Chapter 37
Nursing Care of Patients With Disorders of the Urinary System
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Etiology Acute Poststreptococcal Glomerulonephritis Glomerulonephritis is most commonly associated with a group A beta-hemolytic streptococcal infection 6 to 10 days after a streptococcal infection of the throat or skin. This is the most common cause in children and young adults. Antibodies form complexes with the streptococcal antigen and are deposited in the basement membrane of the glomer- ulus, inducing damage from inflammation. Edema, oliguria, and hypertension result. Goodpasture Syndrome Occasionally, glomerulonephritis is caused by an auto- immune response. In this case, for unknown reasons anti- bodies form against a person’s own glomerular basement membrane. Glomerulonephritis caused by an autoimmune response usually progresses rapidly and leads to CKD. Chronic Glomerulonephritis Chronic glomerulonephritis occurs over years because of glomerular inflammatory disease. There may be no history of renal disease before the diagnosis. Often, proteinuria and hematuria may have been noted before the diagnosis. Systemic lupus erythematosus and type 1 diabetes mellitus may precede chronic glomerular injury. It is often discov- ered during an examination for another concern. Ultrasound, CT scan, or renal biopsy is used to diagnose the cause. Symptoms Symptoms of glomerulonephritis include hematuria, pro- teinuria, electrolyte imbalances, renal insufficiency, edema, hypertension, and thrombotic events (Table 37.4). Edema may begin around the eyes (periorbital edema) and face and progress to the abdomen (ascites), lungs (pleural effusion), and extremities. Flank pain may be present. Complications Adults who develop glomerulonephritis may recover renal function or progress to chronic glomerulonephritis. Some patients develop rapidly progressive glomerulonephritis. This can quickly lead to acute renal injury. Chronic glomer- ulonephritis is a slow process characterized by hypertension, gradual loss of renal function, and eventual CKD. Diagnostic Tests Glomerulonephritis is diagnosed with urinalysis, which shows protein, casts, or RBCs. Urine is dark or cola-colored from old RBCs and may be foamy because of proteinuria. Serum blood urea nitrogen (BUN) and serum creatinine • WORD • BUILDING • nephrosclerosis: nephro—pertaining to the kidney + sclerosis—hardening glomerulonephritis: glomerulo—glomerulus + nephr—kidney + itis—inflammation
Edematous tissue must be protected from injury. Preventing protein malnutrition is challenging but important to maintain- ing normal body functions. Referral to a dietitian is essential. Infection control measures are implemented. Nephrosclerosis Hypertension damages kidneys by causing sclerotic changes in the small arteries and arterioles, such as arteriosclerosis with thickening and hardening of the renal blood vessels ( nephrosclerosis ). Arteriosclerotic changes in the blood vessels of the kidneys decrease blood supply to the kidney (ischemia of the kidney), which can eventually destroy the organ. The remaining nephrons try to compensate with vaso- dilation to increase blood flow to the glomeruli. This results in increased glomerular pressure and filtration, which thick- ens the blood vessels. High pressure in the kidneys causes the vessels to weaken and hemorrhage. Large areas of the kid- ney become damaged. Symptoms of nephrosclerosis include proteinuria, hyaline casts in the urine, and, as it progresses, symptoms of CKD. Treatment for nephrosclerosis is anti- hypertensive medication, a low-sodium diet, and eventually dialysis. The priority nursing diagnosis for the patient with nephrosclerosis is Ineffective Health Maintenance Behaviors with a goal of managing hypertension. Arteriosclerosis increases risk of myocardial infarctions and cerebrovascular accidents. CLINICAL JUDGMENT Mr. Stevens, who is 55 years old, is admitted to the intensive care unit with uncontrolled hypertension and nephrosclerosis. His blood pressure is controlled by IV medication. His laboratory tests show protein and hyaline casts in the urine. 1. What data do you collect for your shift evaluation of Mr. Stevens’s condition? 2. What renal function tests do you review? 3. What education do you reinforce for Mr. Stevens? Suggested answers are at the end of the chapter.
GLOMERULONEPHRITIS
Pathophysiology Glomerulonephritis is an inflammatory disease of the fil- tering unit of the kidney, the glomerulus. It can be caused by a variety of factors, including immunological abnormali- ties, infectious agents, systemic disease, toxins, and vascular disorders. Inflammation occurs because of the deposition of antigen–antibody complexes in the basement membrane of the glomerulus or from antibodies that specifically attack the basement membrane. The resulting immune reaction in the glomerulus causes further inflammation, which in turn causes the glomerulus to be more porous, allowing proteins, WBCs, and RBCs to leak into the urine. Nephrotic syndrome can occur.
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