Submitted by: Adiong, Joanne Ignacio, Dianne Grace Julian, Marivic

Submitted to: Mr. Arthur Barbasa, RN Clinical Instructor

ACUTE GLOMERULONEPHRITIS
Overview Acute glomerulonephritis (AGN) is active inflammation in the glomeruli. Each kidney is composed of about 1 million microscopic filtering "screens" known as glomeruli that selectively remove uremic waste products. Acute glomerulonephritis results when the capillaries in the kidney (glomeruli) that control filtering and excretion become inflamed and unable to function properly. With the selective filtering mechanism damaged, blood and protein are lost in the urine, and excess body fluids accumulate. Most often, the inflammation that triggers the disease stems from an immune response to a specific bacterium called Streptococcus. Other bacteria, viruses, fungi, and parasites may also trigger such a response, but it is less usual. Acute glomerulonephritis may also stem from systemic causes that affect the body as a whole and for a variety of reasons also result in compromised glomerular function. Some of these conditions are hypersensitivity vasculitis, Wegener granulomatosis, systemic lupus erythematosus, polyarteritis nodosa, cryoglobinemia, and Goodpasture syndrome. When there is active inflammation within the kidney, scar tissue may replace normal, functional kidney tissue and cause irreversible renal impairment. There are two forms of acute glomerulonephritis: postinfectious glomerulonephritis and infectious glomerulonephritis. Postinfectious glomerulonephritis typically occurs about 21 days after a respiratory or skin infection with Streptococcus. Infectious glomerulonephritis occurs during or within a few days of streptococcal infection. The disease may result in high blood pressure (hypertension), fluid accumulation (edema), and kidney failure. Of the two types, postinfectious glomerulonephritis (also called acute poststreptococcal glomerulonephritis) is the most common. The most common risk factor for development of postinfectious glomerulonephritis is an untreated streptococcal infection of the respiratory tract and, less commonly, of the skin (impetigo). Anatomy and Physiology The glomerulus is a tiny structure shaped like a ball; in the kidney. It is composed of capillary blood vessels and is actively involved in the filtration of the blood to form urine. The glomerulus is one of the structures that make up the nephron - a key functional unit of the kidney. The Latin word glumus means "a ball of yarn". Glomerulus in Latin means "a small ball of yarn". The glomerulus is literally a ball containing a yarn of blood vessels. Put simply - the glomeruli are tiny filters in our kidneys that take waste out of our blood. The waste is urine. Each kidney has about 1 million glomeruli, which attach to the opening of a small fluidcollecting tube (tubule). A nephron consists of one glomerulus and one tubule. Impure blood enters the nephron, waste (urine) is filtered out, and filtered blood returns to the bloodstream. The tubules modify what the glomerulus filters by saving substances that are needed, such as

protein. The waste (urine) goes from the kidney to the bladder through a tube called the ureter. The urine is then passed out of the body when we go to the toilet (urinate). When the glomeruli are inflamed the patient has 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. 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 bodys 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 red blood cells (causing hematuria which is the primary sign of acute glomerulonephritis) 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. Another large molecule are the proteins, that causes proteinuria. When proteinuria occurs, there is a decrese in the osmotic pressure that leads to generalized edema or anasarca. This decreases the circulating blood volume, which decreases the blood flow and affects the Renin-AngiotensinAldosterone-System, where the Renin promotes vasoconstriction that leads to hypertension.

Etiology In many cases the doctor never finds out what the cause of the glomerulonephritis was. Below is a list of known possible causes or risk factors: y Post-streptococcal glomerulonephritis - strep infections of the throat and impetigo (a skin infection) may cause glomerulonephritis. Impetigo is a much less common cause than throat infection. As treatment for most streptococcal infections improve, this cause is becoming much less common. y TB (tuberculosis) - glomerulonephritis can develop as a complication of tuberculosis. y Syphilis - glomerulonephritis can develop as a complication of syphilis. y Injecting illegal drugs - people who inject illegal drugs are at a much higher risk of developing glomerulonephritis. y Bacterial endocarditis - this is an infection in at least one of the heart valves. Patients with a heart defect have a higher risk of developing bacterial endocarditis and eventually glomerulonephritis. y Some viral infections - people infected with the HIV, hepatitis B and C viruses are more likely to develop glomerulonephritis compared to others.

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Lupus - this is a chronic inflammatory condition caused by an autoimmune disease (the body's immune system attacks itself, its own tissues). People with lupus are more likely to develop compared to people without it. Goodpasture's syndrome - this is also an autoimmune disease which causes lung and kidney disease. The patient may bleed in the lungs and develop glomerulonephritis. IgA nephropathy - immunoglobulin A (IgA) deposits appear in the glomeruli, eventually causing glomerulonephritis. Polyarteritis - this is an autoimmune disease in which the arteries become inflamed (arteritis). As the arteries are involved it can affect any organ in the body, including the kidneys. Wegener's granulomatosis - a rare kind of inflammation of the small arteries and veins (vasculitis) that typically involves the vessels that supply lung, sinus and kidney tissue.

The following conditions may cause scarring of the glomeruli: y Hypertension (high blood pressure) - hypertension can damage the kidneys and subsequently their normal functioning. Glomerulonephritis itself can cause hypertension because kidney function is undermined - the kidneys play a vital role in regulating our blood pressure. y Diabetic nephropathy (diabetic kidney disease) - any patient with diabetes has the potential to develop diabetic nephropathy. Kidney damage may be prevented, or at least significantly slowed down with good diabetes control. y Focal segmental glomerulosclerosis - segmental collapse of glomerular capillaries (small vessels). There may be scattered scarring of some of the glomeruli. y Acute glomerulonephritis - an attack of acute glomerulonephritis may develop into chronic (long-term) glomerulonephritis. If the patient has no history of kidney disease, the first indication of chronic glomerulonephritis will be chronic kidney failure. y Genetic factors - there is a certain type of glomerulonephritis that runs in families. However, most people with glomerulonephritis do not have a family member who has/had the condition. y Long-term medications - some medications, if taken over the long-term, may increase a patient's likelihood of developing glomerulonephritis. Examples include: o NSAIDs (non-steroidal anti-inflammatory drugs), such as ibuprofen and aspirin. o Gold injections, for the treatment of rheumatoid arthritis. o Lithium, for the treatment of depression. o Penicillamine, for the treatment of arthritis. y Hodgkin's disease - this is a type of cancer which can result in glomeruli being damaged. y Sickle cell disease - a genetic blood disease in which there is an abnormal form of hemoglobin. Epidemiology Risk: Males are twice as likely to have the condition as females, and although glomerulonephritis can appear at any age, 90% of cases occur in those under 40 years. The disease most often develops in boys between 2 and 14 years (Kazzi).

Incidence and Prevalence: There has been a significant decline in the incidence of acute glomerulonephritis in developed countries such as the US, and cases are reported only sporadically. The declining incidence rates are probably related to improved nutritional status in these countries and more liberal use of antibiotics. Developing countries, such as those in Africa and the Caribbean, appear to have a higher potential for development of streptococcal infections, and the incidence of acute glomerulonephritis is proportionally higher in these areas. Clinical Manifestations The primary presenting features of acute glomerulonephritis are hematuria, edema, azotemia (concentration of urea and other nitrogenous wastes in the blood), and proteinuria. If the glomeruli are damaged there will be a small amount of blood and/or protein in the urine, which may be visible or will show up in a urine test. The hematuria may be microscopic (identifiable only thought microscopic examination) or macroscopic (visible to the eye). The urine may appear cola-colored because of red blood cells and protein plugs or casts; RBC casts indicate glomerular injury. Some degree of edema and hypertension is present in most patients. Marked proteinuria due to increased permeability of the glomerular membrane may also occur, with associated pitting edema, hypoalbuminemia, hyperlipidemia, and fatty casts in the urine. Blood urea nitrogen and serum creatinine levels may increase as urine output decreases. In addition, anemia may be present. In the more severe form of the disease, patients may also complain of headache, malaise, and flank pain. Elderly patients may experience circulatory overload with dyspnea, engorged neck veins, cardiomegaly, and pulmonary edema. Atypical symptoms also include confusion, somnolence, and seizures. In acute glomerulonephritis, the kidneys become large, edematous, and congested. All renal tissues including the glomeruli, tubules and blood vessels are affected to varying degrees. Kidney biopsy may be needed for definitive diagnosis. If the patient improves, the amount of urine increases and the urinary protein and sediment diminish. Some patients develop severe uremia (an excess of urea and other nitrogenous wastes in the blood) within weeks and require dialysis for survival. A healthy adult urinates between 1 to 1.5 liters per day. People with severe glomerulonephritis may spend two or three days without being able to urinate; and when they do, there may be blood and/or protein in the urine. Patients with glomerulonephritis caused by kidney damage may have the following signs or symptoms: o An elevated body temperature (typically about 38C, 100.4F) o Breathing difficulties (dyspnea), orthopnea o Generalized edema (swelling), especially in the hands, face, feet, ankles or abdomen

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Loss of appetite Nausea and vomiting Oliguria Pallor Vision problems Circulatory congestion Hypertension (high blood pressure) Fatigue and anorexia with possible headache Anemia from loss of RBCs into the urine

Diagnosis History: Individuals may report a recent bacterial (streptococcal) or viral illness. In some cases, symptoms are mild, and individuals may report only vague weakness, loss of appetite (anorexia), and lethargy. In more severe cases, they may complain of cola- or tea-colored urine, fever, chills, weakness, headache, blurred vision (reduced visual acuity), abdominal or flank pain, reduced or no urine output (oliguria or anuria, respectively) for several days, nausea, and vomiting. Physical exam: Examination usually reveals generalized swelling (edema) particularly around the face and eyes (periorbital), fluid in the abdomen (ascites), fluid in the lungs (pulmonary edema) and chest cavity (pleural effusion), elevated blood pressure (hypertension), bloody urine, and skin rashes. Tests: Visual examination of the urine usually provides enough information necessary for a definitive diagnosis of acute glomerulonephritis. The urine, which may be scanty in amount, will typically be dark, smoky, or cola-colored or red or brown in hue. There is usually persistent and excessive foam in the specimen, indicating a high level of protein in the urine. A laboratory test of the urine (urinalysis) may show protein and blood, high acid levels (low pH), and mid- to high-normal range values for specific gravity. Other laboratory tests may include an analysis of how well the kidneys are working (renal function test) and specific blood tests for serum urea nitrogen, creatinine, hyaluronidase, deoxyribonuclease B, and serum complement. The percentage of red blood cells (hematocrit) and the amount of hemoglobin in the blood can be measured using a complete blood count (CBC). A streptozyme test and cultures of the throat and skin may show evidence of the streptococcus bacterium. Kidney biopsy - patients with chronic glomerulonephritis may need to have a small sample of kidney tissue removed for testing to find out how serious the condition is. The doctor extracts tissue samples using a small needle. The patient will normally receive a local anesthetic. A kidney biopsy has a small risk of bleeding. If the doctor finds evidence of damage, diagnostic studies may be ordered so that the kidneys can be visualized. This may include a kidney X-ray, an ultrasound scan, or a CT (computerized tomography) scan. Treatment The goal of treatment is to stop the ongoing inflammation and lessen the degree of scarring that develops. Treatment for acute glomerulonephritis depends on the underlying cause of the disease.

Medical Management In most cases, it is designed to relieve symptoms and reduce the potential for complications. Antibiotic therapy is used to treat the infection that resulted in acute glomerulonephritis (e.g., a penicillin derivative is given for streptococcal bacteria for 10 days). Fluid retention (edema) and high blood pressure (hypertension) are treated with drugs that promote fluid loss (diuretics) and lower blood pressure (angiotensin converting enzyme [ACE] inhibitors). Other drug treatments may include anti-inflammatory drugs (corticosteroids), drugs that decrease the response of the immune system (immunosuppressive), and drugs that prevent clotting (anticoagulants or antiplatelet agents). Usually, potassium and sodium intake is restricted in presence of hyperkalemia, edema or signs of heart failure. Dietary protein is restricted moderately if there is oliguria and the BUN is elevated. A procedure called plasmapheresis may be used for some cases of glomerulonephritis due to immune-related causes. The fluid part of the blood containing antibodies is removed and replaced with intravenous fluids or donated plasma (without antibodies). Removing antibodies may reduce inflammation in the kidney tissues. Persons with this condition should be closely watched for signs that they are developing kidney failure. Dialysis or a kidney transplant may eventually be necessary. Temporary dialysis can help control hypertension and remove surplus fluid. If kidney transplant is not possible, usually because the patient's poor health would not withstand the procedure, dialysis becomes the only available therapy. Kidney dialysis is when a machine is utilized to do the kidney's job of filtering out waste products from the body. Treatment for acute glomerulonephritis may include:
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AGN Diet o High calorie diet o Low protein o Low sodium diet o Low potassium diet o Low phosphorus diet o Calcium supplements o Vitamin B supplements Fluid restriction o Limiting the amount of fluid in the diet Oral corticosteroid medications o Prednisone o Methylprednisolone (Medrol) Diuretic medications o Furosemide (Lasix) Medications that suppress the immune system o Cyclophosphamide (Cytoxan, Neosar, Procytox) Kidney dialysis o For those who develop kidney failure

Nursing management In the hospital setting, carbohydrates are given liberally to provide energy and reduce the catabolism of protein. The nurse must consult the dietitian about a diet high in calories and low in protein, sodium, potassium, and fluids. Instruct patient to schedule follow-up evaluations of blood pressure, urinalysis for protein, electrolyte levels, and BUN and creatinine studies to determine if disease has worsened. Intake and output and daily weight are carefully measured and recorded. Fluids are given according to the patients fluid losses and daily body weight. In addition, explain to the patient taking diuretics that he may experience orthostatic hypotension and dizziness when he changes position quickly. Patient is encourage rest to facilitate diuresis and until renal function test levels normalize. The nurse must assist the client and perform passive range of motion exerecises. Diuresis begins about 1 week after the onset of symptoms with a decrease in edema and blood pressure. Proteinuria and microscopic hematuria may persist for many months and some patients may develop chronic glomerulonephritis. Other nursing interventions focus on patient education about the disease process explanations of laboratory and other diagnostic tests and preparation for safe and effective self care at home. If the patient is cheduled for dialysis, explain the procedure fully. Monitoring the signs and symptoms of heart failure and hypertensive encephalopathy are also included. The nurse must also protect the debilitated patient against secondary infection by providing good nutrition and hygienic technique and preventing contact with infected people.

Complications Complications of acute glomerulonephritis include hypertensive encephalopathy, nephrotic syndrome, chronic kidney failure, end stage kidney disease, hyperkalemia, congestive heart failure, pulmonary edema, and chronic or recurrent urinary tract infection. Hypertensive encephalopathy is a medical emergency, and therapy is directed toward reducing the blood pressure without impairing renal function. This can occur in acute glomerulonephritis or preeclampsia with chronic hypertension of greater than 140/90 mmHg. Rapidly progressive glomerulonephritis is characterized by a rapid decline in renal function. The kidneys can become so damaged that they fail completely if the condition is left untreated. Crescent shape cells accumulate in bowmans space, disrupting the filtering surface. Loss of function of the filtering part of the nephron may result in accumulation of waste products (uremia) - if this happens rapidly the patient can develop acute kidney failure and will need emergency dialysis. Plasma exchange and treatment with high dose corticosteroids and cytotoxic agents have been used to reduce the inflammatory response. If the kidneys gradually lose function and continue to do so the patient will develop chronic kidney failure and/or the end stage renal disease in a matter of weeks or months and will require regular dialysis or a kidney transplant to stay alive.

Prognosis Glomerulonephritis may be a temporary and reversible condition, or it may get worse. Progressive glomerulonephritis may lead to chronic kidney failure and end-stage kidney disease. The prognosis for patients with AGN is favorable and approximately 60% recover completely. Individuals who lose kidney function will have to be treated on an ongoing basis with dialysis, and if there is no meaningful recovery of kidney function, they may be a candidate for a kidney transplant. Generally, adults have a poorer prognosis for acute glomerulonephritis than do young individuals. Drug treatments are usually effective, and very few individuals die as a result of fluid in the lungs (pulmonary edema), brain inflammation (hypertensive encephalopathy), or uncontrolled infection.

References: http://www.healthcommunities.com/acute-glomerulonephritis-agn/index.shtml http://www.nursing-lectures.com/2011/03/acute-glomerulonephritis-and-nursing.html Smeltzer and Bare: Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 11th edition. Philadelphia: Lippincott Williams & Wilkins, 2008.