Genitourinary_System

Glomerulonephritis is a term that refers to a group of kidney disorders characterized by inflammatory injury in the glomerulus, most of which are caused by an immunological reaction. 2. The disorder results in proliferative and inflammatory changes within the glomerular structure. 3. Destruction, inflammation, and sclerosis of the glomeruli of the kidneys occur. 4. Inflammation of the glomeruli results from an antigen-antibody reaction produced by an infection elsewhere in the body. 5. Loss of kidney function develops. B. Causes 1. Immunological diseases 2. Autoimmune diseases 3. Antecedent group A beta-hemolytic streptococcal infection of the pharynx or skin 4. History of pharyngitis or tonsillitis 2 to 3 weeks before Symptoms TYPES Acute: Occurs 2 to 3 weeks after a streptococcal infection Chronic: Can occur after the acute phase or slowly over time COMPLICATIONS 1. Renal Failure 2. Hypertensive encephalopathy 3. Pulmonary edema 4. Heart failure SIGNS AND SYMPTOMS Assessment 1. Periorbital and facial edema that is more prominent in the morning 2. Anorexia 3. Decreased urinary output 4. Cloudy, smoky, brown-colored urine (hematuria) 5. Pallor, irritability, lethargy 6. In the older child, headaches, abdominal or flank pain, dysuria 7. Hypertension 8. Proteinuria that produces a persistent and excessive foam in the urine 9. Azotemia 10. Increased blood urea nitrogen and creatinine levels 11. Increased antistreptolysin O titer (used to diagnose disorders caused by streptococcal infections) MANAGEMENT 1. Monitor vital signs, weight, intake and output, and the characteristics of urine. 2. Limit activity; provide safety measures. 3. Provide high-quality nutrient foods. a. Restrictions depend on the stage and severity of the disease, especially the extent of the edema. b. In uncomplicated cases, a regular diet is permitted but sodium is restricted to a “no added salt to foods” diet. c. Moderate sodium restriction is prescribed for the child with hypertension or edema. d. Foods high in potassium are restricted during periods of oliguria. e. Protein is restricted if the child has severe azotemia resulting from prolonged oliguria. 4. Monitor for complications (e.g., renal failure, hypertensive encephalopathy, seizures, pulmonary edema, heart failure). 5. Administer diuretics (if significant edema and fluid overload are present), antihypertensives (for hypertension), and antibiotics (to the child with evidence of persistent streptococcal infections) as prescribed. 6. Initiate seizure precautions and administer anticonvulsants as prescribed for seizures associated with hypertensive encephalopathy. 7. Instruct the parents to report signs of bloody urine, headache, or edema. 8. Instruct the parents that the child needs to obtain appropriate adequate treatment for infections, specifically for sore throats, upper respiratory infections, and skin infections. AGN * is an inflammation of the glomerular capillaries NEPHROTIC SYNDROME Nephrotic syndrome * is a primary glomerular disease characterized by the following: • Marked increase in protein in the urine (proteinuria) • Decrease in albumin in the blood (hypoalbuminemia) • Edema • High serum cholesterol and low-density lipoproteins (hyperlipidemia) * seriously damages the glomerular capillary membrane and results in increased glomerular permeability. * characterized by the loss of plasma protein, particularly albumin, in the urine. Although the liver is capable of increasing the production of albumin, it cannot keep up with the daily loss of albumin through the kidneys. Thus, hypoalbuminemia results CAUSES * chronic glomerulonephritis * diabetes mellitus with intercapillary glomerulosclerosis * amyloidosis of the kidney * systemic lupus erythematosus * multiple myeloma * renal vein thrombosis SIGNS AND SYMPTOMS * edema {soft and pitting most commonly occurs around the eyes (periorbital), in dependent areas (sacrum, ankles, and hands), and in the abdomen (ascites)} * malaise * headache * irritability * fatigue * Proteinuria (predominately albumin) exceeding 3 to 3.5 g/ { sufficient for the diagnosis of nephrotic syndrome } COMPLICATIONS * infection (due to a deficient immune response) * thromboembolism (especially of the renal vein) * pulmonary emboli * acute renal failure (due to hypovolemia) * accelerated atherosclerosis (due to hyperlipidemia) DIAGNOSTIC EXAMINATION * Protein electrophoresis and immunoelectrophoresis {performed on the urine to categorize the type of proteinuria} * needle biopsy of the kidney {for histologic examination of renal tissue to confirm the diagnosis} * Anti-C1q antibodies –A Recent studies have confirmed the usefulness of serum markers as a means of assessing the disease process. This is the most reliable markers for assessing disease activity in lupus nephritis (Moroni et al., 2001)} MANAGEMENT (objective is to preserve renal function) MEDICAL * Diuretic agents may be prescribed for the patient with severe edema; however, caution must be used because of the risk of reducing the plasma volume to the point of impaired circulation with subsequent prerenal acute renal failure. * The use of angiotensin-converting enzyme (ACE) inhibitors in combination with diuretics often reduces the degree of proteinuria but may take 4 to 6 weeks to be effective. * antineoplastic agents (cyclophosphamide [Cytoxan]) or immunosuppressant medications (azathioprine [Imuran], chlorambucil [Leukeran], or cyclosporine). It may be necessary to repeat treatment with corticosteroids if relapse occurs * low-sodium, liberal-potassium diet to enhance the sodium/potassium pump mechanism, thereby assisting in elimination of sodium to reduce edema. * Protein intake should be about 0.8 g/kg/day, with emphasis on high biologic proteins (dairy products, eggs, meats), and the diet should be low in saturated fats (Deschenes & Doucet, 2000). NURSING In the early stages of the disease, the nursing management is similar to that of the patient with acute glomerulonephritis, but as the disease worsens, management is similar to that of the patient with chronic renal failure * The patient who is receiving corticosteroids or cyclosporine requires instructions about the medications and signs and symptoms that should be reported to the physician. * Dietary instructions may also be necessary. RENAL FAILURE * results when the kidneys cannot remove the body’s metabolic wastes or perform their regulatory functions. The substances normally eliminated in the urine accumulate in the body fluids as a result of impaired renal excretion, leading to a disruption in endocrine and metabolic functions as well as fluid, electrolyte, and acid–base disturbances. * is a systemic disease and is a final common pathway of many different kidney and urinary tract diseases. ACUTE RENAL FAILURE * is a sudden and almost complete loss of kidney function (decreased GFR) over a period of hours to days * Although the exact pathogenesis of ARF and oliguria is not always known, many times there is a specific underlying problem CATEGORIES OF ACUTE RENAL FAILURE 1. Prerenal Failure (hypoperfusion of kidney) * occur as a result of impaired blood flow that leads to hypoperfusion of the kidney and a drop in the GFR CAUSES: • 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 2. Intrarenal Failure (actual damage to kidney tissue) * the result of actual parenchymal damage to the glomeruli or kidney tubules CAUSES: • Prolonged renal ischemia resulting from: * Pigment nephropathy (associated with the breakdown of * blood cells containing pigments that in turn occlude kidney structures) * Myoglobinuria (trauma, crush injuries, burns) * Hemoglobinuria (transfusion reaction, hemolytic anemia) Conditions such as burns, crush injuries, and infections, as well as nephrotoxic agents, may lead to acute tubular necrosis and cessation of renal function. With burns and crush injuries, myoglobin (a protein released from muscle when injury occurs) and hemoglobin are liberated, causing renal toxicity, ischemia, or both. Severe transfusion reactions may also cause intrarenal failure; hemoglobin is released through hemolysis, filters through the glomeruli, and becomes concentrated in the kidney tubules to such a degree that precipitation of hemoglobin occurs. • Nephrotoxic agents such as: * Aminoglycoside antibiotics (gentamicin, tobramycin) * Radiopaque contrast agents * Heavy metals (lead, mercury) * Solvents and chemicals (ethylene glycol, carbon tetrachloride, * arsenic) * Nonsteroidal anti-inflammatory drugs (NSAIDs) * Angiotensin-converting enzyme inhibitors (ACE inhibitors) Medications may also predispose a patient to intrarenal damage, especially nonsteroidal anti-inflammatory drugs (NSAIDs) and ACE inhibitors. These medications interfere with the normal autoregulatory mechanisms of the kidney and may cause hypoperfusion and eventual ischemia. Other potential causes of intrarenal or intrinsic ARF include rhabdomyolysis, which results in accumulation of myoglobin in the glomeruli secondary to damage to skeletal muscle, and nephrotoxicity secondary to herbal remedies (Myhre, 2000). • Infectious processes such as: * Acute pyelonephritis * Acute glomerulonephritis 3. Postrenal Failure (obstruction to urine flow) * the result of an obstruction somewhere distal to the kidney. Pressure rises in the kidney tubules; eventually, the GFR decreases. • Urinary tract obstruction, including: * Calculi (stones) * Tumors * Benign prostatic hyperplasia * Strictures * Blood clots PHASES 1. Initiation period * begins with the initial insult and ends when oliguria develops. 2. Oliguria period * is accompanied by a rise in the serum concentration of substances usually excreted by the kidneys (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. In this phase uremic symptoms first appear and life-threatening conditions such as hyperkalemia develop. Some patients have decreased renal function with increasing nitrogen retention, yet actually excrete normal amounts of urine (2 L/day or more) * ↑ URINE OUTPUT * ↑ BUN * ↑ SERUM CREATININE * EDEMA * HYPERTENSION * HYPERKALEMIA * HYPERMAGNESEMIA * HYPERPHOSPHATEMIA * METABOLIC ACIDOSIS * Lasts for 1-3 weeks 3. Diuresis period * the patient experiences gradually increasing urine output, which signals that glomerular filtration has started to recover. Laboratory values stop rising and eventually decrease. Although the volume of urinary output may reach normal or elevated levels, renal function may still be markedly abnormal. Because uremic symptoms may still be present, the need for expert medical and nursing management continues. The patient must be observed closely for dehydration during this phase; if dehydration occurs, the uremic symptoms are likely to increase. * ↑ URINE OUTPUT (3-5 l/DAY) * HYPOKALEMIA * Lasts for 1 week 4. 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, it is not clinically significant. SIGNS AND SYMPTOMS * Urine output varies (scanty to normal volume), hematuria may be present, and the urine has a low specific gravity (1.010 or less, compared with a normal value of 1.015 to 1.025). * Oliguria (less than 400 mL/day of urine) is the most common clinical situation seen in ARF * Anuria (less than 50 mL/day of urine) and normal urine output are not as common * ↑ serum creatinine (Serum creatinine rises in conjunction with glomerular damage. Serum creatinine levels are useful in monitoring kidney function and disease progression.) * ↑ BUN levels (BUN level rises steadily at a rate dependent on the degree of catabolism (breakdown of protein), renal perfusion, and protein intake. Serum creatinine rises in conjunction with glomerular damage. Serum creatinine levels are useful in monitoring kidney function and disease progression.) * Azotemia (retention of other metabolic waste products) * may appear critically ill and lethargic * persistent nausea, vomiting, and diarrhea * skin and mucous membranes are dry from dehydration * breath may have the odor of urine (uremic fetor) * Central nervous system signs and symptoms include drowsiness, headache, muscle twitching, and seizures * Hyperkalemia (the most life-threatening of the fluid and electrolyte disturbances) * (potassium value more than 5.5 mEq/L [5.5 mmol/L]), electrocardiogram changes (tall, tented, or peaked T waves), and changes in clinical status * (With a decline in the GFR, the patient cannot excrete potassium normally. Patients with oliguria and anuria are at greater risk for hyperkalemia than those without oliguria. Protein catabolism results in the release of cellular potassium into the body fluids, causing severe hyperkalemia (high serum Klevels). Hyperkalemia may lead to dysrhythmias and cardiac arrest. Sources of potassium include normal tissue catabolism, dietary intake, blood in the GI tract, or blood transfusion and other sources (intravenous infusions, potassium penicillin, and extracellular shift in response to metabolic acidosis).) * Metabolic Acidosis (Patients with acute oliguria cannot eliminate the daily metabolic load of acid-type substances produced by the normal metabolic processes. In addition, normal renal buffering mechanisms fail. This is reflected by a fall in the serum CO2-combining power and blood pH. Thus, progressive metabolic acidosis accompanies renal failure.) * Anemia (inevitably accompanies ARF due to reduced erythropoietin production, uremic GI lesions, reduced RBC life span, and blood loss, usually from the GI tract. With use of the parenteral form of erythropoietin (Epogen), anemia is not the major problem it once was) DIAGNOSTIC EXAMINATION * Ultrasonography is a critical component of the evaluation of both acute and chronic renal failure PREVENTION A careful history is obtained to determine whether the patient has been taking potentially nephrotoxic antibiotic agents or has been exposed to environmental toxins. Therefore, in patients taking potentially nephrotoxic medications (aminoglycosides, gentamicin, tobramycin, colistimethate, polymyxin B, amphotericin B, vancomycin, amikacin, cyclosporine), renal function should be monitored closely. Serum BUN and creatinine levels should be obtained at baseline by 24 hours after initiation of these medications and at least twice a week while the patient is receiving them. The kidneys are especially susceptible to the adverse effects of medications because the kidneys are repeatedly exposed to substances in the blood. They receive a large blood flow (25% of the cardiac output at rest; the entire blood volume circulates through the kidneys about 14 times a minute). In addition, the kidney is the major excretory organ for many toxic substances, and during the normal urine concentration process, these substances increase in concentration and can be toxic to the kidneys. 1. Provide adequate hydration to patients at risk for dehydration: * Surgical patients before, during, and after surgery * Patients undergoing intensive diagnostic studies requiring fluid restriction and contrast agents (eg, barium enema, intravenous pyelograms), especially elderly patients who may not have adequate renal reserve * Patients with neoplastic disorders or disorders of metabolism (ie, gout) and those receiving chemotherapy 2. Prevent and treat shock promptly with blood and fluid replacement. 3. Monitor central venous and arterial pressures and hourly urine output of critically ill patients to detect the onset of renal failure as early as possible. 4. Treat hypotension promptly. 5. Continually assess renal function (urine output, laboratory values) when appropriate. 6. Take precautions to ensure that the appropriate blood is administered to the correct patient in order to avoid severe transfusion reactions, which can precipitate renal failure. 7. Prevent and treat infections promptly. Infections can produce progressive renal damage. 8. Pay special attention to wounds, burns, and other precursors of sepsis. 9. Give meticulous care to patients with indwelling catheters to prevent infections from ascending in the urinary tract. Remove catheters as soon as possible. 10. To prevent toxic drug effects, closely monitor dosage, duration of use, and blood levels of all medications metabolized or excreted by the kidneys. MANAGEMENT (The kidney has a remarkable ability to recover from insult. Therefore, 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 take place. Any possible cause of damage is identified, treated, and eliminated.) MEDICAL Prerenal azotemia is treated by optimizing renal perfusion Postrenal failure is treated by relieving the obstruction. Intrarenal azotemia is supportive, with removal of causative agents, aggressive management of prerenal and postrenal failure, and avoidance of associated risk factors 1. maintaining fluid balance * is based on daily body weight, serial measurements of central venous pressure, serum and urine concentrations, fluid losses, blood pressure, and the clinical status of the patient. 2. avoiding fluid excesses * Fluid excesses can be detected by the clinical findings of dyspnea, tachycardia, and distended neck veins. The lungs are auscultated for moist crackles. Because pulmonary edema may be caused by excessive administration of parenteral fluids, extreme caution must be used to prevent fluid overload. The development of generalized edema is assessed by examining the presacral and pretibial areas several times daily. Mannitol, furosemide, or ethacrynic acid may be prescribed to initiate a diuresis and prevent or minimize subsequent renal failure. 3. Medications * The elevated potassium levels may be reduced by administering cation-exchange resins (sodium polystyrene sulfonate [Kayexalate]) orally or by retention enema. Kayexalate works by exchanging a sodium ion for a potassium ion in the intestinal tract. Sorbitol is often administered in combination with Kayexalate to induce a diarrhea-type effect (it induces water loss in the GI tract). * Because many medications are eliminated through the kidneys, medication dosages must be reduced when a patient has ARF. Examples of commonly used medications that require adjustment are antibiotic agents (especially aminoglycosides), digoxin, ACE inhibitors, and medications containing magnesium. * Diuretic agents are often used to control fluid volume, but they have not been shown to hasten the recovery from ARF. * Low-dose dopamine (1 to 3 g/kg) is often used to dilate the renal arteries through stimulation of dopaminergic receptors; however, research has not definitely demonstrated that dopamine prevents ARF or improves outcome in patients with established renal failure. * Atrial natriuretic peptide (ANP), an endogenous hormone synthesized by the cardiac atria, has been shown to improve renal function in multiple animal models of ARF. It has also decreased the need for dialysis in patients with oliguric acute tubular necrosis in a multisite clinical trial of patients. Patients with nonoliguric acute tubular necrosis did not benefit (Lewis, Salem, Chertow et al., 2000). Further research on ANP use is underway. 4. Dialysis * Dialysis may be initiated to prevent serious complications of ARF, such as hyperkalemia, severe metabolic acidosis, pericarditis, and pulmonary edema. Dialysis corrects many biochemical abnormalities; allows for liberalization of fluid, protein, and sodium intake; diminishes bleeding tendencies; and may help wound healing. Hemodialysis, peritoneal dialysis, or any of the new continuous renal replacement therapies may be performed. 5. In patients with severe acidosis, the arterial blood gases or serum bicarbonate levels (CO2-combining power) must be monitored because the patient may require sodium bicarbonate therapy or dialysis. 6. If respiratory problems develop, appropriate ventilator measures must be instituted. The elevated serum phosphate level may be controlled with phosphate-binding agents (aluminum hydroxide).These agents help prevent a continuing rise in serum phosphate levels by decreasing the absorption of phosphate from the intestinal tract. 7. 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. The patient is weighed daily and can be expected to lose 0.2 to 0.5 kg (0.5 to 1 lb) daily if the nitrogen balance is negative (ie, the patient’s caloric intake falls below caloric requirements). If the patient gains or does not lose weight or develops hypertension, fluid retention should be suspected. * Dietary proteins are limited to about 1 g/kg during the oliguric phase to minimize protein breakdown and to prevent accumulation of toxic end products. Caloric requirements are met with high-carbohydrate meals because carbohydrates have a protein sparing effect (ie, in a high-carbohydrate diet, protein is not used for meeting energy requirements but is “spared” for growth and tissue healing). Foods and fluids containing potassium or phosphorus (bananas, citrus fruits and juices, coffee) are restricted. Potassium intake is usually restricted to 40 to 60 mEq/day, and sodium is usually restricted to 2 g/day. The patient may require parenteral nutrition. * After the diuretic phase, the patient is placed on a high-protein, high-calorie diet and is encouraged to resume activities gradually. NURSING 1. 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. 2. reducing metabolic rate * to reduce catabolism and the subsequent release of potassium and accumulation of endogenous waste products (urea and creatinine) * 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. 3. preventing infection * Asepsis is essential with invasive lines and catheters to minimize the risk of infection and increased metabolism. 4. monitoring fluid and electrolyte balance * Hyperkalemia is the most immediate life threatening imbalance seen in ARF. Parenteral fluids, all oral intake, and all medications are screened carefully to ensure that hidden sources of potassium are not inadvertently administered or consumed. * The patient’s cardiac function and musculoskeletal status are monitored closely for signs of hyperkalemia * I and O * Daily weight * Hyperkalemia is treated with glucose and insulin, calcium gluconate, cation-exchange resins (Kayexalate), or dialysis. Fluid and other electrolyte disturbances are often treated with hemodialysis, peritoneal dialysis, or other continuous renal replacement therapies. 5. providing support * Although many of the nurse’s functions are devoted to the technical aspects of the procedure, the psychological needs and concerns of the patient and family cannot be ignored. Continued assessment of the patient for complications of ARF and of its precipitating cause is essential. 6. 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. * Massaging bony prominences * turning the patient frequently * bathing the patient with cool water CHRONIC RENAL DISEASE * is a progressive, irreversible deterioration in renal function in which the body’s ability to maintain metabolic and fluid and electrolyte balance fails, resulting in uremia or azotemia (retention of urea and other nitrogenous wastes in the blood). * As renal function declines, the end products of protein metabolism (which are normally excreted in urine) accumulate in the blood. Uremia develops and adversely affects every system in the body. The greater the buildup of waste products, the more severe the symptoms. The rate of decline in renal function and progression of chronic renal failure is related to the underlying disorder, the urinary excretion of protein, and the presence of hypertension. CAUSES: * systemic diseases, such as diabetes mellitus (leading cause) * hypertension * chronic glomerulonephritis * pyelonephritis * obstruction of the urinary tract * hereditary lesions, as in polycystic kidney disease * vascular disorder * infections * medications * toxic agents (lead, cadmium, mercury, and chromium) STAGES 1. reduced renal reserve * characterized by a 40% to 75% loss of nephron function. The patient usually does not have symptoms because the remaining nephrons are able to carry out the normal functions of the kidney. 2. renal insufficiency * occurs when 75% to 90% of nephron function is lost. * At this point, the serum creatinine and blood urea nitrogen rise, the kidney loses its ability to concentrate urine and anemia develops. * The patient may report polyuria and nocturia. 3. ESRD * occurs when there is less than 10% nephron function remaining. * All of the normal regulatory, excretory, and hormonal functions of the kidney are severely impaired. * ESRD is evidenced by elevated creatinine and blood urea nitrogen levels as well as electrolyte imbalances. SIGNS AND SYMPTOMS Because virtually every body system is affected by the uremia of chronic renal failure, patients exhibit a number of signs and symptoms. The severity of these signs and symptoms depends in part on the degree of renal impairment, other underlying conditions, and the patient’s age. * Hypertension (due to sodium and water retention or from activation of the renin–angiotensin–aldosterone system) * The kidney cannot concentrate or dilute the urine normally in ESRD. Appropriate responses by the kidney to changes in the daily intake of water and electrolytes, therefore, do not occur. 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. * Do Strict fluid volume control (found out to normalize HPN) * heart failure * pulmonary edema (due to fluid overload) * pericarditis (due to irritation of the pericardial lining by uremic toxins) Cardiovascular disease is the predominant cause of death in patients with ESRD * Severe itching (pruritus) * Uremic frost, the deposit of urea crystals on the skin * Anorexia * nausea, vomiting * altered levels of consciousness * muscle twitching * seizures * acidosis * With advanced renal disease, metabolic acidosis occurs because the kidney cannot excrete increased loads of acid. Decreased acid secretion primarily results from inability of the kidney tubules to excrete ammonia (NH3−) and to reabsorb sodium bicarbonate (HCO3−). There is also decreased excretion of phosphates and other organic acids. * Anemia * Anemia develops as a result of inadequate erythropoietin production, the shortened life span of RBCs, nutritional deficiencies, and the patient’s tendency to bleed, particularly from the GI tract. Erythropoietin, a substance normally produced by the kidney, stimulates bone marrow to produce RBCs. In renal failure, erythropoietin production decreases and profound anemia results, producing fatigue, angina, and shortness of breath. * Calcium and phosphorus imbalance * Serum calcium and phosphate levels have a reciprocal relationship in the body: as one rises, the other decreases. With decreased filtration through the glomerulus of the kidney, there is an increase in the serum phosphate level and a reciprocal or corresponding decrease in the serum calcium level. The decreased serum calcium level causes increased secretion of parathormone from the parathyroid glands. * In renal failure, however, the body does not respond normally to the increased secretion of parathormone; as a result, calcium leaves the bone, often producing bone changes and bone disease. In addition, the active metabolite of vitamin D (1,25-dihydroxycholecalciferol) normally manufactured by the kidney decreases as renal failure progresses. Uremic bone disease, often called renal osteodystrophy, develops from the complex changes in calcium, phosphate, and parathormone balance (Barnas, Schmidt, Seidl et al., 2001). DIAGNOSTIC EXAMINATION * 24-hour urinalysis for creatinine clearance (to detect decrease GFR) * Creatinine clearance (As glomerular filtration decreases (due to nonfunctioning glomeruli), the creatinine clearance value decreases, whereas the serum creatinine and BUN levels increase.) **** Serum creatinine is the more sensitive indicator of renal function because of its constant production in the body. The BUN is affected not only by renal disease but also by protein intake in the diet, catabolism (tissue and RBC breakdown), parenteral nutrition, and medications such as corticosteroids. COMPLICATIONS * 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 life span, bleeding in the GI tract from irritating toxins, and blood loss during hemodialysis * Bone disease and metastatic calcifications due to retention of phosphorus, low serum calcium levels, abnormal vitamin D metabolism, and elevated aluminum levels MANAGEMENT Goal: maintain kidney function and homeostasis for as long as possible. MEDICAL diuretic agents inotropic agents such as digitalis or dobutamine sodium bicarbonate supplements- may be needed to correct the acidosis if it causes symptoms Antihypertensives erythropoietin (Epogen) * therapy is initiated to achieve a hematocrit of 33% to 38%, which generally alleviates the symptoms of anemia. * administered either intravenously or subcutaneously three times a week. * It may take 2 to 6 weeks for the hematocrit to rise; therefore, Epogen is not indicated for patients who need immediate correction of severe anemia. * Adverse effects seen with Epogen therapy include hypertension (especially during early stages of treatment) increased clotting of vascular access sites seizures depletion of body iron stores * Management: adjustment of heparin to prevent clotting of the dialysis lines during hemodialysis treatments frequent monitoring of hematocrit 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. * Hypertension that cannot be controlled is a contraindication to recombinant erythropoietin therapy. phosphate-binding agents calcium supplements Antacids * Hyperphosphatemia and hypocalcemia are treated with aluminum-based and calcium carbonate antacids that bind dietary phosphorus in the GI tract. * Both calcium carbonate and phosphorus binding antacids must be administered with food to be effective. Magnesium-based antacids must be avoided to prevent magnesium toxicity. Intravenous diazepam (Valium) or phenytoin (Dilantin) is usually administered to control seizures. Diet (careful regulation of protein intake, fluid restriction,low sodium, low potassium) * The allowed protein must be of high biologic value (dairy products, eggs, meats). 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 is 500 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 from the blood during the dialysis treatment. Dialysis * Hyperkalemia is usually prevented by ensuring adequate dialysis treatments with potassium removal and careful monitoring of all medications, both oral and intravenous, for their potassium content. The patient is placed on a potassium-restricted diet. Occasionally, Kayexalate, a cation-exchange resin, administered orally, may be needed. The patient with increasing symptoms of chronic renal failure is referred to a dialysis and transplantation center early in the course of progressive renal disease. Dialysis is usually initiated when the patient cannot maintain a reasonable lifestyle with conservative treatment. NURSING * 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. * patient’s blood pressure and serum potassium level are monitored to detect hypertension and rising serum potassium levels, which may occur with therapy and the increasing RBC mass. KIDNEY TRANSPLANTATION * Kidney transplantation has become the treatment of choice for most patients with ESRD. During the past 40 years, more than 380,000 kidney transplantations have been performed worldwide, and more than 174,000 have been performed in the United States. This number includes over 10,000 kidney-pancreas transplantations. In January 2003 there were almost 54,000 persons on the waiting list for kidney transplantation (http://www.unos.org., December 25, 2002). * involves transplanting a kidney from a living donor or human cadaver to a recipient who has ESRD * A nephrectomy of the patient’s own native kidneys may be performed before transplantation. The transplanted kidney is placed in the patient’s iliac fossa anterior to the iliac crest. The ureter of the newly transplanted kidney is transplanted into the bladder or anastomosed to the ureter of the recipient