|Mean LOS:||4.5 days|
|Description:||MEDICAL: Other Kidney and Urinary Tract Diagnoses With CC|
Acute glomerulonephritis (AGN) is an inflammatory disease of the specialized tuft of capillaries within the kidney called the glomerulus. In its several forms, glomerulonephritis was the leading cause of chronic renal failure in the United States until the mid-1980s, but because of more aggressive treatment approaches, it is now third, after diabetes mellitus and hypertension. Glomerulonephritis continues to be a fairly common disorder worldwide, however. The inflammatory changes occur because of deposits of antigen-antibody complexes lodged within the glomerular membrane. Antigen-antibody complexes are formed within the circulation in response to an antigen or foreign protein. The antigen may be of external origin, such as a portion of the Streptococcus bacterial cell wall, or of internal origin, such as the changes that occur in systemic diseases like systemic lupus erythematosus (SLE).
Acute poststreptococcal glomerulonephritis (APSGN) results from an infection with nephritogenic strains of group A beta-hemolytic streptococci (GABHS). These infections occur in the skin (impetigo) or throat (pharyngitis). If the source of the causative antigen is temporary, such as a transient infection, the inflammatory changes subside and renal function usually returns to normal; if the source of antigen is long-term or permanent, the AGN may become chronic. During the acute phase of the disease process, major complications include hypertension, hypertensive encephalopathy, acute renal failure, cardiac failure, and seizures. Chronic glomerular nephritis leads to contracted, granular kidneys and end-stage renal disease. Rapidly progressive glomerulonephritis (RPGN; also known as crescentic nephritis), an acute and severe form of kidney inflammation, can cause loss of kidney function within days. Inflammation at the sites of renal filtration (the glomerular basement membrane) causes leakage of blood proteins into the urinary space. The condition is caused by inflammation of cells in the urinary space that form crescents, hence the name crescentic nephritis.
Etiological factors are unclear, but most experts identify an immunological origin for the disease. AGN may occur as an isolated (primary) disorder, as a disorder associated with an infectious disease, or as a secondary disorder. Primary AGN occurs in mesangiocapillary glomerulonephritis and in IgA nephropathy. Infection-associated AGN follows an infection such as a GABHS infection. Nonstreptococcal postinfectious glomerulonephritis may occur after an attack of infective endocarditis, sepsis, pneumococcal pneumonia, viral hepatitis, mumps, or measles. RPGN is associated with vasculitis, SLE, Goodpasture’s syndrome, and IgA nephropathy.
Single-gene disorders with glomerulonephritis as a feature include Fechtner’s syndrome and Barraquer-Simon syndrome. There is also a familial form of IgA nephropathy. Alport’s syndrome is a hereditary nephritis that includes X-linked Alport’s syndrome (80%), autosomal recessive Alport’s syndrome (15%), and autosomal dominant Alport’s syndrome (5%). Mutations in collagen genes (COL4, COL4A4, COL4A5) are associated.
Gender, ethnic/racial, and life span considerations
AGN occurs primarily in the pediatric population, ages 2 to 15, after an infectious event; GABHS is most common in boys ages 3 to 7. About 95% of children and 70% of adults have a full recovery from APSGN. In both men and women, AGN may occur after an infection or with multisystem diseases such as SLE. Because adults may exhibit more signs of cardiovascular compromise than children, treatment of the adult may require more support of the cardiovascular system through medications. RPGN primarily affects adults in their sixth and seventh decades of life. As a whole, twice as many males as females are affected with GN.
Global health considerations
While APSGN has decreased in Western countries, it is common in developing regions of Africa, the Caribbean, and South America and in countries such as India, Pakistan, and Malaysia.
Question the patient or parents about an untreated respiratory tract infection that has occurred in the last 1 to 3 weeks. Ask the patient about the medical history to identify any multisystem diseases. Because patients often describe a history of weight gain and edema of the hands and face, ask the patient if his or her rings are tighter than usual. Some patients may also describe decreased urine volume, changes in urine color (dark, smoky), increased fatigue and activity intolerance, muscle and joint achiness, shortness of breath, and orthopnea. Elderly patients’ symptoms may be more vague and nonspecific, such as achiness and nausea.
The most common symptoms are hematuria, oliguria, and peripheral or periorbital edema. Note any signs of fluid retention, such as edema in the face and hands. As you speak to the patient, you may notice dyspnea and labored breathing. Inspect the neck veins to determine if engorgement is present. The patient’s urine output is usually decreased and is often dark or even coffee colored. When you auscultate the patient’s heart and lungs, you may hear basilar crackles and an S3 heart sound. Most patients have an elevated arterial pressure. Weigh the patient each day, and monitor abdominal girth. Provide ongoing monitoring for visual changes, vomiting, adventitious breath sounds, abdominal distention, and seizure activity. These signs and symptoms indicate the potential onset of the complications and need to be reported to the physician.
Patients and families may be anxious about changes in the patient’s appearance, an uncertain prognosis, and the possibility of lifestyle changes. Older children and adults may be concerned about their appearance. Assess the patient’s and family’s coping mechanisms, support systems, and stress levels.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Creatinine clearance||100–140 mL/min||50 mL/min||Damaged glomerulus no longer able to clear or filter normal amounts of creatinine from blood|
|Serum creatinine||0.5–12 mg/dL||< 2 mg/dL||Decreased ability of glomerulus to filter creatinine leads to accumulation in the blood|
|Urinalysis||Minimal red blood cells; moderate clear protein casts; negative for protein||Red blood cells and red blood cell casts; elevated protein and urine specific gravity||May also have renal tubular cells, white blood cells, increased white blood cell casts|
Other Tests: Supporting tests include cultures of the throat and skin lesions if streptococcus infection is suspected, serum electrolytes, serum potassium, serum blood urea nitrogen, complete blood count, erythrocyte sedimentation rate, C-reactive protein, complement levels, cryoglobulins, serum mucoprotein levels, antistreptolysin O titers, Streptozyme test, and percutaneous renal biopsy.
Primary nursing diagnosis
DiagnosisFluid volume excess related to glomerular inflammation and decreased renal filtration
OutcomesFluid balance; Hydration; Nutrition management; Nutrition therapy; Knowledge: Treatment regime
InterventionsFluid/electrolyte management; Fluid monitoring; Medication administration
Planning and implementation
Most patients with AGN recover spontaneously. During the acute phase, when urine is grossly hematuric and blood pressure is elevated, the patient is placed on bedrest and symptoms are managed pharmacologically. A dietary consultation is necessary to implement dietary restrictions that can manage increased blood pressure, decreased urine output, and the presence of nitrogenous products in the urine. Usually, sodium and fluid restriction is instituted to manage hypertension and edema. Depending on the course of their disease, some patients also need potassium and protein restrictions. If the patient is on fluid restriction, work with the patient and family to devise a schedule of fluid intake that maximizes patient preference and comfort.
|Medication or Drug Class||Dosage||Description||Rationale|
|Antihypertensive and diuretics||Varies with drug||Antihypertensives; hydralazine; diuretics: furosemide||Manage hypertension and fluid overload|
|Antibiotics||Varies with drug for a 10–day course of therapy||Penicillin or erythromycin||Kills streptococcal infection if the disease is believed to be APSGN|
Other Drugs: Antibiotics may be administered for 7 to 10 days if the etiological factor was an infectious agent such as streptococcus. Corticosteroids are controversial and considered by many experts to be of no value. Labetalol may be used for hypertensive encephalopathy and malignant hypertension. Cyclophosphamide may be used for treatment of acute glomerulonephritis due to Wegener’s granulomatosis.
Focus on decreasing discomfort, reducing complications, and providing patient education. Work with the patient to develop a schedule for daily hygiene that limits fatigue and overexertion. Cluster care to provide for rest periods and assist the patient with relaxation techniques. Assist children with the usual bedtime rituals. Increase activity gradually as symptoms subside.
While the patient is on bedrest, perform active or passive range-of-motion exercises each shift and assist the patient to a new position every 2 hours. Monitor the patient’s skin for breakdown. If the patient is recovering from an infection, prevent secondary infection. Take time to answer the patient’s and parents’ questions fully. If you note that the family is coping ineffectively with the illness or prognosis, make a referral to a clinical nurse specialist.
Evidence-Based Practice and Health Policy
Nasr, S.H., Fidler, M.E., Valeri, A.M., Cornell, L.D., Sethi, S., Zoller, A., …D'Agati, V.D. (2011). Postinfectious glomerulonephritis in the elderly. Journal of the American Society of Nephrology, 22(1), 187–195.
- Although glomerulonephritis is primarily a childhood disease, significant population increases in persons ages 65 and older has led to an increased number of diagnoses among the elderly.
- A review of 72 cases of postinfectious glomerulonephritis (PIGN) in patients ages 65 and older revealed complete recovery in 22%, persistent renal dysfunction in 44%, and progression to end-stage renal disease in 33% over a mean follow-up period of 29 months, resulting in a mortality rate of 12.5% (p = 0.02).
- The majority of patients were infected through the skin (28%), followed by the lungs (16%), the urinary tract (13%), and the upper respiratory tract (10%). The most common infectious agent was staphylococcus (46%), followed by streptococcus (16%).
- Cardiovascular responses: Blood pressure, pulse, presence of abnormal heart sounds; presence, location, and severity of edema; daily weights
- Renal responses: Character, amount, odor of urine
- Respiratory responses: Respiratory rate and effort, breath sounds
- Presence of complications: Fever, food intolerance, pulmonary congestion, shortness of breath, increasing peripheral edema, weight gain, skin breakdown, anuria
- Comfort: Type of discomfort, location and intensity, character, response to attempts to provide relief
Discharge and home healthcare guidelines
Inform patients and families about the disease process, prognosis, and treatment plan. Discuss with them the possibility that abnormal urinary findings may persist for years after AGN has been diagnosed. Demonstrate all home care techniques, such as medication administration. Discuss the dosage, action, route, and side effects of all medications. If the patient is placed on antibiotics, encourage her or him to complete the entire prescription. Teach the patient and family to seek professional assistance for all infectious processes (particularly respiratory infections with sore throat and fever); monitor body weight and blood pressure at home or through a clinic; avoid contact with individuals with infectious processes. Discuss the need for ongoing laboratory monitoring of electrolytes and renal function tests during the months of convalescence, as recommended by the physician. Explain that after APSGN, any gross hematuria that occurs when the patient has a viral infection needs to be reported to the physician.