Nausea and vomiting
  • Shortness of breath
  • Disturbed vision
  • High blood pressure
  • Swelling, especially noted in the face, hands, feet, and ankles
  • Blood and protein in the urine, resulting in a smoky or slightly red appearance.

The individual with chronic glomerulonephritis may discover their condition with a routine physical exam revealing high blood pressure, or an eye exam showing vascular or hemorrhagic changes. The kidneys may be reduced to as little as one-fifth their normal size, consisting largely of fibrous tissues.

Diagnosis

Diagnosis of glomerulonephritis is established based on medical history, combined with laboratory studies. A "dipstick" test of urine will reveal increased protein levels. A 24 hour urine collection allows measurement of the excretion of proteins and creatinine. Creatinine clearance from the bloodstream by the kidneys is considered an index of the glomerular filtration rate. Blood studies may reveal a low blood count, and may also be checked for the presence of a streptococcal antibody titer(a sophisticated blood test indicating presence of streptococcal infection). A kidney biopsy may also be performed, using ultrasound to guide the needle for obtaining the specimen.

Treatment

The main objectives in the treatment of acute glomerulonephritis are to:

  • Decrease the damage to the glomeruli
  • Decrease the metabolic demands on the kidneys
  • Improve kidney function.

Bedrest helps in maintaining adequate blood flow to the kidney. If residual infection is suspected, antibiotic therapy may be needed. In the presence of fluid overload, diuretics may be used to increase output with urination. Iron and vitamin supplements may be ordered if anemia develops, and antihypertensives, if high blood pressure accompanies the illness. In order to rest the kidney during the acute phase, decreased sodium and protein intake may be recommended. The amount of protein allowed is dependent upon the amount lost in the urine, and the requirements of the individual patient. Sodium limitations depend on the amount of edema present. Fluid restrictions are adjusted according to the patient's urinary output and body weight.

An accurate daily record of the patient's weight, fluid intake and urinary output assist in estimating kidney function. The patient must be watched for signs of complications and recurrent infection. As edema is reduced and the urine becomes free of protein and red blood cells, the patient is allowed to increase activity. A woman who has had glomerulonephritis requires special medical attention during pregnancy.

Prognosis

In acute glomerulonephritis, symptoms usually subside in two weeks to several months, with 90% of children recovering without complications and adults recovering more slowly. Chronic glomerulonephritis is a disease that tends to progress slowly, so that there are no symptoms until the kidneys can no longer function. The resultant renal failure may require dialysis or kidney transplant.

Prevention

Prevention of glomerulonephritis is best accomplished by avoiding upper respiratory infections, as well as other acute and chronic infections, especially those of a streptococcal origin. Cultures of the infection site, usually the throat, should be obtained and antibiotic sensibility of the offending organism determined. Prompt medical assessment for necessary antibiotic therapy should be sought when infection is suspected. The use of prophylactic immunizations is recommended as appropriate.

Key Terms

Dialysis
A process of filtering and removing waste products from the bloodstream. Two main types are hemodialysis and peritoneal dialysis. In hemodialysis, the blood flows out of the body into a machine that filters out the waste products and routes the cleansed blood back into the body. In peritoneal dialysis, the cleansing occurs inside the body. Dialysis fluid is injected into the peritoneal cavity and wastes are filtered through the peritoneum, the thin membrane that surrounds the abdominal organs.
Glomeruli
Groups of tiny blood vessels with very thin walls that function as filters in the kidney. Glomeruli become inflamed and are destroyed in the disease process of glomerulonephritis.
Renal
Relating to the kidneys, from the Latin word

Further Reading

For Your Information

    Books

  • Branch, William. Office Practice of Medicine. Philadelphia: W. B. Saunders, 1982.
  • Brunner, Lillian & Doris Suddarth. Textbook of Medical-Surgical Nursing. Philadelphia: J. B. Lippincott, 1975.

    Organizations

  • American Association of Kidney Patients. 100 S. Ashley Dr., #280, Tampa, FL 33602. (800)749-2257 or (813)223-7099.
  • American Kidney Fund. 6110 Executive Blvd. #1010, Rockville, MD 20852. (800)638-8299, or (301)881-3052.
  • National Kidney Foundation. 30 E. 33rd St., New York, NY 10016. (800)652-9010 or (212)889-2210.
  • National Kidney Foundation and Urologic Diseases Information Clearinghouse. 3 Information Way, Bethesda, MD 20892-3580. (301)654-4415.

    Other

  • Glomerulonephritis www.healthtouch.com (29March1998).
  • Glomerulonephritis www.thriveonline.com (29March1998)

Gale Encyclopedia of Medicine. Gale Research, 1999.

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