CHRONIC RENAL FAILURE DEFINITION: Chronic renal failure, or ESRD, is a progressive, irreversible deterioration in renal function in which the

e bodys ability to maintain metabolic and fluid and electrolyte balance fails, resulting in uremia or azotemia. CRF defined as either the presence of kidney damage or glomerular filtration rate (GFR) <60 ml/min for 3 months or longer. Kidney damage: Kidney damage is defined as either pathologic abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies. End stage renal disease ( ESRD): Final stage of renal failure characterized by GFR less than 15 ml/min CAUSES:

STAGES OF CHRONIC RENAL DISEASE: Stage 1 - Reduced renal reserve characterized by 40% to 75% loss of nephron function. usually does not have symptoms because the remaining nephrons are able to carry out the normal functions of the kidney. Stage 2 - Renal insufficiency 75% to 90% of nephron function is lost serum creatinine and blood urea nitrogen rise kidney loses its ability to concentrate urine and anemia develops, polyuria and nocturia may occur Stage 3 - End-stage renal disease (ESRD) final stage of chronic renal failure less than 10% nephron function remaining normal regulatory, excretory, and hormonal functions of the kidney are severely impaired evidenced by elevated creatinine and blood urea nitrogen levels as well as electrolyte imbalances. dialysis is indicated.

STAGES: Stages

D e s c r i p t i on

GFR ( m l / m i n / 1 . 7 3 m2 ) 90

Action

Stage I

At increased risk for CKD S Kidney damage with normal or GFR Kidney damage with mild GFR Moderate GFR Severe GFR Kidney failure

Screening CKD risk reduction Diagnosis and treatment Estimation of progression Evaluation and treatment of complications Preparation for renal replacement therapy Dialysis Dialysis Renal replacement (if uremia present)

Stage II Stage III Satge IV Satge V

60-89 30-59 15-29 <15

PATHOPHYSIOLOGICAL CHANGES: 1. Waste Product Accumulation: BUN and serum creatinine levels increase. BUN is increased due to protein intake, fever, corticosteroids, and catabolism. As the BUN increases, nausea, vomiting, lethargy, fatigue, impaired thought processes, and headaches become common as a result of the effects of waste products on the central nervous and GI systems. 2. Hyperkalemia: Hyperkalemia is the most serious electrolyte disorder Fatal dysrhythmias can occur when the serum potassium level reaches 7 to 8 mEq/L Hyperkalemia results from the decreased excretion by the kidneys, the breakdown of cellular protein, bleeding, and metabolic acidosis. 3. Sodium imbalance: Sodium may be normal or low in renal failure. Retainment of large quantities of body water causes dilutional hyponatremia. Sodium retention can leads to edema, hypertension, and heart failure. 4. Metabolic Acidosis: Results from the impaired ability of the kidneys to excrete the acid load and from defective reabsorption and regeneration of bicarbonate. Decrease in plasma bicarbonate reflects its use in buffering metabolic acids. Kussmaul respiration reduces the severity of acidosis by increasing carbon dioxide excretion 5. Infection: Infectious complications are caused by changes in leukocyte function and altered immune response and function related to altered response by both neutrophils and monocytes. Characteristic clinical findings include lymphopenia, lymphoid tissue atrophy, decreased antibody production, and suppression of the delayed hypersensitivity response. Other factors contributing to the increased risk of infection include malnutrition, hyperglycemia, and external trauma 6. Hematologic changes: Normocytic or normochromic anemia is associated with CKD. The anemia is due to decreased production of the hormone erythropoietin by the kidneys Other factors contributing to anemia are nutritional deficiencies, decreased RBC life span, increased hemolysis of RBCs, frequent blood samplings, and bleeding from the GI tract. Megaloblastic anemia resulting from folic acid deficiency may develop 7. Bleeding Tendencies: Defect in platelet function. Dysfunction is caused by impaired platelet aggregation and impaired release of platelet factor III.

8. Gastrointestinal System changes: Inflammation of the mucosa caused by excessive urea Mucosal ulcerations due to increased ammonia Uremic fetor (a urinous odor of the breath) occurs Anorexia, nausea, and vomiting caused by irritation of the GI tract by waste products contribute to weight loss and malnutrition. 9. Neurologic changes: Neurologic changes due to increased nitrogenous waste products, electrolyte imbalances, metabolic acidosis, and axonal atrophy and demyelination of nerve fibers. Depression of the CNS results in lethargy, apathy, decreased ability to concentrate, fatigue, irritability, and altered mental ability. Seizures and coma may result from a rapidly increasing BUN and hypertensive encephalopathy. Peripheral neuropathy results in slowing of nerve conduction to the extremities. Motor involvement may lead to bilateral footdrop, muscular weakness and atrophy, and loss of deep tendon reflexes. Muscle twitching, jerking, asterixis, and nocturnal leg cramps also occur. 10. Renal osteodystrophy: 1.Osteomalacia Demineralization results from slow bone turnover and defective Result of PTH suppression from high calcium intake), high vitamin D dosage, and the presence of diabetes mellitus. 2. Osteitis Jibrosa cystica: Results from decalcification of the bone and replacement of bone tissue with fibrous tissue. 3. Osteitis fibrosa : Result of markedly elevated levels of PTH that cause bone resorption and softening. CLINICAL MANIFESTATIONS:

DIAGNOSTIC STUDIES: History and physical examination Identification of reversible renal disease Renal ultrasound Renal scan CT scan Renal biopsy BUN, serum creatinine, and creatinine clearance levels Serum electrolytes Protein-to-creatinine ratio in first morning voided specimen Urinalysis and urine culture Hematocrit and hemoglobin levels

COLLABORATIVE THERAPY: Correction of extracellular fluid volume overload or deficit Nutritional therapy Erythropoietin therapy Calcium supplementation, phosphate binders, or both Antihypertensive therapy Measures to lower potassium Adjustment of drug dosages to degree of renal function Peritoneal dialysis Peritoneal dialysis uses the lining of the abdominal cavity as a filter to clean blood and remove excess fluid. A catheter is implanted into the abdomen by a minor surgical procedure and a fluid (dialysate solution) is infused through this. The dialysate solution, left for a few hours, capture and eliminate the waste products from your blood. The most common form of peritoneal dialysis called continuous ambulatory peritoneal dialysis (CAPD) changes dialysate four times a day Hemodialysis Hemodialysis uses a mechanical membrane (dialyzer) with a special filter that removes waste and excess water from the blood. The patient is connected to the machine by a tube running from a conduit created surgically between a large artery and vein. The blood is circulated through the artificial kidney, which removes toxins and wastes. The blood is then returned to your body. Hemodialysis typically takes 3-4 hours and is needed 3 times a week. . Hyperkalemia management: Restriction of high-potassium foods and drugs. Acute hyperkalemia is treated with with IV glucose and insulin or IV 10% calcium gluconate. Sodium polystyrene sulfonate (Kayexalate), a cation-exchange resin, is used to lower potassium

 As sodium polystyrene sulfonate exchanges sodium ions for potassium ions, the patient should be observed for sodium and water retention. In dysrhythmias, dialysis may be required to remove excess potassium. Hypertension management: Target BP be less than 130/80 mm Hg for patients with CKD. Treatment of hypertension includes (1) weight loss (2) therapeutic lifestyle changes (3) diet recommendations (4) administration of antihypertensive drugs diuretics(e.g., furosemide), (3-adrenergic blockers (e.g., metoprolol), calcium channel blockers (e.g., nifedipine ), ACE inhibitors (e.g., captopril, enalapril), and angiotensin receptorblocker (ARB) agents (e.g., losartan) Anemia management With the use of recombinant DNA technology , erythropoietin is produced and is administered intravenously or subcutaneously Oral iron supplements are given Parenteral iron sucrose injection (Venofer) or sodium ferric gluconate complex in sucrose injection (Ferrlecit) is given Supplemental folic acid Blood transfusions should be avoided. LIST OF NURSING DIAGNOSES: 1. Excess fluid volume related to inability of kidneys to excrete fluid and excessive fluid intake as evidenced by edemahypertension, bounding pulse, weight gain, shortness of breath, pulmonary edema 2. Risk for injury related to alterations in bone structure due to decreased calcium absorption, retention of phosphate, and altered vitamin D metabolism 3. Imbalanced nutrition: less than body requirements related to restricted intake of nutrients (especially protein), nausea, vomiting, anorexia, and stomatitis as evidenced by loss of appetite and weight Deficient knowledge regarding condition and treatment regimen 4. Activity intolerance related to fatigue, anemia, retention of waste products, and dialysis procedure 5. Low self-esteem related to dependency, role changes, changes in body image, and sexual dysfunction 6. Risk for infection related to suppressed immune system, access sites, and malnutrition secondary to dialysis & uremia 7. Grieving related to loss of kidney function as evidenced by expression of feelings of sadness, anger, inadequacy, hopelessness NURSING INTERVENTIONS: 1. Excess fluid volume related to inability of kidneys to excrete fluid and excessive fluid intake as evidenced by edemahypertension, bounding pulse, weight gain, shortness of breath, pulmonary edema Hypervolemia Management : Monitor respiratory pattern for symptoms of respiratory difficulty that are indicators of fluid excess. Weigh patient daily and monitor trends. Provide appropriate diet to help control edema and hypertension. Instruct patient and/or family on measures instituted to treat the hypervolemia to help monitor and control fluid overload and related hypertension. Dialysis Therapy: Draw blood sample and review blood chemistries before treatment to evaluate response. Record baseline vital signs: weight, temperature, pulse, respirations, and blood pressure, to evaluate response to therapy. Adjust filtration pressure to remove an appropriate amount of fluid.

 Work collaboratively with patient to adjust length of dialysis, diet regulations, fluid limitations, and medications to regulate fluid and electrolyte shifts between treatment 2. Risk for injury related to alterations in bone structure due to decreased calcium absorption, retention of phosphate, and altered vitamin D metabolism Electrolyte Management: Hypocalcemia Monitor trends in serum levels of calcium to provide early intervention Monitor for electrolyte imbalances associated with to determine degree of bone demineralization and potential risk for fracture. Administer appropriate prescribed calcium salt (e.g., calcium carbonate, calcium chloride, and calcium gluconate). Provide adequate intake of vitamin D to facilitate GI absorption of calcium to prevent and/or treat the bone demineralization. Teaching: Disease Process Instruct patient on measures to control/minimize symptoms Discuss lifestyle changes that may be required to prevent future complications (and/or control the disease process to reduce the risk of unsafe practices that might result in a traumatic or pathologic fracture. 3. Imbalanced nutrition: less than body requirements related to restricted intake of nutrients (especially protein), nausea, vomiting, anorexia, and stomatitis as evidenced by loss of appetite and weight Deficient knowledge regarding condition and treatment regimen Nutritional Monitoring: Monitor trends in weight loss and gain to detect changes in status. Monitor albumin, total protein, hemoglobin, and hematocrit levels as indicators of nutritional status, and response to treatments. Monitor caloric and nutrient intake to detect changes. Nutrition Therapy: Provide oral care before meals to prevent stomatitis, remove bad taste, and increase patient's appetite. Refer for diet teaching and planning to ensure adequate intake within prescribed diet restrictions. Provide needed nourishment within limits of prescribed diet to promote adequate nutrition 4. Risk for infection related to suppressed immune system, access sites, and malnutrition secondary to dialysis & uremia Infection Protection: Monitor for systemic and localized signs and symptoms of infection to ensure early identification and treatment. Limit number of visitors to decrease risk of infection. Infection Control: Ensure aseptic handling of all IV lines to prevent the introduction of organisms. Wash hands before and after each patient care activity to prevent transmission of pathogens. Teach patient and family about signs and symptoms of infection and when to report them to the health care provider to obtain early treatment. 5. Grieving related to loss of kidney function as evidenced by expression of feelings of sadness, anger, inadequacy, hopelessness Grief Work Facilitation: Listen to expressions of grief to convey a caring attitude and foster a relationship and/or to determine how patient is handling the situation. Identify sources of community support for continued grief work. Coping Enhancement: Assist patient to solve problems in a constructive manner to help facilitate the grieving process. Encourage family involvement to enable them to assist the patient and foster their support and understanding. Assist patient to grieve and work though the losses of chronic illness and/or disability.