Glo Me Rulo Nephritis

Glomerulonephritis This renal condition can be classified into two: acute and chronic.

Acute Glomerulonephritis Acute glomerulonephritis refers to a group of kidney diseases in which there is an inflammatory reaction in the glomeruli. It is not an infection of the kidney, but rather the result of the immune mechanisms of the body. The glomerular injury is the result of antigen-antibody deposits within the glomeruli. In less than 60 days, patients regain normal renal function. Pathophysiology: The initial reaction is usually either an upper respiratory infection or skin infection due to group A beta-hemolytic streptococcus. This leads to the formation of an antigen-antibody reaction. It is followed by the release of a membrane-like material from the organism into the body’s circulation. Antibodies produced to fight the invading organism also react against the glomerular tissue, thus forming immune complexes. The immune complexes become trapped in the glomerular loop and cause an inflammatory reaction in the affected glomeruli. Changes in the glomerular capillaries reduce the amount of the glomerular filtrate, thereby allowing passage of blood cells and protein into the infiltrate, and reducing the amount of sodium and water that is passed into the tubules for reabsorption. This affects the vascular tone and permeability of the kidney, resulting to tissue injury. Clinical Manifestations:

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History of infection such as pharyngitis or impetigo Tea-colored urine and oliguria Puffiness of face and edematous extremities Fatigue and anorexia with possible headache

High blood pressure Anemia from loss of RBCs into the urine Diagnostic Evaluation: Urinalysis for hematuria, proteinuria, cellular elements and various casts. 24-hour urine collection to determine protein and creatinine clearance. Elevated BUN and serum creatinine levels, low albumin level, increased antistreptolysis titer and decreased

serum complement. Needle biopsy of the kidney reveals obstruction of the glomerular capillaries from proliferation of endothelial cells. Complications: Hypertension, heart failure, endocarditis Hyperkalemia, hyperphosphatemia, hypervolemia Malnutrition

Hypertensive enecephalopathy, seizures ESRD Medical Management: It depends on the symptoms and includes antihypertensives, diuretics, drugs to manage hyperkalemia, H2 blockers and phospate-binding agents. Antibiotic therapy is initiated to eliminate infection. Fluid intake is restricted. Dietary protein is restricted moderately if there is oliguria and the BUN is elevated.

Carbohydrates are increased liberally to provide energy and reduce catabolism of protein. Potassium and sodium intake is restricted in presence of hyperkalemia, edema or signs of heart failure. Nursing Management: Promote renal function.

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Strictly measure and monitor intake and output and maintain dietary restrictions. Encourage rest to facilitate diuresis and until renal function test levels normalize. Administer medications as ordered and evaluate effectiveness of treatment.

Clinical Manifestations:                   Feet are slightly swollen at night Loss of weight and strength Irritability Nocturia Headaches and dizziness Digestive disturbances Appears poorly nourished Yellow-gray pigmentation of the skin Periorbital and peripheral dependent edema Retinal hemorrhage Cardiomegaly Crackles in the lungs Peripheral neuropathy Medical Management: Symptomatic management. Proteins of high biologic value are given. medications are prescribed based on the exhibited symptoms. hypertensive nephrosclerosis. UTI must be treated promptly. . The result is severe glomerular damage that can progress to ESRD. Initiation of dialysis must be considered. as well as ensuring adequate caloric intake. making the surface of the kidney rough and irregular. Chronic Glomerulonephritis This can be due to repeated episodes of acute glomerulonephritis. hyperlipidemia. Improve fluid balance. Numerous glomeruli and their tubules become scarred and the branches of the renal artery are thickened.   Carefully monitor fluid balance and and replace fluids according to patient’s fluid losses. The kidneys are reduced to as little as one-fifth of their normal size. Weight is monitored daily. Monitor for signs and symptoms of heart failure and hypertensive encephalopathy. Bands of scar tissue distort the remaining cortex. chronic tubulointerstitial injury or hemodynamically mediated glomerular sclerosis. Get daily weight.

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