ACUTE GLOMERULONEPHRITIS

DEFINITION OF TERMS:
Glomerulonephritis an inflammation of the glomerulus that can be caused by variety of factors, including immunologic abnormalities, effects of drugs or toxins, vascular disorders, and systemic diseases.

Acute Glomerulonephritis - is frequently associated with group A (nephritogenic strain) poststreptococcal infection (acute poststreptococcal glomerulonephritis [ASPGN]). The disease has been abrupt onset and usually occurs 7 to 10 days after streptococcal infection of the throat or skin, commonly in children. Chronic Glomerulonephritis - may be due to repeated episodes of acute glomerulonephritis, hypertensive nephrosclerosis, hyperlipidemia, chronic tubulointerstitial injury, or hemodynamically mediated glomerular sclerosis.

Hematuria- is the presence of red blood cells (erythrocyte) in the urine

Proteinuria- the presence of an excess of serum proteins in the urine Oliguria- is the low output of urine, it is clinically classified as the an output below 300- 500 mL/day

Types and Causes of Acute Glomerulonephritis

TYPES AND CAUSES

Poststreptococcal Group A Beta-hemolytic streptococcus Rapidly Progressive or crescentic- nonspecific response to glumerular injury; can occur in any severe glomerular disease

Membranoproliferative- usually idiopathic ; associated with hypocomplementemia Type I: activation of classical complement pathway with nephrotic syndrome Type II: activation of alternate complement pathway with hematuria IgA nephropathy (Berger Disease)- usually idiopathic; elevated IgA plasma level
Membranous nephropathy usually idiopathic; can be associated with systemic diseases, i.e., hepatitis B virus, systemic lupus erythematosus, solid malignant tumors

I. Etiology General Etiology - Post infectious GN can occur at any age but usually develops in children. Most cases occur in patients aged 5-15 years; only 10% occur in patients older than 40 years. Outbreaks of PSGN are common in children aged 6-10 years. Acute nephritis may occur at any age, including infancy. Genetic Considerations - Genetic factors influence renal disease progression, and several loci have been linked to the spontaneous development of proteinuria and glomerulosclerosis in animal models. However, the role of genetic susceptibility in glomerulonephritis-induced progressive glomerulosclerosis is unknown. Gender, Ethical/ Racial, and Life span considerations - Acute GN predominantly affects males (2:1 male-to-female ratio). Postinfectious GN has no predilection for any racial or ethnic group. A higher incidence (related to poor hygiene) may be observed in some socioeconomic groups.

Pathophysiology

DIAGNOSTIC STUDIES OR LABORATORY RESULTS

1. Urinalysis Urinalysis during the acute phase characteristically shows hematuria, proteinuria, and increased specific gravity. The specific gravity is moderately elevated and seldom exceeds 1.020. Gross discoloration of urine reflects its red blood cell and hemoglobin content. Microscopic examination of the sediment shows many red blood cells, leukocytes, epithelial cells, and granular and red blood casts. Bacteria are not seen and urine cultures are negative 2. Culture and Sensitivity Cultures of the pharynx are positive for streptococci in only a few cases, and the numbers are not significantly greater than the normal carrier incidence in many communities. Positive cultures help establish a diagnosis. Cultures should be obtained from other household members, and persons positive for group A streptococci should receive a course of antistreptococcal therapy. 3. Serologic Tests Serologic tests are necessary for diagnosis. Antibody responses to the extracellular products of the streptococci provide evidence of previous streptococcal infection. These include antistreptolysin O (ASO), antistreptokinase (ASKase), Antihyaluronidase (AHase). ASO titer is the most familiar and readily available set for streptococcal antibodies. One more important clinical serological diagnosis is measurement of the serum complement level (C3). Serum C3 level is decreased initially but returns to normal 8-10 weeks after onset of glomerulonephritis.

Medical Management
There is no direct medical treatment for acute glomerulonephritis. Usually, when treatment is necessary, it may include mostly of a pharmacological and nursing management like a special diet, monitoring blood pressure and fluid balance and taking of immunosuppressant drugs. Somehow, plasmapheresis is helpful. It is a procedure in which blood taken from a patient is treated to extract the cells and corpuscles, which are then added to another fluid and returned to the patients body. An example of its use is the removal of the harmful antibodies or immune complexes from the blood in autoimmune diseases as such in this case.

PHARMACOLOGIC THERAPY
Antibiotics Antibiotic therapy is indicated for children with evidence of persistent streptococcal infections. Antibiotics do not alter the course of disease but are often recommended to prevent transmission of nephritogenic streptococci to other family members. Authorities are divided in the use of prophylactic antimicrobials for other family members. ACE Inhibitors These drugs work by interfering with the enzymes that convert an inactive chemical known as angiotensin I to an active form, angiotensin II. Angiotensin II increases the retention of salt and water in the body, raising blood pressure. Inhibiting the formation of angiotensin II results in relaxed arterial walls and lowered blood pressure.

Antihypertensive and Cardiovascular Agents Hypertension is managed by intravascular volume control and a variety of antihypertensive agents. Heart failure and pulmonary edema may also require treatment with fluid restriction, low-sodium diets, diuretic agents, inotropic agents such as digoxin (Lanoxin) or dobutamine (Dobutrex), and dialysis. The metabolic acidosis of chronic renal failure usually produces no symptoms and requires no treatment; however, sodium bicarbonate supplements or dialysis may be needed to correct the acidosis if it causes symptoms. Diuretics

Chemical compound that increases the flow of urine and thus eliminates accumulations of water in cells, tissues, blood, and organs. The retention of excess water may occur following injury, as when water accumulates. With acute glomerulonephritis, the filtration rate of glomerulus declines hence, less urine is excreted which then leads to edema. Another cause of low filtration rate is hypertension from which there is an occurrence of increased intravascular pressure.

NURSING MANAGEMENT
General Measures Once the progression of the symptoms for acute glomerulonephritis (e.g. hematuria, edema, azotemia and hypertension) has been declined, bed rest is no longer recommended. Strenuous activities must be restricted especially during the active phase of the disease. Fluid Balance Body weight and fluid intake and output must to be highly measured and checked to monitor the progress of disease and detect its probable complications that may appear at any time during the course of the disease, considering the signs and symptoms of acute glomerulonephritis. Fluid restrictions are difficult for most clients. Offer suggestions about reducing thirst and moistening lips with lip balms, frequent oral hygiene, and taking ice chips and spray bottles rather than drinking. Sodium and water restriction is useful when output is significantly reduced (<2 to 3 dl/24hr). In children, the water allowed is equivalent to the calculated loss plus the volume of urine excreted. When renal failure is not severe, diuretics is helpful if significant edema and fluid overload is present. Management of electrolyte disturbances is also important in cases of children with severe APSGN.

Monitoring vital signs Acute hypertension must be anticipated and identified early. Monitoring vital signs plays an important role in the care of patients with acute glomerulonephritis. Blood pressure must be taken 2-6 hours. Loop diuretics can control significant but not severe hypertension. Pharmacological regimen may be needed in severe cases like antihypertensive drugs such as calcium channel blockers, beta blockers and ACE inhibitors. Nutritional Therapy Like in any conditions, dietary restrictions depend on the stage and the severity of the disease, especially on the extent of edema. Like in patients with a renal failure or other condition.

References:
Gutierrez, K. (1999). Pharmacotherapeutics: Clinical decision-making in Nursing. Philadelphia, Pennsylvania: W.B. Saunders Company. pp. 870-881. Habel, A. (2001). Encyclopedia of child health. London: Chancellor Press. p. 295. Ignatavicus, D. & Workman, M.L. (2002). Medical-Surgical Nursing: Critical thinking for collaborative care. vol 2. (4thed.). United Sates, US: W.B. Saunders Company. Wong, D., Ahmann, E., Wilson, D., et. al. (1999) Whaley & Wongs: Nursing care of infants and children. (5thed.). St. Louis, Missouri:

Mosby, pp. 1296-1301.

Wong, D., Ahmann, E., Wilson, D., et. al. (2001) Whaley & Wongs: Nursing care of infants and children. (6thed.). St. Louis, Missouri: Mosby, pp. 1380-1384. Shau, B. & Laude, T. (2000). Atlas of pediatric clinical diagnosis. United States, US: W.B. Saunders Company. pp.468-470. http://www.mayoclinic.com/health/glumerulonephritis/DS00682/DSECTION=complications http://www.mayoclinic.com/health/acuteglumerulonephriti/ds00280/dsection=complications Microsoft Encarta 2007. 1993-2006 Microsoft Corporation.