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Lab Values of the Renal Failure Patient

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Lab Values

of the Renal Failure Patient

By PATRICIA SENGSTACK, MSN, RN, CCRN

You're looking over the lab reports for the morning when you come across Mr. Norris' numbers. As you puzzle over many of his abnormal serum values, you remember that 63-year-old Mr. Norris has end-stage renal disease as a result of Type 2 diabetes and hypertension. He has been receiving hemodialysis for the past two years. He was admitted because his right forearm arteriovenous graft had clotted and the outpatient dialysis center was unable to dialyze him. His graft has now been declotted and dialysis will be attempted today.

The fact that Mr. Norris has chronic renal failure explains the abnormalities in his lab reports. But sorting out what is "normal" for a renal failure patient and what may require intervention is often confusing. What is the physiology behind abnormal lab values in the chronic renal failure patient and how do you determine when it is appropriate to request medical intervention?

Mr. Norris' lab values and normal ranges are presented in Table 1. In an attempt to make sense of these lab values, it helps to sort them into two categories: 1) values that increase with renal failure, and 2) values that decrease with renal failure (Table 2).

Increasing Serum Levels

Creatinine: The product of creatine phosphate breakdown from the metabolism of skeletal muscle is creatinine. It is produced at a fairly constant rate and is excreted via the kidneys. It is considered the best indicator of renal function (or glomerular filtration rate, (GFR), since it is not affected by diet or fluid intake.2 The higher the serum value, the poorer the renal function. A simple analogy is having a clogged drain causing it to back up. If the creatinine cannot be excreted, it then "backs up" into the blood, raising the level. In renal failure patients, predialysis levels may be seen as high as 20 mg/dl. This is usually not considered an emergency situation, although normal range is 0.6 mg/dl to 1.3 mg/dl, but would indicate the need for dialysis to lower the value.

Blood Urea Nitrogen (BUN): BUN is the nitrogenous end product of protein metabolism. Because it is regulated and excreted by the kidneys, you will note a rise in this level as kidney function deteriorates. Normal kidneys filter urea in the glomerulus then reabsorb it in the tubules to maintain a serum level of 8 mg/dl to 20 mg/dl.3

BUN is not as sensitive an indicator of renal function as creatinine because factors other than renal failure can cause an increase in urea levels. A diet high in protein, excessive tissue breakdown, starvation, gastrointestinal bleeding (from proteins in blood) and dehydration (as GFR drops, tubules have more time to reabsorb urea back into the blood) all can cause an increase in BUN.4 Levels as high as 300 mg/dl have been noted. While there is no need to call a code at this level, it would likely require dialysis.

Potassium: Approximately 90 percent of potassium is excreted via the kidneys. This explains why serum potassium levels rise as renal function deteriorates. Hyperkalemia has the potential of causing lethal arrhythmias and requires close monitoring. In renal failure, levels just slightly above the normal range are treated with either dialysis or medications, such as a cation exchange resin (Kayexalate®, Sanofi Pharmaceuticals), sodium bicarbonate or a combination of insulin and glucose to drive the potassium back into the cells. The referenced "panic value" for hyperkalemia is 7 mEq/L,1 but you should notify the physician for treatment orders at levels above 5.3 mEq/L.4 If your patient has renal failure, this electrolyte is the one to watch.

Magnesium: Like potassium, magnesium is also excreted via the kidneys. Levels rise as kidneys fail. Remember, magnesium is required in multiple processes in the body, including contraction of muscular tissue. At levels of 5 mEq/L and higher, cardioconduction is retarded, at 10 mEq/L, deep tendon reflexes are lost, at 15 mEq/L, respiratory paralysis occurs, and at 25 mEq/L, you can expect cardiac arrest.1 In caring for renal failure patients, make sure you avoid magnesium containing laxatives and antacids.

Phosphorus: Excreted and regulated via the kidneys, phosphorus also rises with renal failure. In the body, phosphorus is mainly (85 percent) combined with calcium in the bone. Its functions include metabolism of carbohydrates and fats, maintenance of the acid-base system and promotion of nerve and muscle activity. Elevated levels are not reported as panic values.1,4

Decreasing Serum Levels

While the above lab values rise as kidney function deteriorates, there are just as many values that will decrease with renal failure.

Hemoglobin/Hematocrit/Red Blood Cells (RBC): There are several reasons for declining levels of these three values. The most influential factor is decreased production of the hormone erythropoietin with renal failure. Erythropoietin, produced by the healthy kidney, stimulates red blood cell formation in the bone marrow. With declining levels of erythropoietin, as kidney failure progresses, you will see these values fall below normal.2,5

Other reasons for decreased levels include: 1. Decreased survival time of RBCs due to elevated uremic toxins; 2. Blood loss during the hemodialysis procedure; 3. Blood loss from frequent laboratory sampling; and 4. Blood loss from gastrointestinal bleeding.5

It is not unusual to see hematocrit levels of 20 percent-25 percent in patients with chronic renal failure. Treatment includes administration of epoetin alfa (Epogen,® Amgen, which has the same biologic effects as endogenous erythropoietin) and/or packed red blood cells.

Calcium: Calcium plays a major role in muscular contraction, cardiac function, transmission of nerve impulses, blood clotting and maintenance of bones.

As renal failure progresses, you will see a declining level for two reasons. First, the kidney is responsible for converting vitamin D to its active form. The active form of vitamin D (1,25-dihydroxoycholecalciferol) promotes calcium absorption from the intestine. Therefore, lower levels of active vitamin D in renal failure result in decreased absorption of calcium from the intestines. Second, remember that in renal failure, serum phosphorus levels increase. This increase in serum phosphorus leads to enhanced binding of phosphorus with calcium in the plasma, therefore, decreasing the plasma concentration of useable (ionized) calcium.6 Panic values for hypocalcemia are reported at 6 mg/dl, which can result in tetany and convulsions.1

pH: This value represents the acidity or alkalinity of body fluids. Since pH is based on the hydrogen ion (H+) concentration, and hydrogen ions contribute to the acidity of fluid, it makes sense that as H+ concentration increases, the acidity of the fluid increases (and pH decreases). This is exactly what happens in renal failure. The kidney is responsible for the secretion of H+ into the renal tubules for excretion or for combination with bicarbonate for buffering. If H+ cannot be secreted, their concentration in the blood increases, lowering the pH and leading to metabolic acidosis.2,3 Values at 7.30 or lower should be considered a panic value and immediately called to the attention of a physician.1

CO2 Content: Remember, this value is different than CO2 gas. Think of the CO2 content as a serum value that is mainly bicarbonate and a base. It is another general measure of the acidity or alkalinity of the blood (in addition to pH). CO2 content is regulated by the kidneys. Here's how: bicarbonate ions (HCO3-) in the renal tubules combine with H+ to form carbonic acid (H2CO3). Carbonic acid then dissociates into water and CO2. Carbon dioxide is a highly lipid soluble and diffuses easily from the renal tubules back into the blood (see Figure). In renal failure, there is a reduction in H+ secretion into the tubules and poorly filtrated bicarbonate, both leading to malfunctioning of this mechanism. As a result, the CO2 content drops.3,6 The low range panic value is 15 mEq/L or less, and is usually associated with metabolic acidosis.4

Albumin: In renal failure, especially chronic renal failure, malnutrition with a lowered albumin level can occur for a variety of reasons. Dietary restrictions, kidney dysfunction, alteration in taste and decreased food intake as a result of anorexia, nausea and vomiting can all contribute to this condition. Serum albumin levels of less than 3.4 gm/dl indicate protein deficiency and should be reported.5 Decreased levels of circulating albumin (below 2.4 gm/ dl) reduces oncotic pressure in the capillaries leading to fluid shifts into the interstitial space resulting in the edema seen clinically.

Review the Facts

Looking back at Mr. Norris' lab report, you see that most of his labs are what you would expect for a patient with chronic renal failure and in need of dialysis. The one value that may require intervention in addition to dialysis is the potassium level. The physician should be notified of his level of 5.5 mEq/L, otherwise, preparing Mr. Norris for dialysis would be your priority.

It is important to understand the physiology of abnormal lab values in the renal failure patient. A better understanding of the pathophysiology of the disease leads to improved decision making and patient education.

The rationale for interventions becomes clear and the need for continued monitoring obvious. Knowing what is "normal" for your renal failure patients and when to intervene will give you the expertise required to provide these patients with top-notch care. *

 

References

1. Fischbach, F. (1996). A manual of laboratory and diagnostic tests, 5th edition. Philadelphia: Lippincott-Raven.

2. Porth, C. (1998). Pathophysiology: Concepts of altered health states, 5th edition. Philadelphia: Lippincott-Raven.

3. Guyton, A., & Hall, J. (1996). Textbook of medical physiology, 9th edition. Philadelphia: W.B. Saunders Co.

4. Kee, J. (1999). Laboratory & diagnostic tests with nursing implications, 5th edition. Stamford, CT: Appleton & Lange.

5. American Nephrology Nurses Association. (1995). Core curriculum for nephrology nurses, 3rd edition. Pittman, NJ: ANNA.

6. Guyton, A., & Hall, J. (1997). Human physiology and mechanisms of disease, 6th edition. Philadelphia: W.B. Saunders Co.

Patricia Sengstack is a clinical nurse specialist in the pulmonary/renal unit of Washington Adventist Hospital, Takoma Park, MD.




     

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