27 Chronic kidney disease
Overview/pathophysiology
Chronic kidney disease (CKD) is a progressive, irreversible loss of kidney function that develops over days to years. Aggressive management of hypertension and diabetes mellitus (DM) and avoidance of nephrotoxic agents may slow progression of CKD; however, loss of glomerular filtration is irreversible, and eventually CKD can progress to end-stage renal disease (ESRD), at which time renal replacement therapy (dialysis or transplantation) is required to sustain life. Before ESRD, the individual with CKD can lead a relatively normal life managed by diet and medications. The length of this period varies, depending on the cause of renal disease and patient’s level of renal function at the time of diagnosis.
Of the many causes of CKD, some of the most common are DM, hypertension, glomerulonephritis (GN), long-term exposure to certain classes of medications (e.g., nonsteroidal antiinflammatories) or metals (e.g., gold therapy, lead), and polycystic kidney disease. Regardless of the cause, clinical presentation of CKD, particularly as the individual approaches ESRD, is similar. Retention of metabolic end products and accompanying fluid and electrolyte imbalances adversely affect all body systems. Alterations in neuromuscular, cardiovascular, and gastrointestinal (GI) function are common. Renal osteodystrophy and anemia are early and common complications, with alterations being seen when the glomerular filtration rate (GFR) decreases to 60 mL/min. The collective manifestations of CKD are termed uremia.
Health care setting
Primary care with possible hospitalization resulting from complications or during ESRD
Assessment
Potential acute complications
Pericarditis:
Heart pain, elevated temperature, presence of pericardial friction or rub on auscultation.
Cardiac tamponade:
Hypotension, distant heart sounds, pulsus paradoxus (exaggerated inspiratory drop in systolic blood pressure [SBP]).
Physical assessment:
Pallor, dry and discolored skin, edema (peripheral, periorbital, sacral); fluid overload, crackles and elevated blood pressure (BP) may be present.
Diagnostic tests
GFR:
May be calculated using a mathematical formula. The Modification of Diet in Renal Disease (MDRD) GFR calculator is:
Creatinine clearance:
Measures kidney’s ability to clear the blood of creatinine and approximates the GFR. Creatinine clearance decreases as renal function decreases. Dialysis is usually begun when the GFR is 12 mL/min if patient is symptomatic or the GFR is less than 6 mL/min. Creatinine clearance normally is decreased in older adults. Creatinine clearance may be measured through collection of a 24-hr urine sample or calculated using the Cockcroft-Gault equation:
Note: Failure to collect all urine specimens during the period of study will invalidate test results.
Blood urea nitrogen (BUN) and serum creatinine:
Both will be elevated. Note: Nonrenal problems, such as dehydration or gastrointestinal (GI) bleeding, also can cause the BUN to increase, but there will not be a corresponding increase in creatinine.
Serum chemistries, chest and hand x-ray examinations, and nerve conduction velocity test:
To assess for development and progression of uremia and its complications.
Kidney-ureter-bladder (KUB) x-ray examination:
Documents presence of two kidneys, changes in size or shape, and some forms of obstruction.
Intravenous pyelogram, renal ultrasound, renal biopsy, renal scan (using radionuclides), and computed tomography (CT) scan:
Additional tests for determining cause of renal insufficiency. Once patient has reached ESRD, these tests are not performed. Note: Acetylcysteine (Mucomyst) may be prescribed as a prophylactic therapy before, during, and/or after administration of intravenous (IV) contrast in order to reduce the risk of further insult to the kidneys or dye-mediated acute renal failure.
Nursing diagnosis:
Imbalanced nutrition: less than body requirements
related to nausea, vomiting, anorexia, and dietary restrictions
Desired Outcome: Within 2 days of admission, patient has stable weight and demonstrates normal intake of food within restrictions, as indicated.
| ASSESSMENT/INTERVENTIONS | RATIONALES |
|---|---|
| See also Imbalanced Nutrition: Less Than Body Requirements in “Acute Renal Failure,” p. 192. | |
| In addition: | |
| Administer multivitamins and folic acid, if prescribed. | Anorexia and nausea and vomiting may occur with increased anorexia. Vitamin supplementation assists with ensuring that patients maintain adequate nutrition. Note: Use of over-the-counter multivitamins is contraindicated in CKD patients because some vitamin levels (e.g., of vitamin A) may be toxic. Multivitamins for patients on dialysis are specially formulated (e.g., Nephro-Vite, Dialyvite). |
| Monitor for proteinuria, and refer to dietitian if excessive protein losses and/or low serum albumin is noted. | Proteinuria results in malnutrition. Patients with poor nutritional status at the start of dialysis have increased risk of mortality. |
Nursing diagnosis:
Impaired skin integrity
related to uremia, hyperphosphatemia (if severe), and edema
Desired Outcome: Patient’s skin remains intact and free of erythema and abrasions.
| ASSESSMENT/INTERVENTIONS | RATIONALES |
|---|---|
| Assess for presence/degree of pruritus. | Pruritus is common in patients with uremia and occurs when accumulating nitrogenous wastes begin to be excreted through the skin, causing frequent and intense itching with scratching. Pruritus also may result from prolonged hyperphosphatemia. |
| Encourage use of phosphate binders and reduction of dietary phosphorus if elevated phosphorus level is a problem. | Pruritus often decreases with a reduction in BUN and improved phosphorus control. Phosphate binders are medications that, when taken with food, bind dietary phosphorus and prevent GI absorption. Calcium carbonate, sevelamer hydrochloride, aluminum hydroxide, and calcium acetate are common phosphate binders. |
| Note: Administer phosphate binders while food is present in the stomach. | Prolonged elevation of serum phosphorus and/or calcium absorption from ingestion of phosphate binders on an empty stomach results in an increased calcium-phosphorus product (serum calcium × serum phosphorus). When this product exceeds a level of 55 (normal product is approximately 40), phosphorus binds with calcium, and the resulting calcium-phosphate complex is deposited in soft tissues of the body. Deposition of these complexes in the skin produces necrotic patches. In addition, elevation in calcium-phosphate product is associated with increased risk of death, aortic calcification, mitral valve calcification, and coronary artery calcification. |
| If necessary, administer prescribed antihistamines. | Antihistamines help control itching. |
| Keep patient’s fingernails short. | If patient is unable to control scratching, short fingernails will cause less damage. |
| Instruct patient to monitor scratches for evidence of infection and to seek early medical attention if signs and symptoms of infection appear. | Uremia retards wound healing; nonintact skin can lead to infection. |
| Encourage use of skin emollients and soaps with high fat content. Advise patient to bathe every other day and to apply skin lotion immediately upon exiting bath/shower. | Uremic skin is often dry and scaly because of reduction in oil gland activity. Patients should avoid harsh soaps, soaps or skin products containing alcohol, and excessive bathing. |
| Advise patient and significant others that easy bruising can occur. | Patients with uremia are at increased risk for bruising because of clotting abnormalities and capillary fragility. |
| Provide scheduled skin care and position changes for patients with edema. | These measures decrease risk of skin/tissue damage resulting from decreased perfusion and increased pressure. |
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