Kidney Disorder First Lecture PDF

Management of patient with Renal disorder Aysha Hoshyia RN,MSN On the end of this lecture, the students will be able to:  1 Describe the key factors associated with the development of renal disorders.  2 Differentiate between the causes of chronic kidney disease and acute an...

Management of patient with Renal disorder Aysha Hoshyia RN,MSN On the end of this lecture, the students will be able to:  1 Describe the key factors associated with the development of renal disorders.  2 Differentiate between the causes of chronic kidney disease and acute and chronic renal failure.  3 Compare and contrast the pathophysiology, clinical manifestations, medical management, and nursing management for patients with renal disorders.  4 Describe the nursing management of patients with acute and chronic renal failure.  5 Compare and contrast the renal replacement therapies including hemodialysis, peritoneal dialysis, and kidney transplantation.  6 Describe the nursing management of the hospitalized patient on dialysis.  7 Develop a postoperative plan of nursing care and teaching plan for the patient undergoing kidney surgery and transplantation.  FLUID AND ELECTROLYTE IMBALANCES IN RENAL DISORDERS  Patients with renal disorders commonly experience fluid and electrolyte imbalances.  The most accurate indicator of fluid loss or gain in an acutely ill patient is weight.  An accurate daily weight must be obtained and recorded. A 1-kg weight gain is equal to 1000 mL of retained fluid.  Clinical Manifestations: Irregular or fast heart rate (arrhythmia). Muscle cramps, muscle spasms or weakness. Nausea and vomiting. Numbness or tingling in limbs, fingers and toes.  Gerontologic Considerations:  With aging, the kidney is less able to respond to acute fluid and electrolyte changes.  Elderly patients may develop atypical and nonspecific signs and symptoms of disturbed renal function and fluid and electrolyte imbalances.  A fluid balance deficit in the elderly can lead to constipation, falls, medication toxicity, urinary tract and respiratory tract infections, delirium, seizures, electrolyte imbalances, hyperthermia, and delayed wound healing (Mentes, 2006). RENAL DISORDERS: Chronic Kidney Disease  Chronic kidney disease (CKD) is describes kidney damage or a decrease in the glomerular filtration rate (GFR) for 3 or more months (Thomas- Hawkins & Zazworsky, 2005).  Untreated CKD can result in end-stage renal disease (ESRD) and necessitate renal replacement therapy (dialysis or kidney transplantation).  Risk factors include cardiovascular disease, diabetes, hypertension, and obesity.  Diabetes is the primary cause of CKD. The second leading cause is hypertension, followed by glomerulonephritis. (U.S. Renal Data System [USRDS], 2007). Pathophysiology  In the early stages of CKD there can be significant damage to the kidneys without signs or symptoms.  The pathophysiology of CKD is not yet clearly understood, but the damage to the kidneys is thought to be caused by prolonged acute inflammation.  Stages of Chronic Kidney Disease:  CKD has been classified into five stages by the National Kidney Foundation (NKF).  Stage 5 results when the kidneys cannot remove the body’s metabolic wastes or perform their regulatory functions and renal replacement therapies are required to sustain life.  Screening and early intervention are important, as not all patients progress to stage 5 CKD.  Patients with CKD are at increased risk for cardiovascular disease, the leading cause of morbidity and mortality (Thomas & Atkins, 2006).  Treatment of hypertension, anemia, and hyperglycemia and detection of proteinuria all help to slow disease progression and improve patient outcomes (Compton, 2007).  Stages are based on the glomerular filtration rate (GFR).  The normal GFR is 125 mL/min/1.73 m2.  Stage 1  GFR 90 mL/min/1.73 m2 Kidney damage with normal or increased GFR  Stage 2  GFR 60–89 mL/min/1.73 m2 Mild decrease in GFR  Stage 3  GFR 30–59 mL/min/1.73 m2 Moderate decrease in GFR  Stage 4  GFR 15–29 mL/min/1.73 m2 Severe decrease in GFR  Stage 5  GFR 15 mL/min/1.73 m2 Kidney failure (end-stage renal disease [ESRD])  Clinical Manifestations  Elevated serum creatinine levels; as the creatinine level increases, symptoms of chronic kidney disease begin.  Anemia, due to decreased erythropoietin production by the kidney.  metabolic acidosis; and abnormalities in calcium and phosphorus herald the development of CKD. Fluid retention, evidenced by both edema and congestive heart failure, develops.  As the disease progresses, abnormalities in electrolytes occur, heart failure worsens, and hypertension becomes more difficult to control. Assessment and Diagnostic Findings  The GFR is the amount of plasma filtered through the glomeruli per unit of time.  Creatinine clearance is a measure of the amount of creatinine the kidneys are able to clear in a 24-hour period.  Normal values differ in men and women.  Medical Management  The management of patients with CKD includes treatment of the underlying causes.  Regular clinical and laboratory assessment is important to keep the blood pressure (BP) below 130/80 mm Hg.  Prevention of complications is accomplished by controlling cardiovascular risk factors; treating hyperglycemia; treating anemia; smoking cessation, weight loss, and exercise programs as needed; and reduction in salt and alcohol intake.  Gerontologic Considerations  Changes in kidney function with normal aging increase the susceptibility of elderly patients to kidney dysfunction and renal failure (Miller, 2009).  In addition, the incidence of systemic diseases, such as atherosclerosis, hypertension, heart failure, diabetes, and cancer, increases with advancing age, predisposing older adults to renal disease associated with these disorders. Therefore, acute problems need to be prevented if possible or recognized and treated quickly to avoid kidney damage.  Elderly patients frequently take multiple prescription and over-the-counter medications. Because alterations in renal blood flow, glomerular filtration, and renal clearance increase the risk for medication-associated changes in renal function.  When elderly patients undergo extensive diagnostic tests or when new medications (eg, diuretic agents) are added, precautions must be taken to prevent dehydration, which can compromise marginal renal function and lead to renal failure (Mentes, 2006). Nephrosclerosis  Nephrosclerosis is most often due to prolonged hypertension and diabetes.  Nephrosclerosis is a major cause of CKD and ESRD secondary to many disorders.  Pathophysiology  There are two forms of nephrosclerosis:  malignant (accelerated) and benign.  Malignant nephrosclerosis is often associated with significant hypertension (diastolic blood pressure higher than 130 mm Hg). It usually occurs in young adults and twice as often in men compared to women. Damage is caused by decreased blood flow to the kidney resulting in patchy necrosis of the renal parenchyma.  Over time, fibrosis occurs and glomeruli are destroyed. The disease process progresses rapidly.  Benign nephrosclerosis can be found in older adults, associated with atherosclerosis and hypertension.  Assessment and Diagnostic Findings  Symptoms are rare early in the disease, even though the urine usually contains protein and occasional casts.  Renal insufficiency and associated signs and symptoms occur late in the disease. Medical Management  Treatment of nephrosclerosis is aggressive antihypertensive therapy. An angiotensin-converting enzyme (ACE) inhibitor, alone or in combination with other antihypertensive medications. (Munar & Singh, 2007).  Primary Glomerular Diseases  Diseases that destroy the glomerulus of the kidney are the third most common cause of stage 5 CKD.  In these disorders, the glomerular capillaries are primarily involved. Antigen–antibody complexes form in the blood and become trapped in the glomerular capillaries , inducing an inflammatory response.  Immunoglobulin G (IgG), the major immunoglobulin (antibody) found in the blood, can be detected in the glomerular capillary walls.  The major clinical manifestations of glomerular injury include proteinuria, hematuria, decreased GFR, decreased excretion of sodium, edema, and hypertension. ACUTE NEPHRITIC SYNDROME  The acute nephritic syndrome is the clinical manifestation of glomerular inflammation (Porth & Matfin, 2009).  Glomerulonephritis is an inflammation of the glomerular capillaries that can occur in acute and chronic forms.  Pathophysiology:  Primary glomerular diseases include post infectious glomerulonephritis, rapidly progressive glomerulonephritis, membrane proliferative glomerulonephritis, and membranous glomerulonephritis.  Post infectious causes are group A beta-hemolytic streptococcal infection of the throat that precedes the onset of glomerulonephritis by 2 to 3 weeks  It may also follow (infection of the skin) and acute viral infections (upper respiratory tract infections, varicella zoster virus, Epstein-Barr virus, hepatitis B, and human immunodeficiency virus [HIV] infection).  Clinical Manifestations  The primary presenting features of an acute glomerular inflammation are hematuria, edema, azotemia, an abnormal concentration of nitrogenous wastes in the blood, and proteinuria or excess protein in the urine (Porth & Matfin, 2009).  The hematuria may be microscopic, or macroscopic (visible to the eye).  The urine may appear cola-colored because of red blood cells (RBCs) and protein plugs or casts; RBC casts indicate glomerular injury.  Glomerulonephritis may be mild and the hematuria discovered incidentally through a routine urinalysis, or the disease may be severe, with acute renal failure (ARF) and oliguria. Some degree of edema and hypertension is present in most patients.  Marked proteinuria due to the increased permeability of the glomerular membrane may also occur, with associated pitting edema, hypoalbuminemia, hyperlipidemia, and fatty casts in the urine. Blood urea nitrogen (BUN) and serum creatinine levels may increase as urine output decreases. In addition, anemia may be present.  In the more severe form of the disease, patients also complain of headache, malaise, and flank pain. Elderly patients may experience circulatory overload with dyspnea, engorged neck veins, cardiomegaly, and pulmonary edema.  Atypical symptoms include confusion, and seizures, which are often confused with the symptoms of a primary neurologic disorder.  Assessment and Diagnostic Findings  In acute nephritic syndrome, the kidneys become large, edematous, and congested. All renal tissues including the glomeruli, tubules, and blood vessels are affected to varying degrees.  Patients with an IgA nephropathy have an elevated serum IgA and low to normal complement levels.  a kidney biopsy may be needed for definitive diagnosis. If the patient improves, the amount of urine increases and the urinary protein and sediment diminish. Some patients develop severe uremia within weeks and require dialysis for survival.  Others, after a period of apparent recovery, insidiously develop chronic glomerulonephritis.  Complications:  Complications of acute glomerulonephritis include:  hypertensive encephalopathy, heart failure, and pulmonary edema.  Hypertensive encephalopathy is a medical emergency, and therapy is directed toward reducing the blood pressure without impairing renal function. This can occur in acute nephritic syndrome or preeclampsia with chronic hypertension of greater than 140/90 mm Hg.  Without treatment, ESRD develops in a matter of weeks or months. Signs and symptoms are similar to those of acute glomerulonephritis (hematuria and proteinuria), but the course of the disease is more severe and rapid.  Crescent-shaped cells accumulate in Bowman’s space, disrupting the filtering surface.  Medical Management  Management consists primarily of treating symptoms, attempting to preserve kidney function, and treating complications promptly.  Treatment may include corticosteroids, managing hypertension, and controlling proteinuria (Glick,2007).  Pharmacologic therapy depends on the cause of acute glomerulonephritis. If residual streptococcal infection is suspected, penicillin is the agent of choice.  Dietary protein is restricted when renal insufficiency and nitrogen retention (elevated BUN) develop. Sodium is restricted when the patient has hypertension, edema, and heart failure.  Plasma exchange (plasmapheresis) and treatment with high-dose corticosteroids and cytotoxic agents have been used to reduce the inflammatory response.  Dialysis is initiated in acute glomerulonephritis if signs and symptoms of uremia are severe (Porth & Matfin, 2009).  Nursing Management:  In a hospital setting, carbohydrates are given liberally to provide energy and reduce the catabolism of protein.  I&O are carefully measured and recorded.  Fluids are given based on the patient’s fluid losses and daily body weight.  If treatment is effective, diuresis will begin, resulting in decreased edema and blood pressure.  Promoting Home and Community-Based Care:  Proteinuria and microscopic hematuria may persist for months; in fact, 20% of patients have some degree of persistent proteinuria or decreased GFR 1 year after presentation (Porth & Matfin,2009).  Patient education is directed toward symptom management and monitoring for complications.  Fluid and diet restrictions must be reviewed with the patient to avoid worsening of edema and hypertension. The patient is instructed to notify the physician if symptoms of renal failure occur (eg, fatigue, nausea, vomiting, diminishing urine output) or at the first sign of any infection.  The importance of follow-up evaluations of blood pressure, urinalysis for protein, and BUN and serum creatinine levels to determine if the disease has progressed is stressed to the patient.  If corticosteroids, immunosuppressant agents, or antibiotic medications are prescribed, a nurse in the outpatient setting uses the opportunity to review the dosage, desired actions, and adverse effects of medications and the precautions to be taken. CHRONIC GLOMERULONEPHRITIS  Chronic glomerulonephritis may be due to repeated episodes of acute nephritic syndrome, hypertensive nephrosclerosis, hyperlipidemia, chronic tubulointerstitial injury, or hemodynamically mediated glomerular sclerosis.  Secondary glomerular diseases that can have systemic effects include lupus erythematosus, diabetic glomerulosclerosis, and amyloidosis. Pathophysiology  The kidneys are reduced to as little as one-fifth their normal size (consisting largely of fibrous tissue). The cortex layer shrinks to 1 to 2 mm in thickness or less.  Bands of scar tissue distort the remaining cortex, making the surface of the kidney rough and irregular. Numerous glomeruli and their tubules become scarred, and the branches of the renal artery are thickened.  The resulting severe glomerular damage can progress to stage 5 CKD and require renal replacement therapies.  Clinical Manifestations  The symptoms of chronic glomerulonephritis vary. Some patients with severe disease have no symptoms at all for many years (Porth & Matfin, 2009).  The condition may be discovered when hypertension or elevated BUN and serum creatinine levels are detected.  Most patients report general symptoms, such as loss of weight and strength, increasing irritability, and an increased need to urinate at night (nocturia). Headaches, dizziness, and digestive disturbances are also common.  The patient appears poorly nourished, with a yellow-gray pigmentation of the skin and periorbital and peripheral (dependent) edema. Blood pressure may be normal or severely elevated. and papilledema.  Anemia causes pale mucous membranes.  Peripheral neuropathy and neurosensory changes occur late in the disease.  The patient becomes confused and demonstrates a limited attention span.  An additional late finding includes evidence of pericarditis  Assessment and Diagnostic Findings:  Urinalysis reveals a fixed specific gravity of about 1.010,  variable proteinuria, and urinary casts (proteins secreted by damaged kidney tubules). As renal failure progresses and the GFR falls below 50 mL/min, the following changes occur:  Hyperkalemia  Metabolic acidosis  Anemia  Hypoalbuminemia with edema secondary to protein loss through the damaged glomerular membrane.  Increased serum phosphorus level  Decreased serum calcium level  Mental status changes  Impaired nerve conduction due to electrolyte abnormalities and uremia.  Chest x-rays may show cardiac enlargement and pulmonary edema.  The electrocardiogram (ECG) may be normal or may indicate left ventricular hypertrophy associated with hypertension and signs of electrolyte disturbances.  Computed tomography (CT) and magnetic resonance imaging (MRI) scans show a decrease in the size of the renal cortex.  Medical Management  Management of symptoms guides the treatment.  antihypertensive agents.  Weight is monitored daily.  and diuretic medications are prescribed to treat fluid overload.  Proteins of high biologic value (dairy products, eggs, meats) are provided to promote good nutritional status.  Urinary tract infections (UTIs) must be treated promptly to prevent further renal damage.  Dialysis is initiated early in the course of the disease to keep the patient in optimal physical condition.  prevent fluid and electrolyte imbalances, and minimize the risk of complications of renal failure.  Nursing Management  the nurse observes the patient for common fluid and electrolyte disturbances in renal disease.  Changes in fluid and electrolyte status and in cardiac and neurologic status are reported promptly to the physician.  Anxiety levels are often extremely high for both the patient and family. Throughout the course of the disease and treatment, the nurse gives emotional support. Promoting Home and Community-Based Care Teaching Patients Self-Care  Instructions to the patient include explanations and scheduling for follow- up evaluations:  blood pressure, urinalysis for protein and casts, and laboratory studies of BUN and serum creatinine levels.  If long-term dialysis is needed, the nurse teaches the patient and family about the procedure, how to care for the access site, dietary restrictions, and other necessary lifestyle modifications.  NEPHROTIC SYNDROME  Nephrotic syndrome is a type of renal failure characterized by increased glomerular permeability and is manifested by massive proteinuria (Porth & Matfin, 2009).  Clinical findings include a marked increase in protein (particularly albumin) in the urine (proteinuria), a decrease in albumin in the blood (hypoalbuminemia), diffuse edema, high serum cholesterol, and low- density lipoproteins (hyperlipidemia).  The syndrome is apparent in any condition that seriously damages the glomerular capillary membrane and results in increased glomerular permeability to plasma proteins.  Pathophysiology:  Nephrotic syndrome occurs with many intrinsic renal diseases and systemic diseases that cause glomerular damage. It is not a specific glomerular disease.(Porth & Matfin, 2009). Clinical manifestations:  The major manifestation of nephrotic syndrome is edema.  It is usually soft and pitting and commonly occurs around the eyes (periorbital), in dependent areas ( ankles, and hands), and in the abdomen (ascites).  Patients may also exhibit irritability, headache, and malaise. Assessment and Diagnostic Findings:  Proteinuria (predominately albumin) is the hallmark of the diagnosis of nephrotic syndrome (Porth & Matfin, 2009).  Protein electrophoresis and immunoelectrophoresis may be performed on the urine to categorize the type of proteinuria. The urine may also contain increased white blood cells (WBCs) as well as granular and epithelial casts.  A needle biopsy of the kidney may be performed for histologic examination of renal tissue to confirm the diagnosis. Complications:  Complications of nephrotic syndrome include:  infection (due to a deficient immune response).  thromboembolism (especially of the renal vein).  pulmonary emboli.  ARF (due to hypovolemia), and accelerated atherosclerosis (due to hyperlipidemia).  Medical Management:  Treatment is focused on treating the underlying disease state causing proteinuria.  slowing progression of CKD, and relieving symptoms.  Typical treatment includes diuretics for edema, ACE inhibitors to reduce proteinuria, and lipid-lowering agents for hyperlipidemia. Nursing Management: In the early stages of nephrotic syndrome, nursing management is similar to that of the patient with acute glomerulonephritis, but as the condition worsens, management is similar to that of the patient with ESRD.  Polycystic Kidney Disease  Pathophysiology  Polycystic kidney disease (PKD) is a genetic disorder characterized by the growth of numerous cysts in the kidneys.  When cysts form in the kidneys, they are filled with fluid, destroying the nephrons. PKD cysts can profoundly enlarge the kidneys while replacing much of the normal structure, resulting in reduced kidney function and leading to kidney failure.  PKD can also cause cysts in the liver and problems in other organs, such as blood vessels in the brain and heart. The number of cysts as well as the complications they cause help distinguish PKD from the usually harmless “simple” cysts.  Two major inherited forms of PKD  exist: Autosomal dominant PKD is the most common inherited form. Symptoms usually develop between the ages of 30 and 40, but they can begin earlier, even in childhood. About 90% of all PKD cases are autosomal dominant PKD.  Autosomal recessive PKD is a rare inherited form. Symptoms of autosomal recessive PKD begin in the earliest months of life or in utero.  When autosomal dominant PKD causes kidneys to fail, which usually happens after many years, the patient requires dialysis or kidney transplantation.  About one half of people with the most common type of PKD progress to CKD stage 5, requiring renal replacement.  Clinical Manifestations:  Signs and symptoms of PKD result from loss of renal function and the increasing size of the kidneys as the cysts grow.  Renal damage can result in hematuria, polyuria, hypertension, development of renal calculi and associated urinary tract infections, and proteinuria.  The growing cysts are noted with reports of abdominal fullness and flank pain (back and lower sides).  Assessment and Diagnostic Findings:  Since PKD is a genetic disease, careful evaluation of family history is necessary.  Palpation of the abdomen will often reveal enlarged cystic kidneys.  Diagnosis is usually made with ultrasound imaging of the kidney (Porth & Matfin, 2009). Medical Management  PKD has no cure and treatment is largely supportive including blood pressure control, pain control, and antibiotics to resolve infections.  Once the kidneys fail, renal replacement therapy is indicated.  Genetic testing and counseling may be indicated.  RENAL CANCER:  The incidence of renal cell carcinoma is higher in both men and women with an increased body mass index. Tobacco use continues to be a significant risk factor for renal carcinoma.  These tumors may metastasize early to the lungs, bone, liver, brain, and contralateral kidney.  Clinical Manifestations:  Many renal tumors produce no symptoms and are discovered on a routine physical examination as a palpable abdominal mass.  The classic signs and symptoms, which occur in only 10% of patients, include hematuria, pain, and a mass in the flank (Cohen & McGovern, 2005).  The usual sign that first calls attention to the tumor is painless hematuria. There may be a dull pain in the back from the pressure produced by compression of the ureter. Colicky pains occur if a clot or mass of tumor cells passes down the ureter.  Symptoms from metastasis may be the first manifestations of renal tumor and may include unexplained weight loss, increasing weakness, and anemia.  Assessment and Diagnostic Findings:  The diagnosis of a renal tumor may require intravenous (IV) urography, cystoscopic examination, renal angiograms, or a CT scan.  Medical Management:  The goal of management is to eradicate the tumor before metastasis occurs.  Surgical Management  Nephrectomy  A radical nephrectomy is the preferred treatment if the tumor can be removed. This includes removal of the kidney (and tumor), adrenal gland, surrounding perinephric fat and fascia, and lymph nodes.  Radiation therapy, hormonal therapy, or chemotherapy may be used along with surgery. (Cohen & McGovern, 2005). Nursing Management:  After surgery, the patient usually has catheters and drains in place to maintain a patent urinary tract, to remove drainage, and to permit accurate measurement of urine output.  Because of the location of the surgical incision, the patient’s position during surgery, and the nature of the surgical procedure, pain and muscle soreness are common.  Pharmacologic management often includes immunosuppressant agents; therefore, patients are monitored for infection (Aschen- brenner, 2007).  The patient requires frequent analgesia during the post operative period and assistance with turning, coughing, use of incentive spirometry, and deep breathing to prevent atelectasis and other pulmonary complications.  Acute Renal Failure:  Treatment is aimed at replacing renal function temporarily to minimize potentially lethal complications and reduce potential causes of increased renal injury.  ARF is a problem seen in hospitalized patients and those in outpatient settings. ARF is increase in serum creatinine above baseline (Best & Counselman, 2008).  Urine volume may be normal, or changes may occur. Possible changes include oliguria (less than 500 mL/day), or anuria (less than 50 mL/day) (Counts,2008).  Pathophysiology:  Although the pathogenesis of ARF and oliguria is not always known, many times there is a specific underlying problem If these conditions are treated and corrected before the kidneys are permanently damaged, the increased BUN and creatinine levels, oliguria, and other signs may be reversed.  Categories of Acute Renal Failure:  The major categories of ARF are prerenal, intrarenal, and postrenal.  Prerenal ARF, which occurs in 60% to 70% of cases, is the result of impaired blood flow that leads to hypoperfusion of the kidney and a decrease in the GFR.  Intrarenal ARF is the result of actual parenchymal damage to the glomeruli or kidney tubules.  Causes of Acute Renal Failure:  Prerenal Failure  Volume depletion resulting from:  Hemorrhage  Renal losses (diuretics, osmotic diuresis)  Gastrointestinal losses (vomiting, diarrhea, nasogastric suction)  Impaired cardiac efficiency resulting from:  Myocardial infarction  Heart failure  Dysrhythmias  Cardiogenic shock  Vasodilation resulting from:  Sepsis  Anaphylaxis  Antihypertensive medications or other medications that cause vasodilation  Intrarenal Failure  Prolonged renal ischemia resulting from:  Pigment nephropathy  Myoglobinuria (trauma, crush injuries, burns)  Hemoglobinuria (transfusion reaction, hemolytic anemia)  Nephrotoxic agents such as:  Aminoglycoside antibiotics (gentamicin, tobramycin)  contrast agents  Heavy metals (lead, mercury)  Nonsteroidal anti-inflammatory drugs (NSAIDs)  Angiotensin-converting enzyme inhibitors (ACE inhibitors)  Infectious processes such as:  Acute pyelonephritis  Acute glomerulonephritis  Postrenal Failure Urinary tract obstruction, including:  Calculi (stones)  Tumors  Benign prostatic hyperplasia  Blood clots  Phases of Acute Renal Failure :  There are four phases of ARF: initiation, oliguria, diuresis, and recovery.  The oliguria period is accompanied by an increase in the serum concentration of substances (urea, creatinine, uric acid, organic acids, and the intracellular cations [potassium and magnesium]).  The minimum amount of urine needed to rid the body of normal metabolic waste products is 400 mL.  The oliguric phase of ARF may last 10 to 20 days,In this phase uremic symptoms first appear and life-threatening conditions such as hyperkalemia develop.  The diuresis period is marked by a gradual increase in urine output, which signals that glomerular filtration has started to recover. Laboratory values stabilize and eventually decrease.  The patient must be observed closely for dehydration during this phase; if dehydration occurs, the uremic symptoms are likely to increase.  The recovery period signals the improvement of renal function and may take 3 to 12 months. Laboratory values return to the patient’s normal level. Although a permanent 1% to 3% reduction in the GFR is common. Assessment and Diagnostic Findings:  In ARF, urine output varies from scanty to a normal volume.  hematuria may be present, and the urine has a low specific gravity.  One of the earliest manifestations of tubular damage is the inability to concentrate the urine (Porth & Matfin,2009).  Patients with prerenal azotemia have a decreased amount of sodium in the urine (less than 20 mEq/L).  Patients with intrarenal azotemia usually have urinary sodium levels greater than 40 mEq/L with urinary casts.  Ultrasonography is a critical component of the evaluation of patients with renal failure.  A renal sonogram or a CT or MRI scan may show evidence of anatomic changes. The BUN level increases steadily at a rate dependent on the degree of catabolism (breakdown of protein), renal perfusion, and protein intake.  Serum creatinine levels are useful in monitoring kidney function and disease progression and increase with glomerular damage.  With a decline in the GFR, oliguria, and anuria, patients are at high risk for hyperkalemia.  Hyperkalemia may lead to dysrhythmias, such as ventricular tachycardia and cardiac arrest.  Progressive metabolic acidosis occurs in renal failure.  There may be an increase in blood phosphate concentrations; calcium levels may be low due to decreased absorption of calcium from the intestine and as a compensatory mechanism for the elevated blood phosphate levels.  Anemia is another common laboratory finding in ARF, as a result of reduced erythropoietin production, uremic GI lesions, and blood loss from the GI tract.  Prevention:  ARF has a high mortality rate that ranges from 25% to 90%.  A careful history is obtained to identify exposure to nephrotoxic agents or environmental toxins.  The kidneys are susceptible to the adverse effects of medications.  Patients taking nephrotoxic medications (eg, aminoglycosides, gentamicin, amphotericin B, vancomycin, amikacin, cyclosporine) should be monitored closely for changes in renal function.  BUN and serum creatinine levels should be obtained at baseline within 24 hours after initiation of these medications and at least twice a week while the patient is receiving them.  Chronic use of analgesic agents, particularly nonsteroidal anti- inflammatory drugs (NSAIDs), may cause interstitial nephritis (inflammation within the renal tissue) and papillary necrosis.  Patients with heart failure or cirrhosis with ascites are at particular risk for NSAID-induced renal failure. Increased age, preexisting renal disease, and the simultaneous administration of several nephrotoxic agents increase the risk for kidney damage.  Radiocontrast-induced nephropathy is a major cause of hospital- acquired ARF.  Administration of N-acetylcysteine and sodium bicarbonate before and during procedures reduces risk, but prehydration with saline is considered the most effective method to prevent AKI (Barreto, 2007).  Medical Management:  The objectives of treatment of ARF are to restore normal chemical balance and prevent complications until repair of renal tissue and restoration of renal function can occur.  Management includes eliminating the underlying cause.  Prerenal azotemia is treated by optimizing renal perfusion, whereas postrenal failure is treated by relieving the obstruction. Intrarenal azotemia is treated with supportive therapy, with removal of causative agents.  Maintenance of fluid balance is based on daily body weight, fluid losses, blood pressure, and the clinical status of the patient.  Fluid excesses can be detected by the clinical findings of dyspnea, tachycardia, and distended neck veins. The patient’s lungs are auscultated for moist crackles. Because pulmonary edema may be caused by excessive administration of parenteral fluids.  The development of generalized edema is assessed by examining the presacral and pretibial areas several times daily. Mannitol (Osmitrol), furosemide (Lasix) may be prescribed to initiate diuresis.  If ARF is caused by hypovolemia secondary to hypoproteinemia, an infusion of albumin may be prescribed. Dialysis may be initiated to prevent complications of ARF, such as hyperkalemia, metabolic acidosis, and pulmonary edema.  Hemodialysis, peritoneal dialysis (PD), or a variety of continuous renal replacement therapies (CRRTs) (methods used to replace normal kidney function by circulating the patient’s blood through a hemofilter) may be performed.  Pharmacologic Therapy  Hyperkalemia is the most life-threatening of the fluid and electrolyte changes that occur in patients with renal disturbances.  Therefore, the patient is monitored for hyperkalemia through serial serum electrolyte levels, ECG changes (tall, tented, or peaked T waves), and changes in clinical status.  Other symptoms of hyperkalemia include irritability, abdominal cramping, diarrhea, and generalized muscle weakness. Muscle weakness may present, and difficulty breathing. As the potassium level increases, making this a true medical emergency (Counts, 2008).  The elevated potassium levels may be reduced by administering cation- exchange resins ( [Kayexalate]) orally or by retention enema. Kayexalate works by exchanging sodium ions for potassium ions in the intestinal tract.  If the patient is hemodynamically unstable (low blood pressure, changes in mental status, dysrhythmia), IV dextrose 50%, insulin, and calcium replacement may be administered to shift potassium back into the cells.  Albuterol sulfate (Ventolin HFA) by nebulizer can lower plasma potassium concentration by 0.5 to 1.5 mEq/L (Best & Counselman, 2008). The shift of potassium into the intracellular space is temporary, so arrangements for dialysis need to be made on an emergent basis.  In addition, many medications have been used in patients with ARF. Diuretic agents are often used to control fluid volume, but they have not been shown to improve recovery from ARF (Dirkes & Hodge, 2007).  In patients with severe acidosis, the arterial blood gases and serum bicarbonate levels must be monitored because the patient may require sodium bicarbonate therapy or dialysis. If respiratory problems develop, appropriate ventilatory measures must be instituted.  The elevated serum phosphate level may be controlled with phosphate- binding agents that help prevent a continuing rise in serum phosphate levels by decreasing the absorption of phosphate from the intestinal tract.  Nutritional Therapy  ARF causes severe nutritional imbalances (because nausea and vomiting contribute to inadequate dietary intake), impaired glucose use and protein synthesis, and increased tissue catabolism.  Replacement of dietary proteins is individualized to provide the maximum benefit and minimize uremic symptoms. Caloric requirements are met with high-carbohydrate meals, because carbohydrates have a protein- sparing effect. Foods and fluids containing potassium or phosphorus are restricted.  The oliguric phase of ARF which followed by the diuretic phase, at which time urine output begins to increase, along with assessment for overhydration or underhydration. Following the diuretic phase, the patient is placed on a high-protein, high-calorie diet and is encouraged to resume activities gradually. Nursing Management:  Monitoring Fluid and Electrolyte Balance  the nurse monitors the patient’s serum electrolyte levels and physical indicators of these complications during all phases of the disorder.  Hyperkalemia is the most immediate life-threatening imbalance seen in ARF.  all oral intake, and all medications are screened carefully to ensure that hidden sources of potassium are not administered or consumed.  The patient’s cardiac function and musculoskeletal status are monitored closely for signs of hyperkalemia.  The nurse monitors fluid status by urine output, apparent edema, distention of the jugular veins, alterations in heart sounds and breath sounds, and increasing difficulty in breathing. Accurate daily weights, as well as I&O records, are essential. Reducing Metabolic Rate:  The nurse takes steps to reduce the patient’s metabolic rate. Bed rest may be indicated to reduce exertion and the metabolic rate during the most acute stage of the disorder. Fever and infection, both of which increase the metabolic rate and catabolism, are prevented or treated promptly.  Promoting Pulmonary Function  Attention is given to pulmonary function, and the patient is assisted to turn, cough, and take deep breaths frequently to prevent atelectasis and respiratory tract infection.  Drowsiness and lethargy may prevent the patient from moving and turning without encouragement and assistance.  Preventing Infection  Asepsis is essential with invasive lines and catheters to minimize the risk of infection and increased metabolism. An indwelling urinary catheter is avoided whenever possible due to the high risk of UTI associated with its use but may be required to provide ongoing data required to monitor fluid I&O.  Providing Skin Care  The skin may be dry or susceptible to breakdown as a result of edema; therefore, meticulous skin care is important. Additionally, excoriation and itching of the skin may result from the deposit of irritating toxins in the patient’s tissues.  Providing Psychosocial Support Chronic Renal Failure (End-Stage Renal Disease):  Pathophysiology  As renal function declines, the end products of protein metabolism accumulate in the blood. Uremia develops and adversely affects every system in the body. The greater the buildup of waste products, the more pronounced the symptoms are.  The rate of decline in renal function and progression of ESRD is related to the underlying disorder, the urinary excretion of protein, and the presence of hypertension.  Clinical Manifestations  The severity of these signs and symptoms depends in part on other underlying conditions that founds, and the patient’s age.  Cardiovascular disease is the predominant cause of death in patients with ESRD (Burrows & Muller, 2007).  Patients complain of severe pain and discomfort. Restless leg syndrome and burning feet can occur in the early stage of uremic peripheral neuropathy (Phillips & Ryr, 2005; Slack & Landis, 2006). Assessment and Diagnostic Findings  Glomerular Filtration Rate  As the GFR decreases, the creatinine clearance decreases, while the serum creatinine and BUN levels increase. Serum creatinine is a more sensitive indicator of renal function than BUN. The BUN is affected not only by renal disease but also by protein intake in the diet, catabolism (tissue and RBC breakdown), and medications such as corticosteroids.  Sodium and Water Retention  Some patients retain sodium and water, increasing the risk for edema, heart failure, and hypertension. Hypertension may also result from activation of the renin–angiotensin–aldosterone axis and the concomitant increased aldosterone secretion.  Other patients have a tendency to lose sodium and run the risk of developing hypotension and hypovolemia. Vomiting and diarrhea may cause sodium and water depletion, which worsens the uremic state.  Acidosis  Metabolic acidosis occurs in ESRD.  Anemia  Anemia develops as a result of inadequate erythropoietin production, the shortened lifespan of RBCs, nutritional deficiencies, and the patient’s tendency to bleed, particularly from the GI tract.  Calcium and Phosphorus Imbalance  Serum calcium and phosphate levels have a reciprocal relationship in the body: As one increases, the other decreases. Complications  Potential complications of chronic renal failure that concern the nurse and necessitate a collaborative approach to care include the following:  Hyperkalemia due to decreased excretion, metabolic acidosis, catabolism, and excessive intake (diet, medications, fluids)  Pericarditis, pericardial effusion, and pericardial tamponade due to retention of uremic waste products and inadequate dialysis  Hypertension due to sodium and water retention and malfunction of the renin–angiotensin–aldosterone system  Anemia due to decreased erythropoietin production, decreased RBC lifespan, bleeding in the GI tract from irritating toxins and ulcer formation, and blood loss during hemodialysis  Bone disease and metastatic and vascular calcifications due to retention of phosphorus, low serum calcium levels, abnormal vitamin D metabolism, and elevated aluminum levels  Medical Management  Pharmacologic Therapy  Complications can be prevented or delayed by administering prescribed phosphate-binding agents, calcium supplements, antihypertensive and cardiac medications, antiseizure medications, and erythropoietin.  Calcium and Phosphorus Binders  Hyperphosphatemia and hypocalcemia are treated with medications that bind dietary phosphorus in the GI tract.  Binders such as calcium carbonate or calcium acetate are prescribed, but there is a risk of hypercalcemia. These medications bind dietary phosphorus in the intestinal tract. All binding agents must be administered with food to be effective.  Antihypertensive and Cardiovascular Agents  Hypertension is managed by intravascular volume control and a variety of antihypertensive agents. Heart failure and pulmonary edema may also require treatment with fluid restriction, low-sodium diets, diuretic agents. The metabolic acidosis of ESRD usually produces no symptoms and requires no treatment; however, sodium bicarbonate supplements or dialysis may be needed to correct the acidosis if it causes symptoms (Molzahn & Butera,2006).  Antiseizure Agents  Neurologic abnormalities may occur, so the patient must be observed for early evidence of slight twitching, headache, delirium, or seizure activity.  If seizures occur, the onset of the seizure is recorded along with the type, duration, and general effect on the patient. The physician is notified immediately.  IV diazepam (Valium) or phenytoin (Dilantin) is usually administered to control seizures.  The side rails of the bed should be raised and padded to protect the patient.  Erythropoietin  Erythropoietin is administered intravenously or subcutaneously three times a week in ESRD.  It may take 2 to 6 weeks for the hematocrit to increase; therefore, the medication is not indicated for patients who need immediate correction of severe anemia.  Management involves adjustment of heparin to prevent clotting of the lines during hemodialysis treatments.  frequent monitoring of hemoglobin and hematocrit, and periodic assessment of serum iron and transferrin levels. Because adequate stores of iron are necessary for an adequate response to erythropoietin, supplementary iron may be prescribed. Common iron supplements include iron sucrose (Venofer).  the patient’s blood pressure and serum potassium level are monitored to detect hypertension and increasing serum potassium levels.  Nutritional Therapy  adequate caloric intake and vitamin supplementation must be ensured. Protein is restricted because urea, uric acid, and organic acids—the breakdown products of dietary and tissue proteins—accumulate rapidly in the blood when there is impaired renal clearance.  The allowed protein must be of high biologic value.High-biologic-value proteins are those that are complete proteins and supply the essential amino acids necessary for growth and cell repair.  Usually, the fluid allowance per day is 500 mL to 600 mL more than the previous day’s 24-hour urine output. Calories are supplied by carbohydrates and fat to prevent wasting.  Vitamin supplementation is necessary because a protein restricted diet does not provide the necessary complement of vitamins. Additionally, the patient on dialysis may lose water-soluble vitamins during the dialysis treatment.  Dialysis  The patient with increasing symptoms of renal failure is referred to a dialysis and transplantation center early in the course of progressive renal disease.  Nursing Management  The patient with ESRD requires astute nursing care to avoid the complications of reduced renal function and the stresses and anxieties of dealing with a life-threatening illness.  Nursing care is directed toward assessing fluid status and identifying potential sources of imbalance, implementing a dietary program to ensure proper nutritional intake within the limits of the treatment regimen, and promoting positive feelings by encouraging increased self-care and greater independence.  A great deal of emotional support is needed by the patient and family because of the numerous changes experienced.  Promoting Home and Community-Based Care:  Teaching Patients Self-Care  A referral to a nutritionist is made because of the dietary changes required.  The patient is taught how to check the vascular access device for patency and appropriate precautions, such as avoiding venipuncture and blood pressure measurements on the arm with the access device.  the patient and family need to know what problems to report to the health care provider. These include the following:  Worsening signs and symptoms of renal failure (nausea, vomiting, change in usual urine output)  Signs and symptoms of hyperkalemia (muscle weakness, diarrhea, abdominal cramps)  Signs and symptoms of access problems (clotted fistula or graft, infection)  These signs and symptoms of decreasing renal function, in addition to increasing BUN and serum creatinine levels, may indicate a need to alter the dialysis prescription. Some elderly patients elect not to undergo dialysis or transplantation. Conservative management, including nutritional therapy, fluid control, and medications such as phosphate binders, may be considered in patients who are not suitable for or elect not to have dialysis or transplantation. RENAL REPLACEMENT THERAPIES  the need for replacement therapy can be acute (short term) or chronic (long term). The main renal replacement therapies include the various types of dialysis and kidney transplantation.  Dialysis Types of dialysis include hemodialysis, CRRT, and PD.  Acute dialysis is indicated when there is a high and increasing level of serum potassium, fluid overload, or impending pulmonary edema, increasing acidosis, pericarditis, and severe confusion. It may also be used to remove medications or toxins (poisoning or medication overdose) from the blood or for edema that does not respond to other treatment, hepatic coma, hyperkalemia, hypercalcemia, hypertension, and uremia (Mosenkis, Kirk & Berns, 2006).  HEMODIALYSIS  More than 90% of patients requiring long-term renal replacement therapy are on chronic hemodialysis (USRDS, 2007).  Most patients receive intermittent hemodialysis that involves treatments three times a week with the average treatment duration of 3 to 4 hours in an outpatient setting.  Vascular Access: Several types of access are available.  Vascular Access Devices Immediate access to the patient’s circulation for acute hemodialysis is achieved by inserting a double-lumen, large-bore catheter into the subclavian, internal jugular, or femoral vein by the physician. This method of vascular access involves some risk (eg, hematoma, pneumothorax, infection, thrombosis of the subclavian vein, inadequate flow). The catheter is removed when no longer needed. Since these catheters have cuffs under the skin, the insertion site heals, sealing the wound and reducing the risk for ascending infection.  Arteriovenous Fistula The preferred method of permanent access is an arteriovenous fistula (AVF) by joining (anastomosing) an artery to a vein. This access will need time, (2 to 3 months) to “mature” before it can be used. As the AVF matures.  Arteriovenous Graft  An arteriovenous graft can be created by subcutaneously interposing a biologic, semibiologic, or synthetic graft material between an artery and vein.  Usually a graft is created when the patient’s vessels are not suitable for creation of an AV fistula. Patients with compromised vascular systems (eg, from diabetes) will require a graft because their native vessels are not suitable for creation of an AV Fistula.  Complications:  With the initiation of dialysis, disturbances of lipid metabolism (hypertriglyceridemia) are accentuated and contribute to cardiovascular complications. Heart failure, coronary heart disease, angina, stroke, and peripheral vascular insufficiency may occur and can incapacitate the patient.  Cardiovascular disease remains the leading cause of death in patients receiving dialysis (Burrows & Muller, 2007).  Anemia is compounded by blood lost during hemodialysis.  Gastric ulcers may result from the physiologic stress of chronic illness, medication, and preexisting medical conditions (eg, diabetes).  Vomiting may occur during the hemodialysis treatment when rapid fluid shifts and hypotension occur. These contribute to the malnutrition seen in patients on dialysis.  Worsening calcium metabolism and renal osteodystrophy can result in bone pain and fractures, interfering with mobility.  As time on dialysis continues, calcification of major blood vessels has been reported and linked to hypertension and other vascular complications.  Phosphorus deposits in the skin can occur and cause itching. Other complications of dialysis treatment may include the following:  Episodes of shortness of breath often occur as fluid accumulates between dialysis treatments.  Hypotension may occur during the treatment as fluid is removed. Nausea and vomiting, diaphoresis, tachycardia, and dizziness are common signs of hypotension.  Painful muscle cramping may occur, usually late in dialysis as fluid and electrolytes rapidly leave the extracellular space.  Dysrhythmias may result from electrolyte and pH changes.  Air embolism is rare but can occur if air enters the vascular system.  Chest pain may occur in patients with anemia or arteriosclerotic heart disease.  Nursing Management:  During dialysis, the patient, the dialyzer, and the dialysate bath require constant monitoring because numerous complications are possible.  Nursing care of the patient and maintenance of the vascular access device are especially important.  Promoting Pharmacologic Therapy  Many medications are removed from the blood during hemodialysis; therefore, dosage or timing of the medication administration may require adjustment.  Medications that are water soluble are readily removed during hemodialysis treatment and those that are fat soluble or adhere to other substances (like albumin) are not dialyzed out very well.  The patient must know when and when not to take the medication. For example, if an antihypertensive agent is taken on a dialysis day, hypotension may occur during dialysis, causing dangerously low blood pressure.  Promoting Nutritional and Fluid Therapy  Goals of nutritional therapy are to minimize uremic symptoms and fluid and electrolyte imbalances; to maintain good nutritional status through adequate protein, calorie, vitamin, and mineral intake; and to enable the patient to eat a palatable and enjoyable diet.  Restricting dietary protein decreases the accumulation of nitrogenous wastes, and may even post-pone the initiation of dialysis for a few months. Restriction of fluid is also part of the dietary prescription because fluid accumulation may occur, leading to weight gain, heart failure, and pulmonary edema.  With the initiation of hemodialysis, the patient usually requires some restriction of dietary protein, sodium, potassium, and fluid intake  If the restrictions are ignored, life-threatening complications, such as hyperkalemia and pulmonary edema, may result.  Meeting Psychosocial Needs  Dialysis alters the lifestyle of the patient and family. The amount of time required for dialysis and physician visits and being chronically ill can create conflict, frustration, guilt, and depression. It may be difficult for the patient, spouse, and family to express anger and negative feelings.  Counseling and psychotherapy may be necessary. Depression may require treatment with antidepressant agents.  Home Hemodialysis:  The patient undergoing home hemodialysis and the caregiver assisting that patient must be trained to prepare, operate, and disassemble the dialysis machine; maintain and clean the equipment; administer medications (eg, heparin) into the machine lines; and handle emergency problems.  Once home hemodialysis is initiated, the home care nurse must visit periodically to evaluate compliance with the recommended techniques, to assess the patient for complications, to reinforce previous teaching, and to provide reassurance.  CONTINUOUS RENAL REPLACEMENT THERAPIES  Continuous renal replacement therapies (CRRTs) may be indicated for patients with acute or chronic renal failure who are too clinically unstable for traditional hemodialysis.  for patients with fluid overload secondary to oliguric (low urine output) renal failure, and for patients whose kidneys cannot handle their acutely high metabolic or nutritional needs.  CRRT does not produce rapid fluid shifts, does not require dialysis machines or dialysis personnel to carry out the procedures, and can be initiated quickly.  PERITONEAL DIALYSIS:  PD may be the treatment of choice for patients with renal failure who are unable or unwilling to undergo hemodialysis or renal transplantation.  Patients who are susceptible to the rapid fluid, electrolyte, and metabolic changes that occur during hemodialysis experience fewer of these problems with the slower rate of PD.  Therefore, patients with diabetes or cardiovascular disease, many older patients, and those who may be at risk for adverse effects of systemic heparin are likely candidates for PD.  In PD, the peritoneal membrane that covers the abdominal organs and lines the abdominal wall serves as the semipermeable membrane.  PD usually takes 36 to 48 hours to achieve what hemodialysis accomplishes in 6 to 8 hours.  Preparing the Patient  Baseline vital signs, weight, and serum electrolyte levels are recorded.  Evaluation of the abdomen for placement of the catheter is done to facilitate self-care.  Typically the catheter is placed on the nondominant side to allow the patient easier access to the catheter connection site when exchanges are done.  The patient is encouraged to empty the bladder and bowel to reduce the risk of puncture of internal organs during the insertion procedure. Complications:  Acute Complications:  Peritonitis  Peritonitis is the most common and serious complication of PD. The first sign of peritonitis is cloudy dialysate drainage fluid.  Diffuse abdominal pain and rebound tenderness occur much later. Hypotension and other signs of shock may also occur with advancing infection.  Drainage fluid is examined for cell count; Gram stain and culture are used to identify the organism and guide treatment.  Antibiotic agents (aminoglycosides or cephalosporins) are usually added. Intraperitoneal administration of antibiotics is as effective as IV administration and therefore most often used. Antibiotic therapy continues for 10 to 14 days.  Careful selection and calculation of the antibiotic dosage are needed to prevent nephrotoxicity and further compromise of residual renal function.  Leakage  Leakage of dialysate through the catheter site may occur immediately after the catheter is inserted.  During this time, it is important to reduce factors that might delay healing, such as undue abdominal muscle activity and straining during bowel movement. In many cases, leakage can be avoided by using small volumes (500 mL) of dialysate, gradually increasing the volume up to 2000 to 3000 mL.  Bleeding  A bloody effluent (drainage) may be observed occasionally, especially in young, menstruating women. (The hypertonic fluid pulls blood from the uterus, through the opening in the fallopian tubes, and into the peritoneal cavity.)  Bleeding is also common during the first few exchanges after a new catheter insertion because some blood enters the abdominal cavity following insertion  obstructing the catheter.  Long-Term Complications  Hypertriglyceridemia is common in patients undergoing long-term PD,Given the high burden of disease in these patients, beta-blockers and ACE inhibitors should be used to control hypertension or protect the heart, and the use of aspirin and statins should be considered.  Other complications that may occur with long-term PD include abdominal hernias probably resulting from continuously increased intra- abdominal pressure. The persistently elevated intra-abdominal pressure also aggravates symptoms of hiatal hernia and hemorrhoids. Low back pain and anorexia from fluid in the abdomen.  To reduce the risk of peritonitis, the patient (and all caregivers) must use meticulous care to avoid contaminating the catheter, fluid, or tubing and to avoid accidentally disconnecting the catheter from the tubing.  Whenever a connection/disconnection is made, hands must be washed and a mask worn by anyone within 6 feet of the area to avoid contamination with airborne bacteria.  Excess manipulation should be avoided and meticulous care of the catheter entry site is provided using a standardized protocol.  Although PD is not as efficient as hemodialysis in removing solute and fluid, it permits a more gradual change in the patient’s fluid volume status and in waste product removal.  Therefore, it may be the treatment of choice for the hemodynamically unstable patient. Exchange times range from 30 minutes to 2 hours.  Nursing Management:  Meeting Psychosocial Needs  In addition to the complications of PD previously described, patients who elect to do PD may experience altered body image because of the presence of the abdominal catheter, bag, tubing, and cycler. Waist size increases from 1 to 2 inches (or more) with fluid in the abdomen.  They may experience depression because they feel overwhelmed with the responsibility of self-care.  Teaching Patients Self-Care,Training usually takes 5 days to 2 weeks.  Vital signs, weight, I&O, laboratory values, and patient status are frequently monitored.  The nurse uses a flow sheet to document each exchange and records vital signs.  The nurse also carefully assesses skin turgor and mucous membranes to evaluate fluid status and monitor the patient for edema.  If the peritoneal fluid does not drain properly, the nurse can facilitate drainage by turning the patient from side to side or raising the head of the bed.  The nurse monitors for complications, including peritonitis, bleeding, respiratory difficulty, and leakage of peritoneal fluid.  Abdominal girth may be measured periodically to determine if the patient is retaining large amounts of dialysis solution.  Additionally, the nurse must ensure that the PD catheter remains secure and that the dressing remains dry.  The patient and family are educated about the procedure and are kept informed about progress.  Because of protein loss with continuous PD, the patient is instructed to eat a high-protein, well-balanced diet.  The patient is also encouraged to increase his or her daily fiber intake to help prevent constipation.  Potassium, sodium, and fluid restrictions are not usually needed. Patients commonly lose about 2 to 3 L of fluid over and above the volume of dialysate infused into the abdomen during a 24-hour period, permitting a normal fluid intake even in an anephric patient (a patient without kidneys). SPECIAL CONSIDERATIONS: NURSING MANAGEMENT OF THE HOSPITALIZED PATIENT ON DIALYSIS:  Protecting Vascular Access  When the patient undergoing hemodialysis is hospitalized for any reason, care must be taken to protect the vascular access.  The nurse assesses the vascular access for patency and takes precautions to ensure that the extremity with the vascular access is not used for measuring blood pressure or for obtaining blood specimens; tight dressings, restraints, or jewelry over the vascular access must be avoided as well.  The bruit, or “thrill,” over the venous access site must be evaluated at least every 8 hours. Absence of a palpable thrill or audible bruit may indicate blockage or clotting in the vascular access.  Clotting can occur if the patient has an infection anywhere in the body (serum viscosity increases) or if the blood pressure has dropped. When blood flow is reduced through the access for any reason (hypotension, application of blood pressure cuff or tourniquet), the access can clot.  If a patient has a hemodialysis catheter or implanted hemodialysis access device, the nurse must observe for signs and symptoms of infection such as redness, swelling, drainage from the exit site, fever, and chills.  The nurse must assess the integrity of the dressing and change it as needed.  Taking Precautions During Intravenous Therapy  When the patient needs IV therapy, the rate of administration must be as slow as possible and should be strictly controlled by a volumetric infusion pump. Because patients on dialysis cannot excrete water, rapid or excessive administration of IV fluid can result in pulmonary edema.  Accurate intake and output records are essential.  Monitoring Symptoms of Uremia  As metabolic end products accumulate, symptoms of uremia worsen. Patients whose metabolic rate accelerates (those receiving corticosteroid medications or parenteral nutrition, those with infections or bleeding disorders, those undergoing surgery) accumulate waste products more quickly and may require daily dialysis.  Detecting Cardiac and Respiratory Complications As fluid builds up, fluid overload, heart failure, and pulmonary edema develop. Crackles in the bases of the lungs may indicate pulmonary edema.  Pericarditis may result from the accumulation of uremic toxins. If not detected and treated promptly, this serious complication may progress to pericardial effusion and cardiac tamponade. Pericarditis is detected by the patient’s report of substernal chest pain (if the patient can communicate), low-grade fever, and pericardial friction rub. A pulsus paradoxus (a decrease in blood pressure of more than 10 mm Hg during inspiration) is often present.  The effusion may progress to life-threatening cardiac tamponade, noted by narrowing of the pulse pressure in addition to muffled or inaudible heart sounds, crushing chest pain, dyspnea, and hypotension.  Controlling Electrolyte Levels and Diet Serum laboratory values are assessed daily. If blood transfusions are required, they may be administered during hemodialysis, if possible, so that excess potassium can be removed.  Dietary intake must also be monitored. Hypoalbuminemia is an indicator of malnutrition in patients undergoing long-term or maintenance dialysis.  Managing Discomfort and Pain Complications such as pruritus and pain secondary to neuropathy must be managed. Antihistamine agents, are commonly ever, because elimination of the metabolites of medications occurs through dialysis rather than through renal excretion. medication dosages may need to be adjusted. Keeping the skin clean and well moisturized using creams or lotions helps promote comfort and reduce itching.  Monitoring Blood Pressure Hypertension in renal failure is common. It is usually the result of fluid overload and, in part, oversecretion of renin. Antihypertensive agents must be withheld before dialysis to avoid hypotension due to the combined effect of the dialysis and the medication.  Preventing Infection Patients with ESRD commonly have low WBC counts, low RBC counts (anemia), and impaired platelet function. Together, these pose a high risk for infection and potential for bleeding after even minor trauma. Preventing and controlling infection are essential because the incidence of infection is high. Infection of the vascular access site and pneumonia are common. And through caring for the Catheter Site.  Administering Medications All medications and the dosage prescribed for any patient on dialysis must be closely monitored to avoid those that are toxic to the kidneys and may threaten remaining renal function. Medications are also scrutinized for potassium and magnesium content, because medications containing potassium or magnesium must be avoided.  Providing Psychological Support  Patients undergoing dialysis for a while may begin to reevaluate their status, the treatment modality, their satisfaction with life, and the impact of these factors on their families and support systems.  KIDNEY SURGERY  A patient may undergo surgery to remove obstructions that affect the kidney (tumors or calculi), to insert a tube for draining the kidney (nephrostomy, ureterostomy), or to remove the kidney involved in unilateral kidney disease, renal carcinoma, or kidney transplantation.  Management of Patients Undergoing Kidney Surgery:  Preoperative Considerations Fluids are encouraged to promote increased excretion of waste products before surgery unless contraindicated because of preexisting renal or cardiac dysfunction. If kidney infection is present preoperatively, broad-spectrum antimicrobial agents may be prescribed to prevent bacteremia. Coagulation studies (prothrombin time, partial thromboplastin time, platelet count) may be indicated if the patient has a history of bruising and bleeding.  Postoperative Management Because the kidney is a highly vascular organ, hemorrhage and shock are the chief complications of renal surgery. Fluid and blood component replacement is frequently necessary in the immediate postoperative period to treat intraoperative blood loss. Abdominal distention and paralytic ileus are fairly common after renal and ureteral surgery and are thought to be due to a reflex paralysis of intestinal peristalsis and manipulation of the colon or duodenum during surgery. Abdominal distention is relieved by decompression through a nasogastric tube. Oral fluids are permitted when the passage of flatus is noted.  If infection occurs, antibiotics are prescribed after a culture reveals the causative organism.  The toxic effects that antibiotic agents have on the kidneys (nephrotoxicity) must be kept in mind when assessing the patient.  Low-dose heparin therapy may be initiated postoperatively to prevent thromboembolism in patients who had any type of urologic surgery. Nursing Management:  Providing Immediate Postoperative Care  Immediate postoperative care of the patient who has undergone surgery of the kidney includes assessment of all body systems. Respiratory and circulatory status.  pain level: Abdominal distention, which increases discomfort, is also noted.  fluid and electrolyte status.  and patency and adequacy of urinary drainage systems are assessed: Urine output and drainage from tubes inserted during surgery are monitored for amount, color, and type or characteristics.  Monitoring and Managing Potential Complications:  Bleeding is a major complication of kidney surgery. If undetected and untreated it can result in hypovolemia and hemorrhagic shock.  The nurse’s role is to monitoring of vital signs, skin condition, the urinary drainage system, the surgical incision, and the level of consciousness is necessary to detect evidence of bleeding, decreased circulating blood, and fluid volume and cardiac output.  Frequent monitoring of vital signs (initially monitored at least at hourly intervals) and urinary output is necessary for early detection of these complications.  If bleeding goes undetected or is not detected promptly, the patient may lose significant amounts of blood and may experience hypoxemia.  Bleeding may be suspected when the patient experiences fatigue and when urine output is less than 30 mL/h. As bleeding persists, late signs of hypovolemia occur, such as cool skin, flat neck veins, and change in level of consciousness or responsiveness.  Pneumonia may be prevented through use of an incentive spirometer, adequate pain control, and early ambulation.  Early signs of pneumonia include fever, increased heart and respiratory rates, and adventitious breath sounds.  Preventing infection is the rationale for using asepsis when changing dressings and handling and preparing catheters, other drainage tubes, central venous catheters, and IV catheters for administration of fluids. Insertion sites are monitored closely for signs and symptoms of inflammation.  Antibiotics are commonly administered postoperatively to prevent infection. If antibiotic agents are prescribed, serum creatinine and BUN values must be monitored closely because many antibiotic agents are toxic to the kidney or can accumulate to toxic levels if renal function is decreased.  Preventing fluid imbalance is critical when caring for a patient undergoing kidney surgery, because both fluid loss and fluid excess are possible adverse effects of the surgery.  Fluid loss may occur during surgery as a result of excessive urinary drainage when the obstruction is removed, or it may occur if diuretic agents are used.  Astute assessment skills are needed to detect early signs of fluid excess (such as weight gain, shortness of breath).  Fluid excess may be treated with fluid restriction and administration of furosemide (Lasix) or other diuretic agents.  Deep venous thrombosis (DVT) may occur postoperatively because of surgical manipulation of the iliac vessels during surgery or prolonged immobility.  Anti-embolism stockings are applied, and the patient is monitored closely for signs and symptoms of thrombosis and encouraged to exercise the legs.  Heparin may be administered postoperatively to reduce the risk of thrombosis. Promoting Home and Community-Based Care:  Teaching Patients Self-Care  preventing infection. Verbal and written instructions and guidelines are provided to the patient and family at the time of hospital discharge.  The importance of strategies to prevent postoperative complications (urinary tract infection and obstruction, DVT, atelectasis, and pneumonia) is stressed to the patient and family.  Kidney Transplantation:  Kidney transplantation is an elective procedure, not an emergency life- saving procedure. Therefore, patients should be in the best possible condition prior to transplantation.  Kidney transplantation involves transplanting a kidney from a living donor or deceased donor to a recipient who no longer has renal function  Transplantation from well-matched living donors who are related to the patient (those with compatible ABO and human leukocyte antigens) is slightly more successful than from cadaver donors.  The success rate further increases if kidney transplantation from a living donor is performed before dialysis is initiated (Danovitch, 2005).  Not everyone is suitable for a kidney transplant. Contraindications include recent malignancy, active or chronic infection, severe irreversible extrarenal disease (chronic lung disease, severe peripheral vascular disease), active autoimmune disease (eg, hepatitis B and C), morbid obesity (body mass index greater than 35).  Donors may be rejected for the same reasons that is determined to have an impact on the remaining kidney. Examples include hypertension and diabetes mellitus since both are known causes of renal disease.  Every precaution must be taken to ensure that the remaining kidney in the donor will remain healthy. If these conditions are met, the donor should remain healthy after donation and have a normal lifespan.  Once the blood supply has been reestablished to the transplanted kidney in the operating room, urine should begin to flow. The production of urine at this stage is an important indicator of the overall success of the procedure. Medical Management A complete physical examination is performed to detect and treat any conditions that could cause complications after transplantation. Tissue typing, blood typing, and antibody screening are performed to determine compatibility of the tissues and cells of the donor and recipient.  The patient must be free of infection at the time of renal transplantation, because after surgery medications to prevent transplant rejection will be prescribed.  These medications suppress the immune response, leaving the patient immunosuppressed and at risk for infection. Therefore, the patient is evaluated and treated for any infections, including gingival (gum) disease and dental caries.  A psychosocial evaluation is conducted to assess the patient’s ability to adjust to the transplant, coping styles, social history, social support available, and financial resources.  A history of psychiatric illness is important to obtain because psychiatric conditions are often aggravated by the corticosteroids needed for immunosuppression after transplantation.  If a dialysis routine has been established, hemodialysis is often performed the day before the scheduled transplantation procedure to optimize the patient’s physical status.  Nursing Management  Patient teaching addresses postoperative, pain management options, dietary restrictions, IV and arterial lines, tubes, and early ambulation.  The patient who receives a kidney from a living related donor may be concerned about the donor and how the donor will tolerate the surgical procedure.  The goal of care is to maintain homeostasis until the transplanted kidney is functioning well. The patient whose kidney functions immediately has a more favorable prognosis than the patient whose kidney does not.  Medical Management:  After a kidney transplant, rejection and failure can occur within 24 hours (hyperacute), within 3 to 14 days (acute), or after many years.  The long-term survival of a transplanted kidney depends on how well it matches the recipient and how well the body’s immune response is controlled.  To overcome or minimize the body’s defense mechanisms, immunosuppressive agents are administered. Optimally, medications modify the immune system enough to prevent rejection, but not enough to allow infections or malignancies to occur.  Combinations of glucocorticoids and medications specifically developed to affect the action of lymphocytes are used to minimize the body’s reaction.  The risks associated with taking these medications include nephrotoxicity, hypertension, hyperlipidemia, hirsutism, tremors, blood dyscrasias, cataracts, gingival hyperplasia, and several types of cancer (American Nephrology Nurses Association, 2006).  Patients receiving cyclosporine may not exhibit the usual signs and symptoms of acute rejection. In these patients, the only sign may be an asymptomatic rise in the serum creatinine level (more than a 20% rise is considered acute rejection).  Nursing Management:  the nurse assesses the patient for signs and symptoms of transplant rejection:  Oliguria.  edema.  fever.  increasing blood pressure.  weight gain, and swelling or tenderness over the transplanted kidney or graft.  Preventing Infection  The patient is closely monitored for infection because of susceptibility to impaired healing and infection related to immunosuppressive therapy and complications of renal failure.  Clinical manifestations of infection include shaking chills, fever, rapid heartbeat (tachycardia), and respirations (tachypnea), as well as either an increase or a decrease in WBCs (leukocytosis or leukopenia).  Urine cultures are performed frequently because of the high incidence of UTI during early and late stages of transplantation.  Any type of wound drainage should be viewed as a potential source of infection because drainage is an excellent culture medium for bacteria.  Catheter and drain tips may be cultured when removed by cutting off the tip of the catheter or drain.  The nurse ensures that the patient is protected from exposure to infection by hospital staff, visitors, and other patients with active infections.  Attention to hand hygiene by all who come in contact with the patient is imperative.  Monitoring Urinary Function  A kidney from a living donor related to the patient usually begins to function immediately after surgery and may produce large quantities of dilute urine.  A kidney from a cadaver donor may undergo acute tubular necrosis and therefore may not function for 2 or 3 weeks, during which time anuria, oliguria, or polyuria may be present.  Therefore, careful monitoring is indicated. The output from the urinary catheter (connected to a closed drainage system) is measured every hour. IV fluids are administered on the basis of urine volume and serum electrolyte levels. Hemodialysis may be necessary postoperatively to maintain homeostasis until the transplanted kidney is functioning well.  After successful renal transplantation, the vascular access device may clot, possibly from improved coagulation with the return of renal function.  GI ulceration and corticosteroid-induced bleeding may occur.  Fungal colonization of the GI tract (especially the mouth) and urinary bladder may occur secondary to corticosteroid and antibiotic therapy.  Closely monitoring the patient and notifying the physician about the occurrence of these complications are important nursing interventions.  In addition, the patient is monitored closely for signs and symptoms of adrenal insufficiency if the treatment has included use of corticosteroids.  Promoting Home and Community-Based Care:  Teaching Patients Self-Care. The nurse works closely with the patient and family to be sure that they understand the need for continuing immunosuppressive therapy as prescribed.  Additionally, the patient and family are instructed to assess for and report signs and symptoms of transplant rejection, infection, or significant adverse effects of the immunosuppressive regimen.  These include decreased urine output; weight gain; malaise; fever; respiratory distress; tenderness over the transplanted kidney; anxiety; depression; and changes in blood pressure.  The patient is instructed to inform other health care providers (eg, dentist) about the kidney transplant and the use of immunosuppressive agents.  Continuing Care. The patient needs to know that follow up care after transplantation is a lifelong necessity.  Individual verbal and written instructions are provided concerning diet, medication, fluids, daily weight, daily measurement of urine, management of I&O, prevention of infection, resumption of activity, and avoidance of contact sports in which the transplanted kidney may be injured.