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Acute Renal Failure 1. Description 1.

Acute renal failure (ARF) is the rapid loss of kidney function from renal \cell damage. Box 62.3 Potentially Nephrotoxic Substances Medications Antibiiotics - anti-infectives Amphotencin B Colistimethate Methicillin Polymyxin B Rifampicin Sulfonamides Tetracycline Hydrochloride Vancomycin Aminoglycoside Antibiotics Gentamycin Kanamycin Neomycin Netilmicin sulfate Tobramycin Antineoplasties Cisplatin Cyclophosphamide Methotrexate Naproxen Oxaprozin Rofecoxib Tolmetin Other Medications Acetaminophen Captopril Cyclosporine Fluorinate anesthetics Penicllamine Phenazopyridine hydrochloride Quinine Other substances Organic solvents Carbon tetrachloride Ethylene glycol Nonpharmacological Chemical Agents Radiographic contrast dye Pesticides Fungicides Myoglobin (from breakdown of skeletal muscle)

Nonsteroidal Anti-inflammatory Drugs (NSAIDs) Celecoxib Heavy Metals and Ions Flurbiprofen Arsenic Ibuprofen Bismuth Indomethacin Copper Sulfate Ketorolac Gold salts Meclofenamate Lead Meloxicam Mercuric chloride Nabumeone

2. Occurs abruptly and can be reversible. 3. ARF leads to cell hypo perfusion, cell death and decompensation of renal function. 4. The prognosis depends on the cause and the condition of the client. 5. Near-normal or normal kidney function may resume gradually. 2. Causes 1. Pre renal: Outside the kidney; caused by intravascular volume depletion, dehydration, decreased cardiac output, decreased peripheral vascular resistance, decreased renovascular blood flow, and pre renal infection or obstruction. 2. Intra renal: Within the parenchyma of the kidney; caused by tubular necrosis, prolonged pre renal ischemia, intra renal infection or obstruction, and nephrotoxicity (Box 62.4) 3. Post renal: Between the kidney and urethral meatus, such as bladder neck obstruction, bladder cancer, calculi, and post renal infection. 3. Phases of ARF and interventions (Box 62.4) 1. Onset: Begins with precipitating event 2. Oliguric phase a. For some clients, oliguria does not occur and the urine output is normal; otherwise the duration of oliguria is 8 to 15 days; the longer the duration, the less chance of recovery. b. Sudden decrease in urine output; urine output is less than 400ml/day. c. Signs of excess fluid volume: Hypertension, edema, pleural and pericardial effusions, dysrhytmias, congestive heart failure (CHF), and pulmonary edema. d. Signs of uremia: Anorexia, nausea, vomiting, and pruritus. e. Signs of metabolic acidosis: Kussmauls respirations. f. Signs of neurological changes: Tingling of extremities, drowsiness progressing to disorientation, and then coma. g. Signs of pericarditis: Friction rub, chest pain with inspiration and low grade fever. h. Laboratory analysis (see Box 62-4) i. Restrict fluid intake; if hypertension is present, daily fluid allowances be 400 mL to 1000 mL plus the measured urinary output. j. Administer medications as prescribed, such as diuretics (furosemide [lasix]), to increase renal blood flow and dieresis. 3. Diuretic phase a. Urine output rises slowly, followed by dieresis (4 to 5L/day). b. Excessive urine output indicates that damaged nephrons are recovering their ability to excrete wastes.

Dehydration, hypovolemia, hypotension, and tachycardia can occur. Level of consciousness improves. Laboratory analysis (see box 62-4) Administer IV fluids as prescribed; which may contain electrolytes to replace loses. 4. Recovery phase (convalescent) a. Recovery is a slow process; complete recovery may take 1 to 2 years. b. Urine volume returns to normal. c. Memory improves. d. Strength increases. e. The older adult is less likely than a younger adult to regain full kidney function. f. Laboratory analysis (see box 62-4) g. ARf can progress to chronic renal failure. (CRF)

c. d. e. f.

Box 62-4 Acute Renal Failure Phases and Laboratory Findings Onset Begins with precipitating event Oliguric phase Elevated blood urea nitrogen and serum creatinine levels. Decreased urine specific gravity (pre renal causes) or nor mal (intra renal causes) Decreased glomerular filtration rate and creatinine clearance. Hyperkalemia Normal or decreased serum sodium level Hypervolemia Hpocalcemia Hyperphosphatemia Diuretic Phase Gradual decline in blood urea nitrogen and serum creatinine levels but still elevated. Continued low creatinine clearance with improving glomerular filtration rate. Hypokalemia Hyponatremia Hypovolemia Recovery Phase Increased glomerular filtration rate. Stabilization or continual decline in blood urea nitrogen and serum creatinine levels toward normal. Complete recovery may take 1 to 2 years.

The signs and symptoms of acute renal failure are primarily caused by the retention of nitrogenous wastes, the retention of fluids, and the inability of the kidney to regulate electrolytes. D. Assessment: Assess objective and subjective data noted in the phases of ARF (see box 62-4) E. Other interventions 1. Monitor vital signs, especially for signs of hypertension, tachycardia, tachypnea, and an irregular heart rate. 2. Monitor urine and intake and output (hourly in ARF) and urine color and characteristics. 3. Monitor daily weight (same scale, same clothes, same time of the day), nothing that an increase of to 1 lb/day indicates fluid retention. 4. Monitor for changes in the BUN, serum creatinine, and serum electrolyte levels. 5. Monitor for acidosis (may be treated with sodium bicarbonate). 6. Monitor urinalysis for protein level, hematuria, casts, and specific gravity. 7. Monitor for altered level of consciousness caused by uremia. 8. Monitor for signs of infection because the client may not exhibit an elevated temperature or an increased white blood cell count. 9. Monitor the lungs for wheezes and rhonchi and monitor for edeme, which can indicate fluid overload. 10. Administer a prescribed diet, which is usually a low to moderate-protein (to decrease the workload on the kidneys) and high-carbohydrate diet. 11. Restrict potassium and sodium intake as prescribed based on the electrolyte level. 12. Administer medications as prescribed; be alert to the mechanism for metabolism and excretion of all prescribed medications. 13. Be alert to nephrotoxic medications, which may be prescribed (see box 62-3). 14. Be alert to the health care providers adjustment of medication dosages for renal failure.

15. Prepare the client for dialysis if prescribed; continuous renal replacement therapy may be used in ARF to treat fluid volume overload or rapidly developing azotemia and metabolic acidosis. 16. Provide emotional support by allowing opportunities for the client to express concerns and fears and by encouraging family interactions. 17. Promote consistency in caregivers. 18. Also refer to the section in this chapter on special problems in renal failure and interventions.

Table 62-1 Progression of Chronic Kidney Disease Stage of CKD At risk normal kidney function (early kidney disease may or may not be present) Mild CKD Moderate CKD Severe CKD ESKD IV. CHRONIC RENAL FAILURE A. Description 1. CRF is a slow, progressive, irreversible loss in kidney function, with a GFR less than or equal to 60 ml/min for 3 months or longer. 2. It occurs in stages and result in uremia or end- stage renal disease (table 62-1). 3. Hypervolemia can occur because of the kidneys inability to excrete sodium and water; hypovolemia can occur because of the kidneys inability to conserve sodium and water. Chronic renal failure affects all major body systems and requires dialysis or kidney transplantation to maintain life. B. Primary causes 1. May follow ARF 2. Diabetes mellitus and other metabolic disorders 3. Hypertension 4. Chronic urinary obstruction 5. Recurrent infections Estimated GFR 90ml/min 60-89ml/min 30-59ml/min 15-29ml/min < 15ml/min

6. Renal artery occlusion 7. Autoimmune disorders C. Assessment 1. Assess body systems for the manifestation of CRF (Box62-5) 2. Assess psychological changes, which could include emotional lability, withdrawal, depression, anxiety, suicidal behavior, denial, dependenceindependence conflict, and changes in body image. D. Interventions 1. Same as the interventions of ARF. 2. Administer a prescribed diet, which is usually a moderate-protein (to decrease the workload on the kidneys), and high-carbohydrate, low-potassium, and lowphosphorus diet. 3. Provide oral care to prevent stomatitis and reduce discomfort from mouth sores. 4. Provide skin care to prevent pruritus. 5. Teach the client about fluid and dietary restrictions and the importance of daily weights. 6. Provide support to promote acceptance of the chronic illness and prepare the client for long-term dialysis and transplantation, or explain to the client about his or her choice to decline dialysis or transplantation. E. Special problems in renal failure and interventions (Box 62-6) 1. Activity intolerance and insomnia. a. Fatigue results from anemia and the buildup of wastes from the diseased kidneys. b. Provide adequate rest periods. c. Teach the client to plan activities to avoid fatigue. d. Administer mild central nervous system depressants as prescribed to promote rest. 2. Anemia a. Anemia results from the decreased secretion of erythropoietin by damaged nephrons resulting in decreased production of red blood cells. b. Monitor for decreased hemoglobin and hematocrit levels. c. Administer epoetin alfa (Epogen, Procrit) or darbepoetin alfa (Aranesp), hematopoietics, as prescribed to promote maturity of the red blood cells. d. Administer folic acid (vitamin B9) as prescribed. e. Administer iron orally as prescribed, but not at the same time as phosphate binders. f. Administer stool softeners as prescribed because of the constipating effects of iron. g. Note that oral iron is not well absorbed by the gastrointestinal tract in CRF and causes nausea and vomiting; parenteral iron (iron sucrose [Venofer] or

sodium ferric gluconate complex [Ferrlecit]) may be used if iron deficiencies persist despite folic acid or oral iron administration. h. Administer blood transfusions if prescribed; blood transfusions are prescribed only when necessary (acute blood loss, symptomatic anemia) because they decrease the stimulus to produce red blood cells; note that certain clients religious beliefs (e.g. Jehovahs Witness) may refuse blood and blood products. i. Blood transfusions also cause the development of antibodies against human tissues, which can make matching for organ transplantation difficult. 3. Gastrointestinal bleeding a. Urea is broken down by the intestinal bacteria to ammonia; ammonia irritates the gastrointestinal mucosa, causing ulceration and bleeding. b. Monitor for decreasing hemoglobin and hematocrit levels. c. Monitor stools for occult blood. d. Instruct the client to use soft toothbrush. e. Avoid the administration of acetylsalicylic acid (aspirin) because it is excreted by the kidneys; if administer, aspirin toxicity can occur and prolong the bleeding time. 4. Hyperkalemia a. Monitor vital signs of hypertension or hypotension and the apical heart rate; an irregular heart rate could indicate dysrhytmias. b. Monitor the serum potassium level; and elevated serum potassium level can cause tall, peaked T waves, flat P waves, a widened QRS complex, and a prolonged PR interval; decreased cardiac output; heart blocks; fibrillation; or a systole (fig. 62-1). c. Provide a low-potassium diet, avoiding foods high in potassium (see Chapter 9 for a listing of foods that are high in potassium). d. Administer electrolyte-binding and electrolye-excreting medications such as oral or rectal sodium polystyrene sulfonate (Kayexalate) as prescribed to lower the serum potassium level. e. Administer prescribed medications: 50% dextrose and insulin may be prescribed to shift potassium into the cell; calcium gluconate IV may be prescribed to reduce myocardial irritability from hyperkalemia; and sodium bicarbonate IV may be prescribed to correct acidosis. f. Administer prescribed loop diuretics to excrete potassium. g. Avoid potassium-sparing medications such as spironolactone (Aldactone) and triamterene (Dyrenium) because these medications will increase the potassium level. h. Prepare the client for peritoneal dialysis or hemodialysis as prescribed.

Place the client with renal failure on continuous cardiac monitoring. The client can develop hyperkalemia resulting in the risk for dysrhytmias. Box 62-5 Key Features of Chronic Renal Failure Neurological Manifestations Asterixis Ataxia (alteration in gait) Coma Inability to concentrate or decreased attention span Lethargy and daytime drowsiness Myoclonus Paresthesias Seizures Slurred speech Cardiovascular Manifestation Cardiac tamponade Cardiomyopathy Heart failure Hypertension Pericardial effusion Pericardial friction rub Peripheral edema Uremic pericarditis Respiratory Manifestation Crackles Deep sighing yawning Depressed cough reflex Kussmauls respirations Pulmonary edema Shortness of breath Tachypnea Uremic halitosis Uremic pneumonia Hematologic Manifestation Abnormal bleeding and bruising Anemia Gastrointestinal Manifestation Anorexia Changes in taste acuity and sensation Constipation Diarrhea Metallic taste in the mouth Nausea Stomatitis Uremic colitis (diarrhea) Uremic fetor Uremic gastritis (possible GI bleeding) Vomiting Urinary Manifestation Diluted, straw-colored appearance Hematuria Oliguria, Anuria (later) Polyuria nocturia (early) Integumentary Manifestation Decreased skin turgor Dry skin Ecchymosis Pruritus Purpura Soft tissue calcifications Uremic frost (late pre morbid) Yellow gray pallor Musculoskeletal Manifestation Bone pain Muscle weakness Pathologic fractures Renal osteodystrophy Reproductive Manifestation Decreased fertility Decreased libido Impotence Infrequent or absent menses

Box 62-6 Special Problems in Renal Failure Activity intolerance and insomnia Anemia Gastrointestinal bleeding Hyperkalemia Hypermagnesemia Hyperphosphatemia Hypertension Hypervolemia Hypocalcemia Hypovolemia Infection Metabolic acidosis Muscle cramps Neurological changes Ocular irritation Potential for injury Pruritus Psychosocial problems

5. Hypermagnesia a. Results from decreased renal excretion of magnesium. b. Monitor for cardiac manifestation such as bradycardia, peripheral vasodilation, and hypotension. c. Monitor central nervous system (CNS) manifestations of decreased nerve impulse transmission, such as drowsiness or lethargy. d. Monitor neuromuscular manifestations, such as reduced or absent deep tendon reflexes or weak or absent voluntary muscle contraction. e. Administer loop diuretics as prescribed, such as furosemide (Lasix). f. Administer calcium as prescribed for resulting cardiac problems. g. Avoid medications that contain magnesium, such as antacids, laxatives, or enemas. h. During severe elevations, avoid foods that increase magnesium levels (see Chapter 9 for a listing of foods that are high in magnesium). 6. Hyperphosphatemia a. As the phosphorus level rises, the calcium level drops; this leads to the stimulation of parathyroid hormone, causing bone demineralization. b. Treatment is aimed at lowering the serum phosphorus level. c. Administer phosphate binders such as calcium carbonate (TUMS), calcium acetate (PhosLo), or sevelamer (Renagel) as prescribed with meals to lower serum phosphate levels. d. Avoid the use of aluminum hydroxide preparations to bind phosphates because they are associated with dementia and osteomalacia. e. Administer stool softeners and laxatives as prescribed because phosphate binders are constipating. f. Teach the client about the need to limit the intake of foods high in phosphorus (see Chapter 9 for listing of foods that are high in phosphorus).

7. Hypertension a. Caused by failure of the kidneys to maintain BP homeostasis. b. Monitor vital signs for elevated blood pressure. c. Maintain fluid and sodium restrictions as prescribed. d. Administer diuretics and antihypertensives as prescribed. e. Administer propranolol (Inderal), a B blocker, as prescribed; propranolol decreases renin release (rennin causes vasoconstriction and subsequent hypertension). 8. Hpervolemia a. Monitor vital signs for an elevated blood pressure. b. Monitor intake and output and daily weight for indications of fluid retention. c. Monitor for periorbital, sacral, and peripheral edema. d. Monitor the serum electrolyte levels. e. Monitor for hypertension and notify the health care provider for sustained elevations. f. Monitor for signs of CHF and pulmonary edema, such as restlessness, heightened anxiety, tachycardia, dyspnea, basilar lung crackles, and blood tinged sputum; notify the physician immediately if signs occur. g. Maintain fluid restriction. h. Avoid administration of large amounts of IV fluids. i. Administer diuretics such a furosemide (Lasix) as prescribed. j. Teach the client to maintain a low-sodium diet. k. Teach the client to avoid antacids, cold remedies, or other products containing sodium bicarbonate.