Important laboratory data for dialysis patients
Important laboratory tests used to monitor dialysis patients include the following:
• Electrolytes (sodium, potassium, chloride, carbon dioxide)
• Blood urea nitrogen (BUN)
• Creatinine
• Hemoglobin
• Hematocrit
• White blood cell count
• Reticulocytes
• Platelets
• Iron and iron-binding capacity
• Ferritin
• Calcium
• Phosphorus
• Magnesium
• Albumin
• Total protein
• Glucose
• Alanine transaminase and aspartate transaminase
• Cholesterol
• Parathyroid hormone (PTH)
• Aluminum
• Hepatitis panel
What are normal laboratory values and how are they interpreted in the patient with chronic kidney disease?
Review of the laboratory reports is included in the overall patient assessment. Any deviations from normal should be further evaluated for what is an acceptable value for a dialysis patient. For example, creatinine and BUN values may not fall within the range of normal because of chronic kidney disease (CKD). However, dialysis personnel should follow a protocol that defines when the BUN and creatinine values exceed the acceptable range for a person on dialysis and take appropriate action. Deviations from the acceptable range of laboratory values should be reported to the dialysis physician for appropriate intervention. Interventions may include a change in the dialysis prescription and/or medication.
What is albumin?
Albumin is a form of protein, which is a good measure of the nutritional status of an individual. It is also the protein of highest concentration in the plasma. Albumin carries smaller molecules in the blood, such as medications, bilirubin, and calcium. Albumin helps to hold fluid in the blood vessels and is a good reflection of the patient’s protein stores. It is well known that albumin is a powerful predictor of morbidity and mortality in the CKD patient. The normal value ranges from 3.5 to 5.4 g/dL. A serum albumin of 4.0 g/dL or greater is desired for the CKD patient.
What are the symptoms of low albumin?
Low albumin will cause edema as fluid shifts from the blood vessels into the tissues. Other symptoms of hypoalbuminemia include weight loss, fatigue, muscle wasting, and hypotension.
Why are dialysis patients at risk for low albumin levels?
Albumin levels are greatly influenced by diet. Dialysis patients are well known for having poor nutrition because uremia causes a loss of appetite. Lack of knowledge regarding adequate protein intake, difficulties with cooking or shopping for food, nausea, and loss of appetite for protein-rich food are all barriers supporting good nutrition in the dialysis patient. Some patients lose albumin into the urine, and peritoneal dialysis patients are at a high risk of lowering their levels as albumin is transported across the peritoneal membrane.
Why do we monitor albumin levels so closely?
A low albumin level (hypoalbuminemia) is linked to higher hospitalization rates and is one of the greatest predictors of death in the dialysis patient. In most studies, the risk for morbidity and mortality increases with a serum albumin level less than 3.5 g/dL (Ahmad, 1999).
What is the relationship between albumin levels and c-reactive protein?
C-reactive protein (CRP) is a protein produced in response to infection, inflammation, and tissue trauma and is used as a marker for inflammation. An elevated level of serum CRP is associated with a low serum albumin level in dialysis patients. A combination of the two factors has been identified as placing the dialysis patient at a higher risk for developing heart disease and inflammation of the blood vessels. CRP is present in the serum of normal individuals at levels between 0 and 5 mg/L. Serum CRP levels increase dramatically during infection or injury. Other factors associated with an increase in CRP levels in the CKD patient include surgery, bioincompatible membranes, periodontal disease, high-flux dialysis, impure dialysate, arthritis, and uremia. Levels may increase 100 times or more during bacterial or viral infection. The CRP level will peak two to three days after an acute infection and begin to decrease one to two weeks after the infection subsides. This is why CRP is useful as an early marker for infection, inflammation, or injury. CRP measurements may help predict low serum albumin levels, evaluate for resistance to epoetin alfa (Epogen) therapy, assess the course of acute bacterial infections and their response to treatment, and detect occult infections or chronic inflammation (Spectra Renal Management, 2009). The National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines suggest a CRP level greater than 5 to 10 mg/L as being indicative of inflammation (NKF, 2006).
Are dialysis patients at risk for aluminum toxicity?
Aluminum is a light metal found in cookware, soft drink and other beverage cans, antacids, cosmetics, antiperspirants, aluminum-containing phosphate binders, and contaminated water. The kidneys are the main organs for the filtration and excretion of aluminum in the body. The majority of aluminum is protein bound so it is not easily diffused through the glomerulus. Deposition of aluminum in the bone, tissues, and brain will be seen with elevated levels.
Aluminum toxicity was once prevalent among dialysis patients because they were exposed to aluminum from the water used in the dialysis treatment and from the oral intake of aluminum-based binders. The use of aluminum-based phosphate binders is now generally avoided due to the harmful effects of aluminum accumulation in the patient. The clinical consequences of aluminum toxicity involve symptoms to the brain, bone, and blood. These may or may not occur concurrently. High serum aluminum levels are associated with progressive neurologic symptoms, such as behavioral changes, slurred speech, and memory loss, that occur very subtly over time. Gastrointestinal (GI) irritation, loss of energy and appetite, anemia, and constipation also are associated with elevated aluminum levels. Dementia may be seen with advanced toxicity. Elevated aluminum levels may also cause epoetin alfa–resistant anemia and aluminum-induced bone disease. Normal serum levels are 0 to 10 mcg/L.
What is the treatment for aluminum toxicity?
Aside from removing the sources of exposure, the chelating agent deferoxamine mesylate (Desferal) may be used to remove the excess aluminum. To chelate means to remove a heavy metal, such as lead, mercury, or aluminum, from the bloodstream. When administered, deferoxamine mesylate will form complexes with the aluminum, which can then be removed from the blood during the dialysis treatment.
How does potassium work inside the body?
Potassium is the major intracellular cation and the second most abundant cation in the body. All but 2% of the total body potassium is within the cells of the body. Potassium is necessary for many cellular functions; neuromuscular control; skeletal, cardiac, and smooth muscle activity; and intracellular enzyme reactions. Potassium is influenced by acid-base balance as potassium ions are shifted out of the cell and replaced with hydrogen ions with acidosis. The majority of excess potassium in the body is excreted by the kidneys in the urine.
What causes hypokalemia?
Hypokalemia is a serum potassium level less than 3.5 mEq/L and may be caused by excessive GI losses, such as vomiting and diarrhea, diuretic use, excessive sweating, poor diet, and burns. Symptoms of low serum potassium include weakness and fatigue, and abnormal heart rhythms.
How is low potassium treated?
Dietary intake of potassium may need to be increased and intravenous potassium may be given if a rapid rise in the serum potassium level is needed. Dialyzing the patient on a higher potassium bath will minimize diffusion of potassium and help to maintain the serum level.
What is hyperkalemia?
Hyperkalemia is a serum potassium level greater than 5.5 mEq/L and usually the result of excessive dietary intake of high-potassium foods. The expected value for a patient on dialysis is 3.6 to 5.0 mEq/L. Other causes of increased serum potassium are catabolic states, tissue or crush injury, blood transfusions, GI bleeding, hemolysis, missed dialysis treatments, and acidosis. Symptoms include abdominal cramps, shortness of breath, dizziness, diarrhea, muscle weakness, hypotension, electrocardiogram changes, arrhythmias, and cardiac arrest. The rapidity of the change in potassium level rather than the actual serum measurement is a greater influence of the degree of symptoms produced.
What is the treatment for hyperkalemia?
A variety of treatment options exist for hyperkalemia. Sodium bicarbonate or glucose and insulin may be given intravenously to help drive the excess potassium into the cell. Sodium polystyrene sulfonate (Kayexalate) is a cation exchange resin that may be given orally or by retention enema. It works by exchanging two sodium ions for one potassium ion and allowing the potassium to be eliminated in the stool. Oral Kayexalate is more effective than retention enema.
The fastest and most efficient way to lower the total body potassium is hemodialysis. The dialysate potassium may be lowered to allow greater diffusion of potassium from the blood into the dialysate. Use with caution in the patient on digoxin therapy because toxicity may develop as the serum potassium is lowered. Potassium levels should always be monitored more frequently for the patient running on a lower potassium dialysate.
Is magnesium ever a problem for the patient with chronic kidney disease?
Magnesium is a mineral and the second most abundant cation in intracellular fluid. Most magnesium is eliminated in the stool, but the kidney is responsible for some of the excretion. Magnesium is responsible for neuromuscular activity and activates various enzymes for carbohydrate and protein metabolism. Magnesium is found in foods and medications, such as antacids, laxatives, and phosphate binders.
Low magnesium levels (hypomagnesemia) may be caused by malnutrition, chronic diarrhea, certain diuretics, and antibiotics, such as amphotericin B and neomycin. Symptoms of low magnesium include twitching, tremors, spasms, confusion, restlessness, and dysrhythmias. Elevated magnesium levels (hypermagnesemia) may occur with dehydration and use of magnesium-based antacids or laxatives. Elevated levels of magnesium will cause excessive perspiration, hypotension, muscle weakness, and sedation. The normal magnesium level is 1.6 to 2.4 mEq/L.
How is the calcium level affected in the patient with kidney disease?
Calcium is the most abundant mineral in the body, with 99% located in the bones and the teeth. Calcium is necessary for blood clotting, bone growth and health, and conduction of neuromuscular impulses. Calcium may be ionized or nonionized. Only ionized calcium is free to be used by the body, and this represents 50% of the calcium in the body. The remaining calcium is bound to proteins.
The CKD patient will normally have a lower serum calcium because calcium absorption is hindered by the suppression of 1,25-dihydroxycholecalciferol (vitamin D) production, decreased phosphorus excretion, and increased phosphorus retention. Normal calcium levels range from 8.5 to 10.5 mg/dL.
Why do we monitor the chronic kidney disease patient’s phosphorus levels?
Phosphorus is normally excreted by the kidneys and accumulates in the patient with CKD. As renal failure progresses, the ability of the kidneys to filter phosphorus decreases. High phosphorus levels are usually the result of decreased glomerular filtration coupled with excessive dietary intake. The normal phosphorus range is 3.5 to 5.5 mg/dL for the CKD patient. The treatment for hyperphosphatemia is phosphate binders, which bind with the phosphorus in the GI tract, allowing it to be excreted through the intestines. Patients with high phosphorus levels would also benefit from dietary counseling.
What role does parathyroid hormone play in maintaining calcium levels?
PTH is secreted by the parathyroid gland and helps to regulate calcium and phosphorus levels. PTH helps the body to absorb calcium and eliminate phosphorus. Low serum calcium levels stimulate PTH secretion. PTH secretion stimulates the movement of calcium out of the bone, increases calcium absorption from the small intestine, and minimizes calcium loss in the urine. Untreated hyperphosphatemia and hypocalcemia may lead to persistent and prolonged secretion of PTH in an attempt to raise calcium levels in the blood. Chronically elevated phosphorus levels will cause secondary hyperparathyroidism and the resultant renal osteodystrophy and calcium phosphorus deposits in the soft tissues of the body. Elevated phosphorus levels need to be controlled with the use of phosphate binders and nutritional education regarding phosphorus restrictions. The expected PTH level for CKD stage 5 patients is 150 to 300 pg/mL.
What is the relationship between calcium and phosphorus?
Phosphorus is a major intracellular anion. Eighty percent of the body’s phosphorus is present in the bone. Phosphorus acts as a urinary buffer in maintaining acid-base balance, helps to maintain cell wall integrity, and is involved with transferring energy to cells in cellular metabolism. Calcium and phosphorus have an inverse relationship. When the phosphorus level is high, the calcium level is low.
What is the importance of the calcium-phosphorus product?
Maintaining the calcium-phosphorus product between 40 and 60 is essential in avoiding bone disease. The calcium-phosphorus product is determined by multiplying the value of the calcium level by the value of the phosphorus level. For example, if the patient’s calcium level is 10 mg and the phosphorus level is 9 mg, the patient would have a calcium phosphorus product of 90. A high product places the patient at risk for developing calcifications in the soft tissues and coronary arteries. The KDOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease recommend that the calcium-phosphorus product should be maintained at <55 mg/dL (NKF, 2003).
Why do we monitor the chronic kidney disease patient’s hematocrit and hemoglobin so closely?
A hemoglobin and hematocrit test is the most commonly monitored laboratory study used to evaluate anemia, and to prescribe a therapeutic dose of epoetin alfa. Both the hematocrit and the hemoglobin are typically low in the CKD patient due to decreased erythropoietin production. Hematocrit is the percentage of red blood cells in whole blood, and hemoglobin measures the oxygen-carrying capacity of red blood cells. Low levels of hematocrit are caused by decreased production of red blood cells, blood loss from the dialysis treatment, and shortened survival time of red blood cells. Low hematocrit values are associated with fatigue, shortness of breath, chest pain, palpitations, and feeling of cold. The normal hematocrit value for kidney disease patients is approximately 30% to 36% if they are on an erythropoiesis-stimulating agent (ESA).
Hemoglobin is a protein that contains the iron that carries oxygen from the lungs to all of the body’s tissues. The target hemoglobin for the CKD patient is approximately 10 to 12 g/dL if on an ESA. Two additional blood tests help determine iron availability: (1) ferritin is a protein that stores the iron until it is needed and (2) transferrin saturation measures the amount of iron immediately available for red blood cell production. The KDOQI guidelines for anemia in CKD suggest that to achieve and maintain the target hemoglobin, sufficient iron should be administered to maintain a transferrin saturation of ≥20% and a serum ferritin level of ≥100 ng/mL (NKF, 2000).
What is reticulocyte hemoglobin count and why is it measured?
Reticulocyte hemoglobin count (CHr) is a sensitive indicator of iron deficiency and a diagnostic tool that can monitor the efficacy of intravenous iron therapy. Reticulocytes are the most recent red blood cells released into the bloodstream and they circulate for only one to two days. CHr provides an assessment of the availability of iron to the red blood cells most recently produced by the bone marrow. Because the CHr is a more sensitive and specific marker of iron status at the reticulocyte level, determining the dose of intravenous iron therapy based on this index should improve hemoglobin levels in the CKD patient.
What is blood urea nitrogen?
Urea is the waste product of protein metabolism.
Why do dialysis patients have elevated blood urea nitrogen levels?
An increased BUN results from renal insufficiency, eating a diet high in protein, digesting blood from GI bleeding, dehydration, infection, injury, or elevated temperature, and could also indicate the need for a longer dialysis time, higher blood flow rate, or larger dialyzer. High levels of BUN will produce symptoms of fatigue, insomnia, irritability, dry and itchy skin, nausea, and an altered sense of taste and smell. The normal BUN level is 7 to 18 mg/dL but the normal level for a dialysis patient (pretreatment) is 60 to 100 mg/dL.
What is dialysis adequacy?
Optimal dialysis can be defined as the dialysis treatment that makes patients feel almost as good and live almost as long as if they did not have end-stage renal disease. The amount of dialysis delivered during a single treatment is measured by the computed Kt/V and urea reduction ratio (URR). The higher the delivered dose of dialysis, the better the patient outcome will be. The NKF sets guidelines for recommended acceptable adequacy levels; however, many dialysis clinics set more stringent goals.
What is the kt/vurea?
Kt/Vurea measures the effectiveness of the dialysis treatment in removing waste products, specifically the ratio of urea clearance and time on dialysis to the volume of urea distribution (total body water). The NKF KDOQI clinical practice guidelines for hemodialysis adequacy suggest that the delivered Kt/Vurea be at least 1.2 when three treatments a week are given (NKF, 2006).
Urea is a good small molecule marker because its level correlates well with the nutritional state of the individual and with protein catabolism. The Kt/Vurea index is the result of complex mathematical modeling of urea kinetics. K is the dialyzer clearance of urea (mL/min), t represents dialysis time (in minutes), and V indicates the volume of distribution of urea in body fluid. Vurea is not a real volume that can be measured. It is derived from pharmacokinetic modeling and involves more than one fluid pool and the rates of transfer between them. These cannot be directly measured.
What is the urea reduction ratio?
The URR measures the reduction of urea in the dialyzed patient from predialysis to postdialysis. The URR reflects the delivered dose of dialysis. The KDOQI clinical practice guidelines for hemodialysis adequacy suggest a delivered dose of at least 65% when three treatments a week are given (NKF, 2006).
What factors affect dialysis adequacy?
The NKF identifies the following factors as instrumental in adversely affecting the prescribed dose of dialysis:
Compromised urea clearance caused by
• Access recirculation
• Inadequate blood flow from vascular access
• Inaccurate estimation of dialyzer performance
• Inadequate dialyzer reprocessing
• Clotted dialyzer fibers
• Errors in blood and dialysate flow rates caused by miscalibrated equipment
• Inadequate blood and dialysate flow rate
• Dialyzer leaks
Reduced treatment time
• Premature discontinuation of treatment
• Time on dialysis incorrectly calculated
• Failure to account for interruption in treatment
Laboratory or blood sampling errors
• Dilution of BUN sample with saline
• Drawing predialysis BUN after initiation of dialysis
• Laboratory error
• Drawing postdialysis BUN before the end of dialysis treatment
• Drawing postdialysis BUN more than five minutes after the end of dialysis
When should serum glucose be monitored in the diabetic patient?
A serum glucose (Chemstick or Accucheck) assessment should be performed at the beginning of the dialysis. Unstable diabetics need more frequent checks. A serum glucose value less than 50 mg/dL may require a bolus of 50 mL of 50% dextrose to prevent hypoglycemic shock. An elevated glucose value may require a dose of regular insulin to prevent diabetic coma (see Chapter 16).
What is creatinine?
Creatinine is a protein produced by muscle and is measured to determine kidney function. The amount produced by any person is relatively constant and the serum volume is determined by the rate it is being removed by the kidney. The amount of creatinine produced is relative to the muscle mass. The elderly will demonstrate lower creatinine levels due to decreased muscle mass. With declining renal function, the serum creatinine will rise. Normal creatinine values are 0.5 to 1.5 mg/dL. The serum creatinine value is a more sensitive marker of renal function because it is not influenced by diet or fluid volume. The expected value for a CKD patient is 12 to 20 mg/dL.
What does it mean to measure the creatinine clearance?
Creatinine clearance is the amount of blood cleared of creatinine per unit of time and is normally expressed in milliliters per minute. The normal creatinine clearance is approximately 85 to 135 mL/min. With CKD there is a decline in creatinine clearance. Normal values may vary slightly from laboratory to laboratory or from textbook to textbook.
What is glomerular filtration rate?
Glomerular filtration rate (GFR) is a measure of renal function and a more sensitive marker of renal impairment than the serum creatinine. The GFR will vary with age, sex, and body size. The normal GFR in young adults is approximately 120 to 130 mL/min/1.73 m2. The GFR will decline with age and with the onset of renal failure. Renal replacement therapy is needed when the GFR falls below 15 mL/min/1.73 m2.