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ACUTE GLOMERULONEPHRITIS
• there are many forms of glomerulonephritis
• APSGN –Acute post streptococcal glomerulonephritis which follows streptococcal infection with certain groups A beta-hemolytic streptococcus . • these infection usually originate as upper respiratory infections, middle ear infections “STREP THROAT”. • certain strains of staphylococcus are occasionally responsible for initiating the immune disorder in the kidney • AGN develops 10 days to 2 weeks after the antecedent infection. • it affects primarily children between the ages of 3 and 7 years especially boys. • PATHOPHYSIOLOGY • the antistreptococcal antibodies, formed as usual from the earlier streptococcal infection • create an antigen-antibody complex that lodges in the glomerular capillaries • activates the complement system to cause an inflammatory response glomeruli of both kidneys • this leads to increased capillary permeability and cell proliferation • And results in leakage of some protein and large numbers of erythrocytes into the filtrate • immunoglobulin G and C3 are present in glomerular tissue and serum C3 is reduced • when the inflammatory response is severe, the congestion and cell proliferation interfere with filtration in the kidney causing decreased GFR and retention of fluid and wastes • ARF is possible if blood flow is sufficiently impaired • the decreased blood flow in the kidney is less likely to trigger renin secretion which leads to elevated BP and edema. • severe prolonged inflammation will cause scarring of the kidneys • SIGNS AND SYMPTOMS • the urine become dark and cloudy (“smoky or coffee colored urine”) because of the protein and red blood cells leaked into it • facial and periorbital edema occur initially, followed by generalized edema as the colloid osmotic pressure of the blood drops and sodium and water are retained • BP is elevated owing to increased renin secretion and decreased GFR • Flank or back pain develops as the kidney tissue swells and stretches the capsule • general signs of inflammation are present, including malaise, fatigue, headache, anorexia, and nausea • urine output decreases (oliguria) as GFR declines • LABORATORY ASSESSMENT • urinalysis shows hematuria and proteinuria – early morning urine is preferred because the urine is most acidic and formed elements are more intact • BUN levels are increased • urea and creatinine are elevated as GFR decreases • blood levels of streptococcal antibodies, ANTISTREPTOLYSIN O (ASO) and exoenzyme antistreptokinase ASK are elevated • metabolic acidosis with decreased serum bicarbonate and low serum pH is present • INTERVENTIONS • sodium restrictions • protein and fluid intake is decreased • glucocorticoid to reduce the inflammation • antihypertensive to reduce high BP • ANTIBIOTICS LIKE penicillin, erythromycin or azithromycin • for clients with fluid overload hypertension and edema, diuretics, sodium and water restrictions are prescribed • instruct patient and so the purpose and desired effects of prescribed medications • ensure that the client and family understand dietary or fluid modification including methods of detecting fluid retention • advise patient to weigh himself and measure BP daily at th same time each day. • CHRONIC GLOMERULONEPHRITIS • chronic nephrotic syndrome • develops 20 to 30 years or even longer • cause is not known because the kidneys are atrophied and tissue is not available for biopsy • SIGNS AND SYMPTOMS • mild proteinuria and hematuria • hypertension • occasional edema • Changes in the renal tissue because of hypertension • kidney tissue atrophies and the number of functional nephron is greatly reduced • biopsy in the late stages show glomerular changes,cell loss, protein and colagen deposits • eventually chronic glomerulonephritis leads to renal failure • assess for uremic symptoms such as slurred speech, ataxia, tremors • DIAGNOSTIC ASSESSMENT • urinalysis shows proteinuria • presence of RBC in the urine • serum creatinine is elevated • BUN is increased • kidneys are abnormally small on x-ray • INTERVENTION • focus on the slowing the progression of the disease and preventing complications. • treatment consist of diet changes, fluid intake sufficient to prevent reduced blood flow volume to the kidneys • drug therapy to control the problems from uremia