Chronic glomerulonephritis may be due to repeated episodes of acute glomerulonephritis, hypertensive nephrosclerosis, hyper-lipidemia, chronic tubulointerstitial injury, or hemodynamically mediated glomerular sclerosis. The kidneys are reduced to as lit-tle as one-fifth their normal size (consisting largely of fibrous tis-sue). The cortex shrinks to a layer 1 to 2 mm thick or less. Bands of scar tissue distort the remaining cortex, making the surface of the kidney rough and irregular. Numerous glomeruli and their tubules become scarred, and the branches of the renal artery are thickened. The result is severe glomerular damage that results in ESRD.
The symptoms of chronic glomerulonephritis vary. Some pa-tients with severe disease have no symptoms at all for many years. Their condition may be discovered when hypertension or ele-vated BUN and serum creatinine levels are detected. The diag-nosis may be suggested during a routine eye examination when vascular changes or retinal hemorrhages are found. The first in-dication of disease may be a sudden, severe nosebleed, a stroke, or a seizure. Many patients report that their feet are slightly swollen at night. Most patients also have general symptoms, such as loss of weight and strength, increasing irritability, and an in-creased need to urinate at night (nocturia). Headaches, dizziness, and digestive disturbances are common.
As chronic glomerulonephritis progresses, signs and symp-toms of renal insufficiency and chronic renal failure may develop. The patient appears poorly nourished, with a yellow-gray pig-mentation of the skin and periorbital and peripheral (dependent) edema. Blood pressure may be normal or severely elevated. Reti-nal findings include hemorrhage, exudate, narrowed tortuous ar-terioles, and papilledema. Mucous membranes are pale because of anemia. Cardiomegaly, a gallop rhythm, distended neck veins, and other signs and symptoms of heart failure may be present. Crackles can be heard in the lungs.
Peripheral neuropathy with diminished deep tendon reflexes and neurosensory changes occurs late in the disease. The patient becomes confused and demonstrates a limited attention span. An additional late finding includes evidence of pericarditis with a peri-cardial friction rub and pulsus paradoxus (difference in blood pres-sure during inspiration and expiration of greater than 10 mm Hg).
A number of laboratory abnormalities occur. Urinalysis reveals a fixed specific gravity of about 1.010, variable proteinuria, and uri-nary casts (protein plugs secreted by damaged kidney tubules). Asrenal failure progresses and the GFR falls below 50 mL/min, the following changes occur:
· Hyperkalemia due to decreased potassium excretion, acido-sis, catabolism, and excessive potassium intake from food and medications
· Metabolic acidosis from decreased acid secretion by the kid-ney and inability to regenerate bicarbonate
· Anemia secondary to decreased erythropoiesis (production of RBCs)
· Hypoalbuminemia with edema secondary to protein loss through the damaged glomerular membrane
· Increased serum phosphorus level due to decreased renal excretion of phosphorus
· Decreased serum calcium level (calcium binds to phospho-rus to compensate for elevated serum phosphorus levels)
· Hypermagnesemia from decreased excretion and inadver-tent ingestion of antacids containing magnesium
· Impaired nerve conduction due to electrolyte abnormalities and uremia
Chest x-rays may show cardiac enlargement and pulmonary edema. The electrocardiogram may be normal or may indicate left ventricular hypertrophy associated with hypertension and signs of electrolyte disturbances, such as tall, tented (or peaked) T waves associated with hyperkalemia. Serum markers, including vascular endothelial growth factor and thrombospondin-1, are being evaluated for their reliability in assessing renal disease (Kang et al., 2001).
Symptoms guide the course of treatment for the patient with chronic glomerulonephritis. If the patient has hypertension, the blood pressure is reduced with sodium and water restriction, anti-hypertensive agents, or both. Weight is monitored daily, and di-uretic medications are prescribed to treat fluid overload. Proteins of high biologic value (dairy products, eggs, meats) are provided to promote good nutritional status. Adequate calories are also im-portant to spare protein for tissue growth and repair. UTIs must be treated promptly to prevent further renal damage.
Initiation of dialysis is considered early in the course of the dis-ease to keep the patient in optimal physical condition, prevent fluid and electrolyte imbalances, and minimize the risk of compli-cations of renal failure. The course of dialysis is smoother if treat-ment begins before the patient develops significant complications.
If the patient is hospitalized or seen by the nurse in the home, the nurse observes the patient for changes in fluid and electrolyte status and for signs and symptoms of deterioration of renal function. Changes in fluid and electrolyte status and in cardiac and neurologic status are reported promptly to the physician. Anxiety levels are often extremely high for both the patient and family. Throughout the course of the disease and treatment, the nurse gives emotional support by providing opportunities for the patient and family to verbalize their concerns, have their ques-tions answered, and explore their options.
The nurse has a major role inteaching the patient and family about the prescribed treatment plan and the risks associated with noncompliance. Instructions to the patient include explanations and scheduling for follow-up evaluations: blood pressure, urinalysis for protein and casts, and blood studies of BUN and creatinine levels. If long-term dialysis is needed, the patient and family are taught about the procedure, how to care for the access site, dietary restrictions, and other nec-essary lifestyle modifications.
Periodic hospitalization, visits to the outpatient clinic or of-fice, and home care referrals provide the nurse in each setting with the opportunity for careful assessment of the patient’s progress and continued education about changes to report to the primary health care provider (worsening signs and symptoms of renal failure, such as nausea, vomiting, and diminished urine output). Specific teaching may include explanations about recommended diet and fluid modifications and medications (purpose, desired effects, adverse effects, dosage, and administration schedule).
Periodic evaluation of creatinine clearance andserum BUN and creatinine levels is carried out to assess residual renal function and the need for dialysis or transplantation. If dial-ysis is initiated, the patient and family will require considerable assistance and support in dealing with therapy and its long-term implications. The patient and family are reminded of the importance of participation in health promotion activities, including health screening. The patient is instructed to inform all health care providers about the diagnosis of glomerulonephritis so that all medical management, including pharmacologic therapy, is based on altered renal function.
Copyright © 2018-2020 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.