Renal failure, chronic
Although chronic renal failure is usually the result of a gradually progressive loss of renal function, it occasionally results from a rapidly progressive disease of sudden onset. Few symptoms develop until after more than 75% of glomerular filtration is lost; then, the remaining normal parenchyma deteriorates progressively, and symptoms worsen as renal function decreases.
If this condition continues unchecked, uremic toxins accumulate and produce potentially fatal physiologic changes in all major organ systems. If the patient can tolerate it, maintenance dialysis or kidney transplantation can sustain life.
Causes
Chronic renal failure may result from:
❑ chronic glomerular disease such as glomerulonephritis
❑ chronic infection, such as chronic pyelonephritis or tuberculosis
❑ a congenital anomaly such as polycystic kidneys
❑ vascular disease, such as renal nephrosclerosis or hypertension
❑ an obstructive process such as calculi
❑ collagen disease such as systemic lupus erythematosus
❑ nephrotoxic drug therapy such as long-term aminoglycoside therapy
❑ endocrine disease such as diabetic neuropathy.
Such conditions gradually destroy the nephrons and eventually cause irreversible renal failure. Similarly, acute renal failure that fails to respond to treatment becomes chronic renal failure.
Chronic renal failure may progress through the following stages:
❑ reduced renal reserve (glomerular filtration rate [GFR] is 40 to 70 ml/ minute)
❑ renal insufficiency (GFR is 20 to 40 ml/ minute)
❑ renal failure (GFR 10 to 20 ml/ minute)
❑ end-stage renal disease (GFR is < 10 ml/minute).
Signs and symptoms
Chronic renal failure produces major changes in all body systems.
Renal and urologic changes
Initially, salt-wasting and consequent hyponatremia produce hypotension, dry mouth, loss of skin turgor, listlessness, fatigue, and nausea. Later, somnolence and confusion develop.
As the number of functioning neph-rons decreases, so does the kidneys’ capacity to excrete sodium, resulting in sodium retention and overload. Accumulation of potassium causes muscle irritability and then muscle weakness as the potassium level continues to rise.
Fluid overload and metabolic acidosis also occur. Urine output decreases; urine is very dilute and contains casts and crystals.
Cardiovascular changes
Renal failure leads to hypertension and arrhythmias, including life-threatening ventricular tachycardia or fibrillation. Other effects include cardiomyopathy, uremic pericarditis, pericardial effusion (and possibly cardiac tamponade), heart failure, and peripheral edema.
Respiratory changes
Pulmonary changes include reduced pulmonary macrophage activity with increased susceptibility to infection, pulmonary edema, pleuritic pain, pleural friction rub and effusions, uremic pleuritis, and uremic lung (or uremic pneumonitis). Dyspnea from heart failure also occurs, as do Kussmaul’s respirations as a result of acidosis.
GI changes
Inflammation and ulceration of GI mucosa cause stomatitis, gum ulceration and bleeding and, possibly, parotitis, esophagitis, gastritis, duodenal ulcers, lesions on the small and large bowel, uremic colitis, pancreatitis, and proctitis. Other GI signs and symptoms include a metallic taste in the mouth, uremic fetor (ammonia smell to breath), anorexia, nausea, and vomiting.
Cutaneous changes
Typically, the skin is pallid, yellowish bronze, dry, and scaly. Other cutaneous signs and symptoms include severe itching; purpura; ecchymoses; petechiae; uremic frost (most common in critically ill or terminal patients); thin, brittle fingernails with characteristic lines; and dry, brittle hair that may change color and fall out easily.
Neurologic changes
Restless leg syndrome, one of the first symptoms of peripheral neuropathy, causes pain, burning, and itching in the legs and feet, which may be relieved by voluntarily shaking, moving, or rocking them. Eventually, this condition progresses to paresthesia and motor nerve dysfunction (usually bilateral footdrop) unless dialysis is initiated.
Other signs and symptoms include muscle cramping and twitching, shortened memory and attention span, apathy, drowsiness, irritability, confusion, coma, and seizures. EEG changes indicate metabolic encephalopathy.
Endocrine changes
Common endocrine abnormalities include stunted growth in children (even with elevated growth hormone levels), infertility and decreased libido in both sexes, amenorrhea and cessation of menses in women, and impotence and decreased sperm production in men. Other changes include increased aldosterone secretion (related to increased renin production) and impaired carbohydrate metabolism (causing increased blood glucose levels similar to those found with diabetes mellitus).
Hematopoietic changes
Anemia, decreased red blood cell (RBC) survival time, blood loss from dialysis and GI bleeding, mild thrombocytopenia, and platelet defects occur. Other problems include increased bleeding and clotting disorders, demonstrated by purpura, hemorrhage from body orifices, easy bruising, ecchymoses, and petechiae.
Skeletal changes
Calcium-phosphorus imbalance and consequent parathyroid hormone imbalances cause muscle and bone pain, skeletal demineralization, pathologic fractures, and calcifications in the brain, eyes, gums, joints, myocardium, and blood vessels. Arterial calcification may produce coronary artery disease. In children, renal osteodystrophy (renal rickets) may develop.
Diagnosis
Clinical assessment, a history of chronic progressive debilitation, and gradual deterioration of renal function as determined by creatinine clearance tests lead to a diagnosis of chronic renal failure.
The following laboratory findings also aid in diagnosis:
❑ Blood studies show elevated blood urea nitrogen, creatinine, and potassium levels; decreased arterial pH and bicarbonate levels; and low hemoglobin (Hb) levels and hematocrit (HCT).
❑ Urine specific gravity becomes fixed at 1.010; urinalysis may show proteinuria, glycosuria, erythrocytes, leukocytes, and casts, depending on the cause.
❑ Renal or abdominal X-ray, abdominal computed tomography scan, magnetic resonance imaging, or ultrasonography shows reduced kidney size.
❑ X-ray studies include kidney-ureter-bladder radiography, excretory urography, nephrotomography, renal scan, and renal arteriography.
❑ Kidney biopsy allows histologic identification of underlying pathology.
Treatment
Conservative treatment aims to correct specific symptoms, minimize complications, and slow progression of the disease. Underlying conditions that cause chronic renal failure must be controlled.
Diet
A low-protein diet reduces the production of end products of protein metabolism that the kidneys can’t excrete. (A patient receiving continuous peritoneal dialysis should receive a high-protein diet.)
A high-calorie diet prevents ketoacidosis and the negative nitrogen balance that results in catabolism and tissue atrophy. Such a diet also restricts sodium and potassium.
Fluid status
Maintaining fluid balance requires careful monitoring of vital signs, weight changes, and urine volume (if present). Loop diuretics, such as furosemide (if some renal function remains), and fluid restriction can reduce fluid retention. A cardiac glycoside may be used to mobilize edema fluids; an antihypertensive, especially an angiotensin-converting enzyme inhibitor, to control blood pressure and associated edema.
Treatment of GI and blood problems
An antiemetic taken before meals may relieve nausea and vomiting; cimetidine, omeprazole, or ranitidine may decrease gastric irritation. Methylcellulose or docusate can help prevent constipation.
Treatment may also include regular stool analysis (guaiac test) to detect occult blood and, as needed, cleansing enemas to remove blood from the GI tract.
Anemia necessitates iron and folate supplements; severe anemia requires infusion of fresh frozen packed cells or washed packed cells. However, transfusions relieve anemia only temporarily. Synthetic erythropoietin (epoetin alfa) may be given to stimulate the division and differentiation of cells within the bone marrow to produce RBCs. An-drogen therapy (testosterone or nandrolone) may increase RBC production.
Drug therapy, surgery, and dialysis
Drug therapy can help relieve associated symptoms: an antipruritic, such as trimeprazine or diphenhydramine, to relieve itching and aluminum hydroxide gel to lower serum phosphate levels.
CLINICAL TIP: Be alert for aluminum toxicity, an adverse reaction to aluminum hydroxide.
The patient may also benefit from supplementary vitamins (particularly B vitamins and vitamin D) and essential amino acids.
Careful monitoring of serum potassium levels is necessary to detect hyperkalemia. Emergency treatment for severe hyperkalemia includes dialysis therapy and administration of 50% hypertonic glucose I.V., regular insulin, calcium gluconate I.V., sodium bicarbonate I.V., and cation exchange resins such as sodium polystyrene sulfonate. Cardiac tamponade resulting from pericardial effusion may require emergency pericardial tap or surgery.
Blood gas measurements may indicate acidosis; intensive dialysis and thoracentesis can relieve pulmonary edema and pleural effusions.
Hemodialysis or peritoneal dialysis (particularly continuous ambulatory peritoneal dialysis and continuous cyclic peritoneal dialysis) can help control most manifestations of end-stage renal disease. (See Continuous ambulatory peritoneal dialysis, page 718.) Altering dialyzing bath fluids can correct fluid and electrolyte disturbances. However, anemia, peripheral neuropathy, cardiopulmonary and GI complications, sexual dysfunction, and skeletal defects may persist.
Maintenance dialysis may produce complications, such as protein wasting, refractory ascites, and dialysis dementia. A kidney transplant may eventually be the treatment of choice for some patients with end-stage renal disease.
Special considerations
❑ Provide good skin care. Bathe the patient daily, using superfatted soaps, oatmeal baths, and skin lotion to ease pruritus. Give good perineal care, using mild soap and water. Pad the side rails to guard against ecchymoses. Turn the patient often, and use a convoluted foam mattress to prevent skin breakdown.
❑ Provide good oral hygiene. Brush the patient’s teeth often with a soft brush or sponge tip to reduce breath odor. Hard candy and mouthwash minimize bad taste in the mouth and alleviate thirst.
❑ Offer small, palatable meals that are also nutritious; try to provide favorite foods within dietary restrictions. Encourage intake of high-calorie foods. Instruct the outpatient to avoid high-sodium, high-protein, and high-potassium foods.
❑ Encourage adherence to fluid and protein restrictions. To prevent constipation, stress the need for exercise and sufficient dietary fiber.
❑ Watch for hyperkalemia. Cramping of the legs and abdomen and diarrhea are indications of it. As potassium levels rise, watch for muscle irritability and a weak pulse rate. Monitor electrocardiogram results for indications of hyperkalemia — tall, peaked T waves; widening QRS complex; prolonged PR interval; and disappearance of P waves.
❑ Carefully assess hydration status. Check for jugular vein distention and auscultate the lungs for crackles. Measure daily intake and output carefully, including all drainage, vomitus, diarrhea, and blood loss. Record daily weight, presence or absence of thirst, axillary sweat, dryness of tongue, hypertension, and peripheral edema.
❑ Monitor the patient for bone and joint complications. Prevent pathologic fractures by turning the patient carefully and ensuring his safety. If the patient is bedridden, provide passive range of-motion exercises.
❑ Encourage deep breathing and coughing to prevent pulmonary congestion. Listen often for crackles, rhonchi, and decreased breath sounds. Be alert for signs and symptoms of pulmonary edema (such as dyspnea, restlessness, and crackles). Administer a diuretic and other medications as needed.
❑ Maintain strict aseptic technique. Use a micropore filter during I.V. therapy. Watch for signs of infection (such as listlessness, high fever, and leukocytosis). Urge the outpatient to avoid contact with infected persons during the cold and flu season.
❑ Carefully observe and document seizure activity. Infuse sodium bicarbonate for acidosis and a sedative or an anticonvulsant for seizures. Pad the side rails, and keep an oral airway and suction setup at bedside. Assess neurologic status periodically, and check for Chvostek’s and Trousseau’s signs, indicators of low serum calcium levels.
❑ Observe the patient for signs of bleeding. Watch for prolonged bleeding at puncture sites and at the vascular access site used for hemodialysis. Monitor Hb and HCT, and check stools, urine, and vomitus for blood.
❑ Watch for signs of pericarditis, such as a pericardial friction rub and chest pain. Also, watch for the disappearance of friction rub, with a drop of 15 to 20 mm Hg in blood pressure during inspiration (paradoxical pulse) — an early sign of pericardial tamponade.
❑ Schedule medications carefully. Give iron before meals, aluminum hydroxide gels after meals, and an antiemetic, as necessary, a half hour before meals. Administer an antihypertensive at appropriate intervals.
❑ If the patient requires a rectal infusion of sodium polystyrene sulfonate for dangerously high potassium levels, apply an emollient to soothe the perianal area. Be sure the sodium polystyrene sulfonate enema is expelled; otherwise, it will cause constipation and won’t lower potassium levels.
❑ Recommend antacid cookies as an alternative to aluminum hydroxide gels needed to bind GI phosphate.
If the patient requires dialysis:
❑ Prepare the patient by fully explaining the procedure. Be sure that he understands how to protect and care for the arteriovenous shunt, fistula, or other vascular access.
❑ Check the vascular access site every 2 hours for patency and the extremity for adequate blood supply and intact nervous function (temperature, pulse rate, capillary refill time, and sensation).
❑ If a fistula is present, palpate for a thrill and listen for a bruit. Use a gentle touch to avoid occluding the fistula. Note any signs of clotting.
❑ Don’t use the arm with the vascular access site to take blood pressure readings, draw blood, or give injections; these procedures may rupture the fistula or cause scarring that occludes blood flow.
❑ Withhold the 6 a.m. (or morning) dose of antihypertensive on the morning of dialysis, and instruct the outpatient to do the same.
❑ Check the patient’s hepatitis antigen status. If it’s positive, he’s a carrier of hepatitis B, and stool, needle, blood, and excretion precautions should be instituted.
❑ Monitor Hb and HCT. Assess the patient’s tolerance of his levels; some individuals are more sensitive to lower levels than others. Instruct the anemic patient to conserve energy and to rest frequently.
❑ After dialysis, check for disequilibrium syndrome, a result of sudden correction of blood chemistry abnormalities. Signs and symptoms range from a headache to seizures. Also, check for excessive bleeding from the dialysis site. Apply a pressure dressing or absorbable gelatin sponge as indicated. Monitor blood pressure carefully after dialysis.
❑ A patient undergoing dialysis is under a great deal of stress, as is his family. Refer them to appropriate counseling agencies for assistance in coping with chronic renal failure.
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Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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