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    Acute Glomerulonephritis (AGN) : Group A Beta Hemolytic Stretococcus

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    Kristine Danielle Dejelo
    1. Acute glomerulonephritis (AGN) is caused by an immune complex reaction in the kidneys following a streptococcal infection, resulting in inflammation of the glomeruli. 2. Symptoms include hematuria, edema, high blood pressure, and decreased kidney function. 3. Treatment involves bed rest, a low-sodium diet, medications to control blood pressure and infection, and monitoring for complications like renal failure.

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    Acute Glomerulonephritis (AGN) : Group A Beta Hemolytic Stretococcus

    Uploaded by

    Kristine Danielle Dejelo
    209 views3 pages
    1. Acute glomerulonephritis (AGN) is caused by an immune complex reaction in the kidneys following a streptococcal infection, resulting in inflammation of the glomeruli. 2. Symptoms include hematuria, edema, high blood pressure, and decreased kidney function. 3. Treatment involves bed rest, a low-sodium diet, medications to control blood pressure and infection, and monitoring for complications like renal failure.

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    1. Acute glomerulonephritis (AGN) is caused by an immune complex reaction in the kidneys following a streptococcal infection, resulting in inflammation of the glomeruli. 2. Symptoms include hematuria, edema, high blood pressure, and decreased kidney function. 3. Treatment involves bed rest, a low-sodium diet, medications to control blood pressure and infection, and monitoring for complications like renal failure.

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    209 views3 pages

    Acute Glomerulonephritis (AGN) : Group A Beta Hemolytic Stretococcus

    Uploaded by

    Kristine Danielle Dejelo
    1. Acute glomerulonephritis (AGN) is caused by an immune complex reaction in the kidneys following a streptococcal infection, resulting in inflammation of the glomeruli. 2. Symptoms include hematuria, edema, high blood pressure, and decreased kidney function. 3. Treatment involves bed rest, a low-sodium diet, medications to control blood pressure and infection, and monitoring for complications like renal failure.

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    http://www.asianbearmen.com/search/label/Short%20Stories Acute Glomerulonephritis (AGN) -caused by defective immune mechanism.

    Hypersensitivity reaction of the kidneys to Group A Beta Hemolytic Stretococcus. - refers to inflammation of the kidneys caused by antigen- antibody reaction following an infection. Etiology -some parts of the body involves damage to both kidneys resulting from filtration and trapping of antibody- antigen complexes within the glumoruli. - As a result, inflammatory and generative changes affect all renal tissue. - Often follows some form of streptococcal infection such as tonsillitis, pharyngitis, otitis media, sinusitis, impetigo, inflammatory pustular skin disease caused by staphylococcus, chronic cellulitis of the skin, and granulation of tissue. - Seen in school-age children, peak at 6 to 7 years of age - More common in boys than girls Pathophysiology: AGN is believed from an antigen- antibody reaction that occurs after previous streptococcal infection. The latent period of about 7 days between the streptococcal infection and onset of glumerulonephritis. Following the infection, there is release of membrane like materials that serves as antigen to illicit antibody formation, an immune complex reaction, and injury. The complement and IgG have been demonstrated on the glumerular basement using immunofluorescent techniques. The abnormal immune reactions results in immune complexes being trapped in the glumerular membrane and iliciting inflammation The endothelial cells of the membrane proliferate and the capillary membrane swells and is permeable to plasma proteins and blood cells. Decreased glumerular filtration leads to greater tubular reabsorption of filtered sodium and consequently contributes to edema. General vascular disturbances including loss of capillary integrity and spasm are secondary to kidney changes these are responsible for much of the symptomatology of the disease. Complications: Hypertensive encephalopathy Acute cardiac failure Acute renal failure SIGNS AND SYMPTOMS -Due to release of the histamine by damaged cells

    1. Presenting symptoms; hematuria (urine is brown or cola-or-tea-colored and cloudy) and edema. 2. Scanty, smoky reddish or brownish urine 3. Pallor 4. Mild to hypertension- first felt as headache 5. Shortness of breath, malaise, fatigue, anorexia with occasional vomiting, lethargy 6. Fever 7. Tachycardia 8. Periorbital edema and generalized edema, weight gain, and electrolyte imbalance 9. Costovertebral tenderness Laboratory Data Increased antistreptolysin O ASO titer. (normal- 250U) the child was exposed to streptococci Urinalysis reveals RBC, leukocytes, epithelial cells, protein and casts in the urine (+3 or +4 urine protein) Serum chemistr level -increased BUN and creatinine levels Decreased HgB and hct transient anemia X-ray reveals cardiac enlargement and pulmonary congestion Management Complete bed rest- most important aspect of treatment Diet-low sodium (because of anemia), low protein (if with high BUN), limited K(because of oliguria) Increase fluid intake, MIO Medications such as; antihypertensive, magnesium sulphate, digitalis if failure, Penicillin- drug of choice exerts bacteriostatic effect by suppressing the formation of bacterial cell wall. Weigh daily Elevate head for periostal edema Renal biopsy- possible prone for 12hrs after biopsy to prevent hemorrhage. Nursing Diagnosis Excess fluid volume related to plasma protein deficit in sodium & water retention Rationale: When proteins are lost in the urine, the osmotic pressure of plasma falls, fluid shifts into the interstitial spaces. The body response to this fluid shift by any sodium & water to maintain intravascular volume, leading to excess fluid volume. Fatigue related to plasma protein loss & anorexia Rationale: Fatigue is a common manifestations of glomerular disorders. Anemia , loss of proteins, anorexia compound this fatigue. The ability to maintain usual physical & mental activities are impaired. Risk for infection related to compromised immune system secondary to medical treatment Rationale: The effects of both glomerular & treatment with anti-inflammatory & cytotoxic drugs can depress the immune system, increasing the risk for infection. The antiinflammatory effects of corticosteroid may also mask early manifestations of infections. Nursing management 1. Assess fluid status by monitoring intake and output, taking & recording daily weights, and observing for edema.

    2. Ensure early detection of complications by closely monitoring blood pressure and rspiratory rate. 3. Administer prescribed medications. a. An antihypertensive drugs, such as a calcium channel blocker, a beta-adrenergic blocker, or an angiotensin-converting enzyme inhibitor, may be needed in severe cases. b. An anticonvulsant for seizure activity associated with hypertensive encephalopathy. c. An antibiotic for persistent streptococcal infection. 4. Promote desired nutritional intake. a. Increase caloric intake to decreased protein breakdown, unless restricted. Imposed sodium, potassium, or fluid restrictions, when prescribed. b. Dietary restrictions depend on the stage and severity of disease. Normally, a regular diet is allowed, but sodium is limited (no added salt). Moderate sodium restriction is for children with hypertension or edema, and potassium-rich food are limited during period of oliguria. Protein is restricted only for those with severe azotemia. 5. Stimulate the child by providing quiet play activities. 6. Provide child and family teaching. a. Instruct about the need for medical evaluation & tissue culture of all sore throats. b. Discuss home care measures, including: - urine testing - blood pressure monitoring - activity and diet restrictions - infection prevention measures - signs and symptoms of potential complications to watch for and report ( the child will require monthly urinalysis & blood pressure monitoring for 6 months & then every 3 to 6 months until he has been symptomfree for 1 year) c. Explain all medications (i.e, dosage, administration, and adverse effects). d. Discuss the possible need for peritoneal dialysis or hemodialysis if renal failure occur. Prognosis Generally benign in young children. Not excellent in older children because it can progress on to chronic renal disease and eventually renal failure.

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