Albumin, the body's predominant serum-binding protein, has several important functions, as follows:

Albumin comprises 75-80% of normal plasma colloid oncotic pressure and 50% of protein content. When plasma proteins, especially albumin, no longer sustain sufficient colloid osmotic pressure to counterbalance hydrostatic pressure, edema develops. Albumin transports various substances, including bilirubin, fatty acids, metals, ions, hormones, and exogenous drugs. One consequence of hypoalbuminemia is that drugs that are usually protein bound are free in the plasma, allowing for higher drug levels, more rapid hepatic metabolism, or both. Alterations in albumin level affect platelet function.

Albumin.

Reference serum values range from 3.5-4.5 g/dL, with a total body content of 300-500 g. Synthesis occurs only in hepatic cells at a rate of approximately 15 g/d in a healthy person, but the rate can vary significantly with various types of physiologic stress. The half-life

of albumin is approximately 21 days, with a degradation rate of approximately 4% per day. Hypoalbuminemia is a common problem among persons with acute and chronic medical conditions. At the time of hospital admission, 20% of patients have hypoalbuminemia. Hypoalbuminemia can be caused by various conditions, including nephrotic syndrome, hepatic cirrhosis, heart failure, and malnutrition; however, most cases of hypoalbuminemia are caused by acute and chronic inflammatory responses. Serum albumin level is an important prognostic indicator. Among hospitalized patients, lower serum albumin levels correlate with an increased risk of morbidity and mortality. The presentation, physical examination findings, and laboratory results associated with hypoalbuminemia depending on the underlying disease process.

Normally, the kidney is the site of hormone production and secretion, acid-base homeostasis, fluid and electrolyte regulation, and waste-product elimination. In the presence of renal failure, these functions are not performed adequately and metabolic abnormalities, such as anemia, acidemia,hyperkalemia, hyperparathyroidism, malnutrition, and hypertension, can occur. Uremia usually develops only after the creatinine clearance falls to less than 10 mL/min, although some patients may be symptomatic at higher clearance levels, especially if renal failure acutely develops. The syndrome may be heralded by the clinical onset of nausea, vomiting, fatigue, anorexia,[2] weight loss, muscle cramps, pruritus, and change in mental status.

Anemia
Anemia-induced fatigue is thought to be one of the major contributors to the uremic syndrome. Erythropoietin (EPO), a hormone necessary for red blood cell production in bone marrow, is produced by peritubular cells in the kidney in response to hypoxia. Anemia associated with renal failure can be observed when the glomerular filtration rate (GFR) is less than 50 mL/min or when the serum creatinine is greater than 2 mg/dL. Diabetic patients may experience anemia with a GFR of less than 60 mL/min. In a study of 832 hospitalized patients with diabetes, Almoznino-Sarafian et al determined that 334 of the patients had anemia, a rate (40%) higher than that reported in ambulatory patient populations. The investigators found that the anemic patients tended to be older (mean age 71.4 years) than were the nonanemic patients with diabetes (mean age 64.4 years) and that a greater percentage were female (52.4% vs 44.4% of the nonanemic patients). In addition, 39% of the anemic patients had renal dysfunction.[3] Anemia associated with chronic kidney disease is characteristically normocytic, normochromic, and hypoproliferative. In the setting of CRF, anemia may be due to other clinical factors or diseases, such as iron deficiency, vitamin deficiencies (eg, folate, vitamin B-12), hyperparathyroidism, hypothyroidism, and decreased red blood cell survival. Iron deficiency, which may occur as a result of occult GI bleeding or frequent blood draws, should be excluded in all patients. Elevated PTH levels are thought to be associated with marrow calcification, which may suppress red blood cell production and lead to a hypoproliferative anemia. Parathyroid-induced marrow calcification tends to regress after parathyroidectomy.

Coagulopathy
Bleeding diatheses are characteristic findings in patients with end-stage renal disease (ESRD). The pathogenesis of uremic bleeding tendency is related to multiple dysfunctions of the platelets. The platelet numbers may be reduced slightly, while platelet turnover is increased. The reduced adhesion of platelets to the vascular subendothelial wall is due to reduction of GPIb and altered conformational changes of GPIIb/IIIa receptors. Alterations of platelet adhesion and aggregation are caused by uremic toxins, increased platelet production of NO, PGI(2), calcium and cAMP as well as renal anemia. Correction of uremic bleeding is caused by treatment of renal anemia

with recombinant human erythropoietin or darbepoetin alpha, adequate dialysis, desmopressin, cryoprecipitate, tranexamic acid, or conjugated estrogens.

Acidosis
Acidosis is another major metabolic abnormality associated with uremia. Metabolic acidbase regulation is controlled primarily by tubular cells located in the kidney, while respiratory compensation is accomplished in the lungs. Failure to secrete hydrogen ions and impaired excretion of ammonium may initially contribute to metabolic acidosis. As kidney disease continues to progress, accumulation of phosphate and other organic acids, such as sulfuric acid, hippuric acid, and lactic acid, creates an increased aniongap metabolic acidosis. In uremia, metabolic acidemia may contribute to other clinical abnormalities, such as hyperventilation, anorexia, stupor, decreased cardiac response (congestive heart failure), and muscle weakness.

Hyperkalemia
Hyperkalemia (potassium, >6.5 mEq/L) may be an acute or chronic manifestation of renal failure, but regardless of the etiology, a potassium level of greater than 6.5 mEq/L is a clinical emergency. As renal function declines, the nephron is unable to excrete a normal potassium load, which can lead to hyperkalemia if dietary intake remains constant. In addition, other metabolic abnormalities, such as acidemia or type IV renal tubular acidosis, may contribute to decreased potassium excretion and lead to hyperkalemia. However, remember that most cases of hyperkalemia are multifactorial in etiology. Hyperkalemia can occur in several instances, which include (1) excessive potassium intake in patients with a creatinine clearance of less than 20 mL/min, (2) hyporeninemic hypoaldosteronism or type IV renal tubular acidosis in patients with diabetes, urinary obstruction, or interstitial nephritis, (3) significant acidemia, or (4) with drug therapy. Hyperkalemia is common when drugs, such as potassium-sparing diuretics (eg, spironolactone, amiloride, triamterene), ACE inhibitors, angiotensin-receptor blockers, beta-blockers, or nonsteroidal anti-inflammatory drugs are used in the setting of renal insufficiency or renal failure.

Calcium, parathyroid, and vitamin D abnormalities

In the setting of renal failure, there are a number of abnormalities of the calcium-vitamin D metabolic pathway, such as hypocalcemia, hyperphosphatemia, and increased PTH levels, that ultimately lead to renal bone disease (osteodystrophy). After exposure to the sun, vitamin D-3 is produced in the skin and transported to the liver for hydroxylation (25[OH] vitamin D-3). Hydroxylated vitamin D-3 is then transported to the kidney, where a second hydroxylation occurs, and 1,25(OH)2 vitamin D-3 is formed. As the clinically active form of vitamin D, 1,25(OH)2 vitamin D-3 is responsible for GI absorption of calcium and phosphorus and suppression of PTH. During renal failure, 1,25(OH)2 vitamin D-3 levels are reduced secondary to decreased production in renal tissue as well as hyperphosphatemia, which leads to decreased calcium absorption from the GI

tract and results in low serum calcium levels. Hypocalcemia stimulates the parathyroid gland to excrete PTH, a process termed secondary hyperparathyroidism. In this setting, the vitamin deficiency can be replaced orally or intravenously with 1,25(OH)2 vitamin D-3 (calcitriol). There are several new vitamin D analogs that have become available for use and are more specific for vitamin D receptors in the parathyroid gland. Use of one of these analogs, paracalcitol, has been found to be associated with improved survival compared to use of calcitriol.[4] In addition, these new vitamin D analogs cause less elevation in serum calcium and phosphorus levels. [5] Also, cinacalcet, a new medication that stimulates the calcium sensing receptor in the parathyroid gland and causes negative feedback on PTH production and release, can be used to treat secondary hyperparathyroidism. In addition to the calcium abnormalities, hyperphosphatemia occurs as excretion of phosphate decreases with progressive renal failure. Hyperphosphatemia stimulates parathyroid gland hypertrophy and stimulates increased production and secretion of PTH. Elevated PTH levels have been associated with uremic neuropathy and other metabolic disturbances, which include altered pancreatic response, erythropoiesis, and cardiac and liver function abnormalities. The direct deposit of calcium and phosphate in the skin, blood vessels, and other tissue, termed metastatic calcification, can occur when the calcium-phosphate product is greater than 70.[6]

Endocrine abnormalities
Other endocrine abnormalities that may occur in the setting of uremia include changes in carbohydrate metabolism, decreased thyroid hormone excretion, and abnormal sexual hormone regulation. Reduced insulin clearance and increased insulin secretion can lead to increased episodes of hypoglycemia and normalization of hyperglycemia in diabetic patients. Glycemic control may appear to be improved; however, this may be an ominous sign of renal function decline. Consider appropriate decreases in doses of antihyperglycemia medications (ie, insulin and oral antihyperglycemic medications) as renal function declines to avoid hypoglycemic reactions. Levels of thyroid hormones, such as thyroxine, may become depressed, while reverse triiodothyronine levels may increase because of impaired conversion of triiodothyronine to thyroxine. Reproductive hormone dysfunction is common and can cause impotence in men and infertility in women. Renal failure is associated with decreased spermatogenesis, reduced testosterone levels, increased estrogen levels, and elevated luteinizing hormone levels in men, all of which contribute to impotence and decreased libido. In women, uremia reduces the cyclic luteinizing hormone surge, which results in anovulation and amenorrhea. Infertility is common and pregnancy is rare in women with advanced uremia and renal failure, but this may be reversed with renal transplantation.

Cardiovascular abnormalities

Cardiovascular abnormalities, including uremic pericarditis, pericardial effusions, calcium and phosphate depositionassociated worsening of underlying valvular disorders, and uremic suppression of myocardial contractility, are common in patients with CRF.[7] Left ventricular hypertrophy is a common disorder found in approximately 75% of patients who have not yet undergone dialysis. Left ventricular hypertrophy is associated with increased ventricular thickness, arterial stiffening, coronary atherosclerosis, and/or coronary artery calcification. Patients are at increased risk for cardiac arrhythmias due to underlying electrolyte and acid-base abnormalities. Renal dysfunction may contribute to associated fluid retention, which may lead to uncontrolled hypertension and congestive heart failure.

Malnutrition
Malnutrition usually occurs as renal failure progresses and is manifested by anorexia, weight loss, loss of muscle mass, low cholesterol levels, low BUN levels in the setting of an elevated creatinine level, low serum transferrin levels, and hypoalbuminemia. However, whether uremia stimulates protein catabolism directly remains controversial.[8] Comorbid diseases, such as diabetes, congestive heart failure, or other diseases, that require reduced food intake or restrictions of certain foods may contribute to anorexia. Numerous epidemiologic studies have shown that a decreased serum albumin concentration is a very strong and independent predictor of mortality among dialysis patients. Thus, it is important that dialysis be initiated prior to the occurrence of significant malnutrition.
Technique for ABG Sampling Allens Test Once arterial site is selected, must test for collateral circulation Allen test used for radial and ulnar arteries Simultaneously compress the radial and ulnar arteries, ask client to make fist until hand blanches, ask client to open fist, release pressure from ulnar artery, check for return of pinkness to hand

What is the nursing responsibilities for patient before during and after blood transfusion?
Answer:
the nurse is responsible for insuring that the right unit of blood is to be administered to the right patient after typing and crossmatching by the lab. this is done by checking the lot, serial numbers, blood type, and expiration date with another nurse or qualified lab personnell. then the unit of blood has to be checked

off with another nurse before administration. only registered nurses are allowed by law to administer blood products. before administering the unit, the nurse has to get consent forms signed by the patient or a qualified representative of the patient, except in the cases of trauma or life saving situations if the patient is unable to make that decision. all patients have the right to refuse transfusions. after consents are signed and the blood is checked by appropriate personnell, the nurse has to take a complete set of vital signs for a baseline. after starting the transfusion, the vital signs must be checked after 15 minutes, then 30 minutes from then, then at one hour. then vital signs must be checked every hour, according to hospital protocol. the vital signs are checked this often to monitor for a reaction to the blood. if a reaction occurs, then the transfusion must be stopped immediately and normal saline infused. blood can only be transfused with normal saline. some hospitals may give premedications before transfusion to reduce the chance of a reaction. a unit of whole blood (packed red blood cells) must be infused over 3.5-4 hours, but not over 4 hours from the time of the start of the transfusion. Source(s): i am a registered nurse the nurse is responsible for insuring that the right unit of blood is to be administered to the right patient after typing and crossmatching by the lab. this is done by checking the lot, serial numbers, blood type, and expiration date with another nurse or qualified lab personnell. then the unit of blood has to be checked off with another nurse before administration. only registered nurses are allowed by law to administer blood products. before administering the unit, the nurse has to get consent forms signed by the patient or a qualified representative of the patient, except in the cases of trauma or life saving situations if the patient is unable to make that decision. all patients have the right to refuse transfusions. after consents are signed and the blood is checked by appropriate personnell, the nurse has to take a complete set of vital signs for a baseline. after starting the transfusion, the vital signs must be checked after 15 minutes, then 30 minutes from then, then at one hour. then vital signs must be checked every hour, according to hospital protocol. the vital signs are checked this often to monitor for a reaction to the blood. if a reaction occurs, then the transfusion must be stopped immediately and normal saline infused. blood can only be transfused with normal saline. some hospitals may give premedications before transfusion to reduce the chance of a reaction. a unit of whole blood (packed red blood cells) must be infused over 3.5-4 hours, but not over 4 hours from the time of the start of the transfusion.