Acute Glomerulonephritis PDF

ACUTE GLOMERULONEPHRITIS Epidemiology Glomerulonephritis is an inflammation of the glomeruli of the kidney. It is the third-leading cause of renal failure in the United States. It is caused by autoimmune disorders, such as Goodpasture’s syndrome or lupus, vasculitis (blood vessel inflammation), or...

ACUTE GLOMERULONEPHRITIS Epidemiology Glomerulonephritis is an inflammation of the glomeruli of the kidney. It is the third-leading cause of renal failure in the United States. It is caused by autoimmune disorders, such as Goodpasture’s syndrome or lupus, vasculitis (blood vessel inflammation), or an infection such as Streptococcus. Glomerulonephritis is typically classified as acute or chronic based on the presentation of symptoms. Acute glomerulonephritis develops rapidly, typically as a result of a complication from an infection. It can be found in patients across the life span but is most often seen in children and young adults. Chronic glomerulonephritis can result from some of the same causes as acute or may be genetic. It develops more slowly with fewer symptoms and may result in irreversible damage. It may also result from unresolved acute glomerulonephritis. The prognosis of the disease is based on the causative agent and the extent of damage to the glomeruli and surrounding renal structures and functions. Risk factors associated with glomerulonephritis are infections such as recent strep infections, immune diseases such as lupus, vasculitis, hypertension, and diabetes. Pathophysiology Glomerulonephritis is an inflammation of the glomeruli within the Bowman’s capsule of the kidney triggered by an immunological mechanism. The glomerulus is a key structure in the nephron consisting of a network of capillaries and is where the first step of filtration and urine formation takes place. There are two types of antibody-induced immunological conditions affecting the glomerulus in glomerulonephritis. In type 1, the antibodies produced are specific for antigens within the glomeruli and glomerulus basement membrane (GBM). As a result of that interaction, immunoglobulins and complement are deposited along the basement membrane. In type 2, the antibodies react to antigens not specific to the glomerulus but still deposit immune complexes along the GBM. Both type 1 and type 2 result in the accumulation of antigens, antibodies, and complement in the glomeruli and GBM, which ultimately results in injury to the glomerular membrane and a decrease in effective filtration through the glomeruli. There is an overall decrease in the glomerular filtration rate (GFR) and an increase in permeability to larger-size proteins. Clinical Manifestations As a result of the increased permeability, protein and blood are seen in the urine as well as WBCs and casts. Patients present edematous, with decreased urine output and hypertension. Renal laboratory tests such as BUN and creatinine are elevated. See Table 62.1 for a brief discussion of differences between nephrotic syndrome and nephritic syndrome; two different presentations of glomerular disease. Interprofessional Management Medical Management Diagnosis Diagnostics of glomerulonephritis include a complete medical history and physical examination and laboratory tests. A urinalysis may reveal the presence of WBCs, RBCs, proteins, and casts. Other laboratory tests include the CBC and differential, which would demonstrate increased WBCs and serum chemistries indicating increased serum BUN and creatinine levels. Decreased albumin and complement levels would also be present. Decreased complement components indicate an immune-mediated response. The diagnosis of acute post-streptococcal glomerulonephritis is made based on a history of group A beta-hemolytic streptococci infection in the throat or a skin lesion. Erythrocyte casts in the urine also suggest acute post-streptococcal glomerulonephritis. Treatment Treatment is based on the cause of the disease and symptom management. Medications focus on antibiotic treatment, most specifically penicillin for post-streptococcal glomerulonephritis if the infection is actively present. Diuretics and other antihypertensives may need to be added to treat hypertension. The edema is treated with the restriction of sodium and fluids. If the BUN is elevated, reductions in dietary protein may be necessary to reduce the build-up of metabolic waste. Corticosteroids are not always recommended but may be indicated to modulate the inflammatory response triggered by an immunological mechanism. Plasmapheresis may also be considered to reduce the immune-triggered inflammation. Plasmapheresis is an extracorporeal separation of the blood components to filter out immune complexes created as a part of the immunological response. The filtered plasma is discarded while the red blood cells and a replacement colloid such as donor plasma are returned to the patient. Last, rest is the most important means of restoration and symptom relief. Complications Ninety-five percent of patients with glomerulonephritis recover if the condition is treated early in the course of the illness, but if untreated or if the patient is unresponsive to treatment, acute or chronic kidney disease may develop. A rapidly progressive form of glomerulonephritis can progress to renal failure within weeks to months. Nursing Management Assessment and Analysis The clinical manifestations of glomerulonephritis are present because of the damage to the GBM. They include the following: Hematuria Oliguria Periorbital edema Peripheral edema of lower extremities Generalized body edema Ascites Abdominal or flank pain Hypertension Nursing Diagnoses/Problem List Impaired urinary elimination related to effects of damage to the glomerular membrane Ineffective therapeutic regimen management related to lack of knowledge regarding the treatment regimen Nursing Interventions Assessments Vital signs Hypertension is a common finding because of fluid retention associated with glomerulonephritis. Hypertension is a risk factor for cardiovascular disease, stroke, and renal failure. Daily weights Weight gain is associated with sodium and water retention. Intake and output Measuring intake and output of fluids is essential in assessing the accumulation of fluids. Increases in fluid retention can develop because of the potential sodium retention associated with renal impairment. Fluid retention is a risk factor for elevated blood pressure and heart failure. Measuring abdominal girth or extremity size Measuring abdominal girth and extremity size is important in assessing fluid retention. Fluids tend to pool in dependent areas such as the abdomen or extremities. Skin condition Edema can increase the risk of skin breakdown. Monitor dietary intake. A patient with glomerulonephritis has the potential for malnourishment from the excessive loss of protein in the urine because of the damage of the glomeruli. Excess sodium intake can cause fluid retention, resulting in elevated blood pressure and heart failure. Protein intake may need to be limited if the BUN is elevated and there are no signs of malnutrition. Laboratory analysis Renal function tests BUN/creatinine should be monitored to track renal function. WBC count Elevations in WBC indicate infection. Urinalysis Protein and RBCs can be found in the urine because of damage in the GBM. Actions Administer antihypertensives as ordered. Diuretics are used to combat sodium and fluid retention. Other antihypertensives such as ACE inhibitors may be prescribed to control blood pressure adequately. Administer corticosteroids as ordered. Corticosteroid agents may be indicated to modulate the inflammatory response triggered by the immunological mechanism.  Maintain low- to moderate-protein diet. Care must be taken to limit protein intake if the BUN is elevated, but a low- to moderate-protein diet may be needed to treat protein loss through the urine. Dietary sodium and fluid restriction Sodium and fluid restriction is necessary to prevent fluid retention, which can cause elevated blood pressure and heart failure. Teaching Overview of the disease process It is important for the patient and family to understand the disease process and the signs and symptoms associated with glomerulonephritis. Prescribed medications It is essential for the patient and family to understand the medications and their side effects and to report the side effects to the healthcare provider. Medication adherence must be emphasized. Dietary restrictions It is important for the patient and family to understand the salt and water restrictions and the rationale for the restrictions. The amount of protein intake must be followed as prescribed in order to obtain the necessary amount in the event of protein loss. Avoid infections. The patient and family should be instructed on avoiding exposure to infectious diseases, especially if on corticosteroids. Evaluating Care Outcomes Evaluating care is based on improvements in kidney function and the symptoms associated with glomerulonephritis. Monitoring serum BUN, creatinine, and electrolytes is important in assessing the condition of the patient. Patient teaching can be evaluated by the patient’s verbalization of information regarding the condition. A well-managed patient has a blood pressure within normal limits, no edema, and renal function within normal limits.