Kidney Clinical Assessment and Diagnostic Procedures

Published on 07/03/2015 by admin

Filed under Critical Care Medicine

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 2 (1 votes)

This article have been viewed 3369 times

Kidney Clinical Assessment and Diagnostic Procedures

Mary E. Lough

Understanding the anatomic structures and physiologic workings of the kidneys provides the basis for understanding the clinical manifestations that signal kidney or renal vascular dysfunction. The body produces many clinical signs and symptoms that indicate kidney disorders. However, these signs and symptoms are often subtle, and although some symptoms point directly to the kidneys, many are exhibited by other body systems. A detailed history and careful physical examination help focus on the kidneys as the source of symptoms and often uncover the cause of the problem.

History

The history begins with a description of the chief complaint, stated in the patient’s own words. A description of the chief complaint includes the onset, location, duration, and factors or strategies that lessen or aggravate the problem.1 The individual should be encouraged to describe the effects of any treatment for the problem, prescription and nonprescription medications taken to alleviate symptoms, efforts taken to determine the cause of the problem, and procedures performed to improve the problem. A careful history that explores symptoms fully is an essential component of the clinical assessment.

Predisposing factors for acute kidney dysfunction are obtained during the history, including the use of over-the-counter medicines, recent infections requiring antibiotic therapy, antihypertensive medicines, and any diagnostic procedures performed using radiopaque contrast.2 Nonsteroidal anti-inflammatory medications (e.g., ibuprofen), antibiotics (especially aminoglycosides), antihypertensives (especially medicines that block angiotensin),3 and iodine-based dyes may cause an acute or chronic decline in kidney function. A history of recent onset of nausea and vomiting or appetite loss caused by taste changes (uremia often causes a metallic taste) may provide clues to the rapid onset of kidney problems.2 Symptoms that indicate rapid fluid volume gains are explored. For example, weight gains of more than 2 pounds per day, sleeping on additional pillows, and sitting in a chair to sleep are signals of volume overload and potential cardiac stress related to kidney dysfunction.

In addition to determining the immediate reason for admission to the critical care unit, compiling a complete medical and social history is important. Similar symptoms, problems, or treatment for similar complaints in the past may help establish the cause of the current problem or provide clues for treatment. For example, a history of obstructive urologic problems, frequent kidney infections, or previous acute kidney injury or failure may signal risk factors for current kidney problems. The patient, family member, or significant other should be encouraged to provide as much detail as possible during the history.

The family history may provide important information that points to the kidneys as the source of the patient’s symptoms. For example, the patient may reveal that one or two close family members have always had swelling of the extremities or high blood pressure. These symptoms should lead to questions about a history of kidney problems in the family. Box 26-1 summarizes the information gained from a kidney history.

Box 26-1   Data Collection

Kidney History

Physical Examination

In the critical care area, nursing assessment does not routinely include a full physical examination of the kidneys and urologic system. However, many of the assessment parameters for the kidneys provide information related to the volume status of the individual and are helpful in a large number of patients regardless of kidney function or status. Although not often performed in the depth described in the following sections, the critical care nurse must be aware of how to perform a thorough kidney assessment in stable patients and as needed in patients with kidney dysfunction.

Inspection

Bleeding

Visual inspection related to the kidneys focuses on the patient’s flank and abdomen. Kidney trauma is suspected if a purplish discoloration is present on the flank (Grey-Turner sign) or near the posterior 11th or 12th ribs.1 Bruising, abdominal distention, and abdominal guarding may also signal kidney trauma or a hematoma around a kidney. Individuals who have experienced a traumatic injury should be carefully assessed for signs of kidney trauma.

Volume

Inspection is especially helpful in looking for signs of volume depletion or overload that may signal or lead to kidney problems. Fluid volume assessment begins with an inspection of the patient’s jugular neck veins. The supine position facilitates normal jugular venous distention. An absence of distention (flat neck veins) indicates hypovolemia. Assessment continues with the head of the bed elevated 45 to 90 degrees.1 Fluid overload exists when the neck veins remain distended more than 2 cm above the sternal notch when the bed is at 45 degrees.4

Hand vein inspection may be helpful in assessing volume status, and is performed by observing for venous distention when the hand is held in the dependent position. Venous filling that takes longer than 5 seconds suggests hypovolemia. When the hand is elevated, the distention should disappear within 5 seconds. If distention does not disappear within 5 seconds after the hand is elevated, fluid overload is suspected.

Assessment of skin turgor provides additional data for identifying fluid-related problems. To assess turgor, the skin over the forearm is picked up and released.5 Normal elasticity and fluid status allow an almost immediate return to shape after the skin is released. In fluid volume deficit, however, the skin remains raised and does not return to its normal position for several seconds.5 Because of the loss of skin elasticity in older persons, skin turgor assessment may not be as accurate a fluid assessment measure for this age group.

Inspection of the oral cavity provides clues to fluid volume status. When a fluid volume deficit exists, the mucous membranes of the mouth become dry. However, mouth breathing and some medicines (e.g., antihistamines) can also dry the mucous membranes temporarily. The most accurate way to assess the oral cavity is to inspect the mouth using a tongue blade and light. Dryness of the oral cavity is more indicative of fluid volume deficit than are complaints of a dry mouth.4

Edema

Edema is the presence of excess fluid in the interstitial space, and it can be a sign of volume overload. In the presence of volume excess, edema may develop in dependent areas of the body, such as the feet and legs of an ambulatory person or the sacrum of an individual confined to bed. However, edema does not always indicate fluid volume overload. A loss of albumin from the vascular space can cause peripheral edema despite hypovolemia or normal fluid states. A critically ill patient may have a low serum albumin level (hypoalbuminemia) because of inadequate nutrition after surgery, a burn, or a head injury and may exhibit edema as a result of the loss of plasma oncotic pressure and not as a result of volume overload. Edema also may signal circulatory difficulties. An individual who is fluid balanced but who has poor venous return may experience pedal edema after prolonged sitting in a chair with the feet dependent. Similarly, an individual with heart failure may experience edema because the left ventricle is unable to pump blood effectively through the vessels. A key feature that distinguishes edema due to excess volume or hypoalbuminemia from circulatory compromise is that the edema does not reverse with elevation of the extremity.

Edema can be assessed by applying fingertip pressure on the swollen area over a bony prominence, such as the ankles, pretibial areas (shins), and sacrum. If the indentation made by the fingertip does not disappear within 15 seconds, pitting edema exists. Pitting edema indicates increased interstitial volume, and it usually is not evident until significant weight gain has occurred. Edema also may appear in the hands and feet, around the eyes, and in the cheeks. Dependent areas, such as the feet and sacrum, are the areas most likely to demonstrate edema in patients confined to a wheelchair or bed. One way of measuring the extent of edema is by using a subjective scale of 1 to 4, with 1 indicating only minimal pitting and 4 indicating severe pitting (Table 26-1).1 Other scales for assessing and measuring edema can be used (see Table 13-3).

TABLE 26-1

PITTING EDEMA SCALE

RATING APPROXIMATE EQUIVALENT
+1 2-mm depth
+2 4-mm depth (lasting up to 15 sec)
+3 6-mm depth (lasting up to 60 sec)
+4 8-mm depth (lasting longer than 60 sec)

Auscultation

Auscultation of the kidneys yields virtually no useful information. However, the renal arteries are auscultated for a bruit, a blowing or swishing sound that resembles a cardiac murmur (Fig. 26-1). The examiner listens for bruits above and to the left and right of the umbilicus.1 A renal artery bruit usually indicates stenosis, which may lead to acute or chronic kidney dysfunction due to compromised blood flow to one or both kidneys. A bruit over the upper portion of the abdominal aorta may indicate an aneurysm or a stenotic area that can decrease blood flow to the kidneys.

image
FIGURE 26-1 Sites for auscultation of bruits.

Auscultation is especially helpful in providing information about extracellular fluid (ECF) volume status. Listening for specific sounds in the heart and lungs provides information about the presence or absence of increased fluid in the interstitium or vascular space.

Blood Pressure

Blood pressure and heart rate changes are very useful in assessing fluid volume deficit.3 In stable critically ill patients or in patients on a telemetry unit, orthostatic vital sign measurements provide clues to blood loss, dehydration, unexplained syncope, and the effects of some antihypertensive medications. A drop in systolic blood pressure of 20 mm Hg or more, a drop in diastolic blood pressure of 10 mm Hg or more, or a rise in pulse rate of more than 15 beats/min from lying to sitting or from sitting to standing indicates orthostatic hypotension. Box 26-2 describes how to assess for orthostatic hypotension. The drop in blood pressure occurs because a sufficient preload is not immediately available when the patient changes position. The heart rate increases in an attempt to maintain cardiac output and circulation. Orthostatic hypotension produces subjective feelings of weakness, dizziness, or faintness. Orthostatic hypotension occurs with hypovolemia, prolonged bed rest, or as a side effect of medications that affect blood volume or blood pressure.

Box 26-2   Orthostatic Hypotension Assessment

BP, Blood pressure; HR, heart rate.

Palpation

Although rarely performed in critically ill patients, palpation of the kidneys in stable patients provides information about the kidneys’ size and shape. Palpation of the kidneys is achieved through the bimanual capturing approach. Capturing is accomplished by placing one hand posteriorly under the flank of the supine patient with the examiner’s fingers pointing to the midline and placing the opposite hand just below the rib cage anteriorly.1,2 The patient is asked to inhale deeply while pressure is exerted to bring the hands together (Fig. 26-2). As the patient exhales, the examiner may feel the kidney between the hands. After each kidney is palpated in this manner, the two should be compared for size and shape. Each kidney should be firm and smooth, and the two organs should be of equal size. The examiner is usually unable to palpate a normal left kidney. The right kidney is more easily palpated because of its lower position, caused by downward displacement by the liver. Problems should be suspected if a mass (cancer) or an irregular surface (polycystic kidneys) is palpated, a size difference is detected, the kidney extends significantly lower than the rib cage on either side, or there is evidence of recent blunt trauma.1

image
FIGURE 26-2 Palpation of the kidney. (From Barkauskas V, et al. Health and Physical Assessment. 3rd ed. St. Louis: Mosby; 2002.)

Percussion

Percussion is performed to detect pain in the area of a kidney or to determine excess accumulation of air, fluid, or solids around the kidneys. Percussion of the kidneys also provides information about kidney location, size, and possible problems. Like palpation, percussion of the kidneys is not a routine part of a nursing assessment in critical care. However, the information gained through percussion can provide important patient-care data.

Kidneys

Percussion of a kidney is performed with the patient in a side-lying or sitting position, with the examiner’s hand placed over the costovertebral angle (lower border of the rib cage on the flank).1 Striking the back of the hand with the opposite fist produces a dull thud, which is normal. Pain may indicate infection (e.g., urinary tract infection that has extended into the kidneys) or injury resulting from trauma. Traumatic injury to the kidneys should be assessed in the presence of a penetrating abdominal wound, with blunt abdominal trauma, or with a fractured pelvis or ribs.

Abdomen

Observation and percussion of the abdomen may help in assessing fluid status. Percussing the abdomen with the patient in the supine position generally yields a dull sound (solid bowel contents or fluid) or a hollow sound (gaseous bowel).1

Ascites, or excess fluid accumulation and distention of the abdominal cavity, is an important observation in determining fluid overload. Differentiating ascites from distortion caused by solid bowel contents is accomplished by producing a fluid wave. A fluid wave is elicited by exerting pressure to the abdominal midline while one hand is placed on the right or left flank.1 Tapping the opposite flank produces a wave in the accumulated fluid that can be felt under the hands (Fig. 26-3). Other signs of ascites include a protuberant, rounded abdomen and abdominal striae.1

image
FIGURE 26-3 Test for the presence of a fluid wave. (From Barkauskas V, et al. Health and Physical Assessment. 3rd ed. St. Louis: Mosby; 2002.)

Individuals with kidney failure may have ascites caused by volume overload, which forces fluid into the abdomen due to increased capillary hydrostatic pressures. However, ascites may or may not represent fluid volume excess. Severe ascites in persons with compromised liver function may result from decreased plasma proteins. The ascites occurs because the increased vascular pressure associated with liver dysfunction forces fluid and plasma proteins from the vascular space into the interstitial space and abdominal cavity. Although the individual may exhibit marked edema, the intravascular space is volume depleted, and the patient is hypovolemic.

Additional Assessments

Weight Monitoring

One of the most important assessments of kidney and fluid status is the patient’s weight. In the critical care unit, weight is monitored for each patient every day and is an important vital signs measurement. Significant fluctuations in body weight over a 1- to 2-day period indicate fluid gains and losses. Rapid weight gains or losses of more than 2 pounds per day usually indicate fluid rather than nutritional factors. One liter of fluid equals 1 kg, or approximately 2.2 pounds.

Whenever possible, the patient is weighed during admission to the critical care unit. It is important to document whether the current weight differs significantly from the weight 1 to 2 weeks before admission to the hospital. The patient is weighed daily for comparison with the previous day’s weight. The weight is obtained at the same time each day, with the patient wearing the same amount of clothing and using the same scales. The individual’s weight is of critical importance to the dialysis nurse caring for a patient with acute or chronic kidney failure. The differences in weight from day to day are used to calculate the amount of fluid to remove during a dialysis treatment.6

Intake and Output Monitoring

Like patient weight, intake and output are monitored for all patients in the critical care unit. Intake and output can be compared with the patient’s weight to more accurately evaluate fluid gains or losses. Urinary output plus insensible fluid losses (perspiration, stool, and water vapor from the lungs) can vary by 750 to 2400 mL/day. When intake exceeds output (e.g., excessive intravenous fluid, decreased urine output), a positive fluid balance exists. In impaired kidney function, the positive fluid balance results in fluid volume overload. Conversely, if output exceeds intake (e.g., fever, increased respiration, profuse sweating, vomiting, diarrhea, gastric suction, diuretic therapy), a negative fluid balance exists, and volume deficit results. During a 24-hour period, fever can increase skin and respiratory losses by as much as 75 mL per 1° F increase in temperature.

Individuals with acute kidney injury (AKI) often exhibit a decrease in urine output, or oliguria (less than 0.5 mL/kg/hr in adults; less than 1 mL/kg/hr in infants and young children). However, there may be a fairly normal or only slightly decreased urine output that reflects water removal without solute removal in the early phases of AKI. Although urine output is a sensitive indicator, kidney function cannot be accurately determined by urine output alone. For additional information on AKI see Chapter 27.

Abnormal output of body fluids creates fluid imbalances and causes electrolyte and acid–base disturbances. For example, gastrointestinal suction or loss by diarrhea can result in fluid deficit, sodium and potassium deficits, and metabolic acidosis from excessive loss of bicarbonate.

In maintaining daily records of intake and output, all gains or losses must be recorded. A standard list of the fluid volume held in various containers (e.g., milk cartons, juice containers) expedites this process. Discussions about the importance of accurate intake and output with the patient and family or friends are necessary and can improve the accuracy of intake and output volumes assessment.

Hemodynamic Monitoring

Body fluid status is accurately reflected in measurements of cardiovascular hemodynamics. Measurements such as central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP), cardiac index (CI), and mean arterial pressure (MAP) provide a clear picture of the increases or decreases in vascular volume returning to and being ejected from the heart.7 Volume depletion and volume overload are easily detected by use of central venous or arterial catheters, from which pressure measurements can be obtained (Table 26-2).

TABLE 26-2

HEMODYNAMIC ASSESSMENT OF FLUID STATUS

MEASUREMENT VOLUME DEPLETION VOLUME OVERLOAD
Central venous pressure (CVP) <2 mm Hg >5 mm Hg
Pulmonary artery occlusion pressure (PAOP) <5 mm Hg >12 mm Hg
Cardiac index (CI) <2.2 L/min/m2 >4 L/min/m2
Mean arterial pressure (MAP) Decreased Increased

A central venous catheter often is inserted to evaluate fluid volume status and to measure the CVP. The CVP represents the filling pressure of the right atrium and is a measurement of right ventricular preload. The CVP changes with fluctuations in volume status. A normal CVP is 2 to 5 mm Hg. In volume depletion, the CVP is less than 2 mm Hg, whereas volume overload is reflected by readings of more than 5 mm Hg (see “Bedside Hemodynamic Monitoring” in Chapter 14 for more information on CVP interpretation).

If the patient has coexisting cardiopulmonary disease or if more information about hemodynamic function is required, a pulmonary artery catheter may be inserted. This catheter provides information about left ventricular filling pressures and cardiac output. The PAOP represents the left atrial pressure required to fill the left ventricle. When the left ventricle is full at the end of diastole, it represents the volume of blood available for ejection. It is also known as left ventricular preload and is measured by the PAOP. The normal PAOP is 5 to 12 mm Hg. In fluid volume excess, the PAOP increases. In fluid volume deficit, the PAOP is low.7

The CI demonstrates the cardiac output, or amount of blood ejected by the left ventricle over 1 minute, standardized for body size. The normal CI is 2.2 to 4 L/min/m2. Compensatory mechanisms in early hypovolemic shock maintain the CI at or near normal. With prolonged fluid loss, the CI decreases. Fluid volume overload increases heart rate, which increases cardiac output, but only to a point. Left ventricular failure may result from massive volume overload, such as with acute heart failure resulting from kidney failure, in which case the CI decreases. The most common cause of AKI in which hemodynamic monitoring is indicated is severe sepsis.7

MAP is regulated by cardiac output and systemic vascular resistance (SVR), and it represents an averaged blood pressure within the arterial system. Changes in cardiac output or SVR inevitably result in corresponding MAP changes. For example, an increase in SVR during the early stages of hypovolemic shock leads to elevation of the MAP. Ongoing fluid losses eventually lead to a decreased cardiac output, which leads to a reduction in MAP. The net effect of a decreased MAP to the kidneys is a reduction in effective blood flow, which may lead to AKI.

Other Observations

Kidney system dysfunction often leads to fluid and electrolyte imbalances and the retention of metabolic waste products. Some of the disturbances in fluid, electrolyte, and waste product levels are accompanied by clinical manifestations less observable or measurable than those previously mentioned but that indicate a change from normal function. Box 26-3 summarizes important aspects to consider during kidney and fluid and electrolyte assessment.

Box 26-3   Fluid and Electrolyte Assessment

Sudden or slowly developing changes in cognitive function and mental status must be investigated. For example, acidosis often results in disorientation. Lethargy, decreased attention or memory, coma, and confusion may result from sodium, calcium, or magnesium excess or deficit or retained waste products. Apprehension or anxiety may result from sodium deficit, a shift of fluid from the plasma to the interstitium, or respiratory changes caused by fluid volume overload. In older adults, new-onset confusion or a fall incurred by a previously mobile, alert individual may signal volume deficit in the absence of apparent acute illness.8

Apathy and withdrawal may accompany hypovolemic states. Patients with kidney failure and the accompanying systemic increases in electrolytes, fluids, and nitrogenous waste products may exhibit apathy, restlessness, confusion, and withdrawal.2 The speed of onset depends on how rapidly or slowly the kidney failure progresses and alters homeostasis.

Laboratory Assessment

There is no single or ideal laboratory test or marker that detects a decrease in kidney function.11 Laboratory tests (serum and urine) used to detect and diagnose kidney dysfunction have limitations, but when reviewed daily for changes or trends, they provide valuable information concerning the status of the kidneys. Small changes in kidney function are associated with short- and long-term outcomes for hospitalized patients.9 In addition to the history and physical examination, laboratory data are extremely helpful in the diagnosis, management, and ongoing evaluation of kidney system dysfunction.

Serum Components

Blood Urea Nitrogen

Blood urea nitrogen (BUN) is a byproduct of protein and amino acid metabolism. The normal value for BUN is 5 to 20 mg/dL, which is increased when kidney function deteriorates. With kidney dysfunction, the BUN is elevated because of a decrease in the glomerular filtration rate (GFR) and resulting decrease in urea excretion. Elevations in the BUN can be correlated with the clinical manifestations of uremia; as the BUN rises, symptoms of uremia become more pronounced.2 However, a drop in the GFR with an increase in the BUN also may be caused by hypovolemia and dehydration, nephrotoxic medications, or a sudden hypotensive episode. In these cases, the rise in BUN is caused by a decreased GFR in the presence of normal kidney function. BUN is also increased by changes in protein metabolism that occur with excessive protein intake and catabolism. A catabolic state may occur with starvation (or chronic poor nutrition in a critically ill patient), severe infection, surgery, or trauma. The BUN level also may be elevated as the result of hematoma resorption, gastrointestinal bleeding, excessive licorice ingestion, or steroid or tetracycline therapy. A decrease in the BUN level may indicate volume overload, liver damage, severe malnutrition (as a result of depleted protein stores), use of phenothiazines, or pregnancy.

Creatinine

Creatinine is a byproduct of muscle and normal cell metabolism, and it appears in serum in amounts generally proportional to the body muscle mass. Although slightly higher in males than females, the normal serum creatinine level is about 0.5 to 1.2 mg/dL. Creatinine is freely filtered by the glomerulus, easily excreted by the kidney tubules, and minimally resorbed or secreted in the tubules.2 Creatinine levels are fairly constant and are affected by fewer factors than BUN. As a result, the serum creatinine level is a more sensitive and specific indicator of kidney function than BUN. Creatinine excess occurs most often in persons with kidney failure resulting from impaired excretion. However, the body’s production and release of creatinine may vary during muscle wasting in acute illness, leading to a falsely low serum level of creatinine. Elevated levels of creatinine are seen in muscle growth disorders such as acromegaly, with traumatic skeletal muscle injury, and with some medications that decrease creatinine removal (e.g., trimethoprim, cimetidine) in the absence of kidney dysfunction. Malnutrition can result in transient increases in creatinine levels as the rapid muscle catabolism associated with malnutrition releases increased amounts of creatinine into the circulation.

BUN to Creatinine Ratio.

Another useful diagnostic parameter in kidney disease is the ratio of blood urea nitrogen (BUN) to creatinine. The usual ratio of BUN to creatinine is 10 to 1, and a change in the ratio may indicate kidney dysfunction. For example, if BUN and creatinine levels are elevated and maintained at an approximate ratio of 10 to 1, the disorder is intrarenal, or affecting the tubules of the kidneys. If the ratio of BUN to creatinine levels is greater than 10 to 1, the cause is most likely prerenal (e.g., hypovolemia). In prerenal kidney failure, the creatinine is excreted by functioning tubules, but the urea nitrogen is retained because of the poor GFR and hemoconcentration, leading to the increased ratio. In the diagnosis of prerenal kidney failure, the ratio is a more useful indicator of kidney function than the separate tests of BUN and creatinine.

Creatinine Clearance

The urine creatinine clearance is a measure of how well the kidneys remove creatinine. Because of the relatively constant rate at which creatinine is produced and the nearly complete removal of creatinine by normal kidneys, the ability of the kidneys to remove (clear) creatinine from the blood is an indication of how well the glomeruli and tubules are working. Measuring the creatinine clearance—the amount of creatinine in the excreted urine and the amount of creatinine in the blood over 24 hours—provides a reliable and accurate estimate of glomerular filtration and therefore of kidney function.2 The normal value for creatinine clearance is 110 to 120 mL/min; values less than 50 mL/min indicate significant kidney dysfunction. The creatinine clearance is traditionally measured using a 12- or 24-hour urine collection and blood sample. Newer methods use a random, smaller-volume urine specimen and blood sample. Creatinine clearance can also be estimated from the serum creatinine level (Box 26-4), a method commonly used in the critical care unit. The estimated or calculated creatinine clearance is widely used to determine changes in medication dosing with kidney dysfunction because of the many medications excreted by the kidneys.

Box 26-4   Creatinine Clearance Calculations*

*Online calculators available from the National Kidney Foundation at http://www.kidney.org/professionals.

†Both risk factor assessments apply for African American women. The number would be multiplied by both 0.742 (woman) and 1.210 (African American).

Cystatin C

Although not widely used in practice, cystatin C is another serum marker for kidney function. Cystatin C is a substance synthesized and released by most cells in the body at a constant rate.10 Like creatinine, cystatin C is filtered easily by the glomerulus and not secreted or resorbed by the tubules. The advantage of cystatin C is that it is metabolized by the tubules. In normal kidney function, cystatin C levels are very low because the glomerulus filters it and the tubules metabolize it. In kidney dysfunction, the glomerular filtration of cystatin C is reduced and therefore not provided to the tubules for metabolism. Cystatin C is affected by fewer factors (e.g., age, gender, muscle mass) than creatinine, and a change in its level can be detected earlier during AKI than creatinine.10 Cystatin C and other kidney-related biomarkers may become more widely used as a kidney function marker as additional clinical validation studies are completed.10

Osmolality

The serum osmolality reflects the concentration or dilution of vascular fluid and measures the dissolved particles in the serum. The normal serum osmolality is 275 to 295 mOsm/L.3 An elevated osmolality level indicates hemoconcentration or dehydration, and a decreased osmolality level indicates hemodilution or volume overload. When the serum osmolality level increases, antidiuretic hormone (ADH) is released from the posterior pituitary gland and stimulates increased water resorption in the kidney tubules. This expands the vascular space, returns the serum osmolality level back to normal, and results in more concentrated urine and an elevated urine osmolality level. The opposite occurs with a decreased serum osmolality level, which inhibits the production of ADH. The decreased ADH results in increased excretion of water in the tubules, producing dilute urine with a low osmolality, and returns the serum osmolality level back to normal. Sodium accounts for 85% to 95% of the serum osmolality value; doubling the serum sodium level gives an estimate of the serum osmolality level in healthy individuals. Other particles in the serum can increase the osmolality and need to be considered in individuals with common comorbid conditions. A more precise estimation of serum osmolality can be calculated from the following formula:

2×Na(mEq / L)+BUN / 3(mg / dL)+Glucose / 18(mg / dL)

image

The calculated serum osmolality level is a useful tool while awaiting full laboratory results. Measured serum osmolality is a useful parameter in determining fluid balance and fluid replacement therapy for critically ill patients. Serum osmolality is also a useful parameter in determining disorders of ADH secretion that may occur in critically ill patients. A decreased serum osmolality level may indicate syndrome of inappropriate ADH secretion (SIADH), or too much ADH, whereas an elevation of the serum osmolality level may indicate diabetes insipidus (DI), or too little ADH.

Anion Gap

The anion gap is a calculation of the difference between the measurable extracellular plasma cations (sodium and potassium) and the measurable anions (chloride and bicarbonate).3 In plasma, sodium is the predominant cation and chloride is the predominant anion. Extracellular potassium concentration in plasma is so small that it is generally ignored, leaving the following equation for calculation of the anion gap:

[Na+]−([Cl−]+[HCO3−])

image

The normal anion gap is 8 to 16 mEq/L, a range that has been verified in a healthy population of adults.11 The “gap” represents the unmeasurable ions present in the ECF (phosphates, sulfates, ketones, lactate). An increased anion gap level usually reflects overproduction or decreased excretion of acid products and indicates metabolic acidosis; a decreased anion gap indicates metabolic alkalosis.

Acute and chronic kidney failure can increase the anion gap because of retention of acids and altered bicarbonate resorption.12 The anion gap is also increased in diabetic ketoacidosis caused by ketone production. The measurement of the anion gap is a rapid method for identifying acid–base imbalance but cannot be used to pinpoint the source of the acid–base disturbance specifically.

Hemoglobin and Hematocrit

The hemoglobin and hematocrit levels can indicate increases or decreases in intravascular fluid volume. Hemoglobin and hematocrit values vary between genders; the hemoglobin level in males is normally 13.5 to 17.5 g/dL, and in females, it is 12 to 16 g/dL. The hematocrit level is 40% to 54% in males and 37% to 47% in females. Hematocrit levels are higher in newborns (up to 65%) and decrease to adult ranges between the ages of 4 and 10 years. Hemoglobin transports oxygen and carbon dioxide and is important in maintaining cellular metabolism and acid–base balance.3

The hematocrit value is the proportion or concentration of red blood cells (RBCs) in a volume of whole blood and is expressed as a percentage. The hematocrit level is approximately three times the hemoglobin level if the individual is in a normal fluid balance. An increase in the hematocrit value often indicates a fluid volume deficit, which results in hemoconcentration. Although rare, true disorders of RBC production, such as polycythemia, can result in an increased hematocrit level.

Conversely, a decreased hematocrit value can indicate fluid volume excess because of the dilutional effect of the extra fluid load. Decreases also can result from anemias, blood loss, liver damage, or hemolytic reactions. In individuals with acute kidney failure, anemia may occur early in the disease.13 A decreased hematocrit level may indicate the anemia of kidney failure or may reflect fluid volume overload. If the hematocrit value is decreasing but the hemoglobin concentration remains constant, the cause is fluid volume overload. Decreased hematocrit values and hemoglobin concentrations indicate a true loss of RBCs. The history and bedside assessment, including hemodynamic monitoring data, aid in determining whether fluid imbalances or disease states, or both, are responsible for changes in hematocrit levels in the critically ill patient.

Albumin

Slightly more than 50% of the total plasma protein is serum albumin. It is manufactured in the liver, and a normal blood level is 3.5 to 5 g/dL. Albumin is primarily responsible for the maintenance of colloid osmotic pressure, which functions to hold fluid in the vascular space. The blood vessel walls, because of their impermeability to plasma proteins, prevent albumin from leaving the vascular space. However, in some disease states such as severe burns (cell membrane destruction) or nephrotic syndrome (increased glomerular capillary permeability to protein and protein loss in the urine), albumin is lost from the vascular space.

Decreased albumin levels in the vascular space result in a fluid shift from the plasma to the interstitium, creating peripheral edema. A decreased albumin level can result from protein-calorie malnutrition, which occurs in many critically ill patients in whom available stores of albumin are depleted. A decrease in the plasma oncotic pressure results, and fluid shifts from the vascular space to the interstitial space. Liver disease or severe injury to the liver also causes a decrease in albumin levels as the diseased liver fails to synthesize sufficient albumin. Severe portal hypertension can force albumin and other plasma proteins into the abdominal cavity, resulting in ascites.

Increased albumin levels are rare. The body uses a fixed amount of protein for energy and body cell replacement and converts excess protein into stored fat. If all plasma protein levels are elevated, fluid volume deficit (hemoconcentration) is suspected.

Urinalysis

Analysis of the urine provides excellent information about the patient’s kidney function and condition relative to fluids and electrolytes. Specific tests and abnormal indications are presented in Table 26-3. In the critically ill patient a routine urinalysis specimen may be obtained to rule out the presence of urinary protein or glucose. A sterile urine culture may be obtained if a urinary tract infection (UTI) is suspected.

TABLE 26-3

URINALYSIS RESULTS

TEST NORMAL POSSIBLE CAUSES FOR INCREASED VALUES POSSIBLE CAUSES FOR DECREASED VALUES
pH 4.5-8.0 Alkalosis Acidosis
      Intrarenal AKI
Specific gravity 1.003-1.030* Volume deficit Volume overload
    Glycosuria Intrarenal AKI
    Proteinuria  
    Prerenal AKI (>1.020)  
Osmolality 300-1200 mOsm/kg Volume deficit Volume excess
    Prerenal AKI (urine > serum osmolality) Intrarenal AKI (urine < serum osmolality)
Protein 30-150 mg/24 hr† Trauma  
    Infection  
    Intrarenal AKI  
    Transient with exercise  
    Glomerulonephritis  
Sodium 40-220 mEq/24 hr High-sodium diet Prerenal AKI
    Intrarenal AKI  
Creatinine 1-2 g/24 hr   Intrarenal AKI
      Chronic kidney failure
Urea 6-17 g/24 hr   Intrarenal AKI
      Chronic kidney failure
Myoglobin Absent Crush injury  
    Rhabdomyolysis  
RBCs 0-5‡ Trauma  
    Intrarenal AKI  
    Infection  
    Strenuous exercise  
    Renal artery thrombus  
WBCs 0-5‡ Infection  
Bacteria None to few Infection  
Casts None to few RBC: glomerular disease  
    WBC: pyelonephritis  
    Glomerular disease  
    Nephrotic syndrome  
    Epithelial: glomerular disease  

image

AKI, Acute kidney injury; RBCs, red blood cells; WBCs, white blood cells.

*Adult value; newborn value is slightly lower at 1.001-1.020.

†Higher values usually apply for persons after exercise; lower values apply for persons at rest.

‡Cells per low-power field.

Urine pH

Urine pH indicates the acidity or alkalinity of the urine. The normal urinary pH is acidic but has a range from 4.5 to 8.14 The kidneys regulate acid–base balance; more hydrogen ions are excreted than bicarbonate ions, causing the acidity of the urine. Changes in metabolic function and kidney function produce changes in urinary pH.

An increase in urinary acidity (decreased pH) indicates retention of sodium and acids by the body, which occurs in intrarenal AKI. A decrease in urinary acidity (increased pH or more alkaline) means the body is retaining bicarbonate. In the presence of normal kidney function, urinary pH levels are greatly affected by diet and medications. Certain food groups, such as citrus fruits and vegetables, lead to alkaline urine, whereas a diet high in protein can produce acidic urine. In the critical care unit, patients receiving total parenteral nutrition or a high-protein tube-feeding formula may have acidic urine because of high protein intake.

Urine Specific Gravity

Specific gravity measures the density or weight of urine compared with that of distilled water. The normal urinary specific gravity is 1.005 to 1.025.14 For comparison, the specific gravity of distilled water is 1.000. Because urine is composed of many solutes and substances suspended in water, the specific gravity should always be higher than that of water.

The specific gravity reflects hydration status and indicates the ability of the kidneys to dilute or concentrate the urine. Decreases in specific gravity reflect the inability of the kidneys to excrete the usual solute load into the urine (less dense with fewer solutes). Increases in specific gravity are caused by dehydration (more concentrated urine), or with additional glucose (diabetes) or protein (glomerular dysfunction) that increase urine density.14 A fixed specific gravity (does not vary with fluid intake) suggests early kidney dysfunction because the kidneys are unable to excrete or resorb water and solutes.

Urine Protein

Protein normally is absent from urine because protein molecules are too large to be filtered across the intact glomerular capillary membrane. Protein amounts greater than 150 mg/day signal compromise of the glomerular membrane and intrinsic kidney damage.14

Traditionally, quantitative measurement of the amount of protein in the urine required a 24-hour urine collection.14 A “spot” or random urine sample can also be used as the correlation between the two tests is very strong.14 Both the amount of protein and the amount of creatinine in the urine specimen are measured. A normal urine protein to urine creatinine ratio is less than 0.2; a protein-to-creatinine ratio of 3.5 indicates approximately 3.5 grams of protein are being excreted per day, indicating severe protein loss by the kidneys.

Urine Glucose

Glycosuria is defined as glucose in the urine. Glucose normally is completely resorbed by the kidney tubules, and the urine should be free of glucose. Urinary glucose should not exceed 130 mg per day.14 In the presence of acute or chronic kidney failure, glycosuria may not be a reliable indicator of the level of hyperglycemia because of the damaged nephrons. In the critical care unit, the serum glucose is measured, not urine values.

Urine Electrolytes

Levels of electrolytes in the urine are not measured as often as levels in serum, but they can yield information about kidney function. To measure urinary electrolyte levels, a 24-hour urine sample may be needed, although potassium and sodium can be measured in a randomly collected specimen.

Urine Sodium.

The most commonly measured electrolyte in the urine is sodium. Urinary sodium is a reflection of the action of aldosterone and subsequent retention or excretion of sodium by the kidney tubules to maintain fluid balance. In the presence of hypovolemia, the kidney tubules retain sodium (and therefore water), and the amount of sodium in the urine and the fractional excretion of sodium are very low. The opposite is true with volume overload and with kidney diseases that cause sodium wasting. The amount of sodium in the urine can help in determining the pathology of AKI as long as diuretics have not been administered. In prerenal AKI due to ineffective circulation reaching the kidneys, the urine sodium level is low. If the AKI results from damage to the kidney tubules, the urine sodium level is normal or elevated.

Urine Sediment

The presence of sediment such as epithelial cells and casts in urine aids in identifying problems related to the kidneys.14 A fresh urine specimen, tested 30 to 60 minutes following collection, is important.14 Urine becomes more alkaline after it has been collected, resulting in a change in the urine sediment (e.g., casts dissolve, cells lyse). The presence or absence of urine sediment can be helpful in identifying the cause of AKI. In prerenal AKI, the kidneys are not injured, and urinary sediment is absent. However, in intrarenal AKI, the kidney glomeruli or tubules are damaged, allowing urinary sediment containing casts and epithelial cells in the urine.14

Casts are cylindrical structures composed mainly of mucoprotein (Tamm-Horsfall protein), which is secreted by epithelial cells lining the loops of Henle, the distal tubules, and the collecting ducts. Casts may form in the presence of epithelial cells, RBCs, or WBCs in the tubular lumen. These cells or clumps of cellular breakdown products can adhere to and be surrounded by the fibrillar mucoprotein matrix, and the resulting casts are washed out of the kidney tubular system in the urinary flow. Casts differ in composition and size and correlate with the severity and type of kidney damage. For example, WBC casts indicate pyelonephritis, or they may occur during acute glomerulonephritis. RBC casts indicate glomerulonephritis. Hyaline casts, which consist of Tamm-Horsfall protein, are associated with kidney parenchymal disease and glomerular capillary membrane inflammation. Consistent appearance of epithelial cells shed by the lining of the nephron may indicate nephritis. Although small numbers of epithelial cells normally appear in the urine and an occasional cast may be found, their consistent appearance is abnormal.14

Hematuria

Obvious and microscopic hematuria may signal kidney damage. Although a few RBCs in the urine are normal, discernibly bloody urine usually indicates bleeding within the urinary tract or kidney trauma. Microscopic hematuria may occur normally after strenuous exercise or the insertion of a retention catheter but should disappear within 48 hours.

The presence of myoglobin can make the urine appear red. Microscopic examination of the urine fails to reveal RBCs, with myoglobin being present instead. Myoglobin in the urine may result from skeletal muscle damage (e.g., traumatic crush injury) or rhabdomyolysis. Rhabdomyolysis may develop in patients admitted to a critical care unit for many reasons, including traumatic injury, cocaine abuse, status epilepticus, heat prostration, or collapse during intense physical exercise (e.g., running a marathon race on a hot day). Myoglobin is released by the muscle cells and blocks the tubules that can result in intrarenal AKI.

Urine Toxicology Screen

Urine can be screened to detect the presence of alcohol, illegal drugs, prescription and nonprescription medications, and other substances that are excreted via the kidneys.15 The is often referred to as a Urine Drug Screen (UDS).15 Urine toxicology tests conducted in the emergency department or the critical care unit are considered screening tests and are not diagnostic of a disease state.15 These analyses are typically undertaken to provide information about causes of an altered level of consciousness rather than to identify kidney-related problems.

Imaging Studies

Although laboratory assessment is used most often in diagnosing kidney problems in the critically ill patient, imaging studies can confirm or clarify causes of particular disorders. Imaging assessment includes the use of ultrasound and radiologic techniques. Ultrasound is a noninvasive imaging technique that is available in most hospitals. Kidney ultrasound is especially useful in determining the size, shape, and contour of the kidneys, the presence of masses or cysts, and the presence of renal artery stenosis.16 Radiologic assessment ranges from basic to more complex (Table 26-4) and provides information about abnormal masses, abnormal fluid collections, obstructions, vascular supply alterations, and other disorders of the kidneys and urinary tract.16

TABLE 26-4

KIDNEY IMAGING TESTS

TEST COMMENTS
Kidney-ureter-bladder (KUB) radiograph Flat-plate radiograph of the abdomen; determines position, size, and structure of the kidneys, urinary tract, and pelvis; useful for evaluating the presence of calculi and masses; usually followed by additional tests
Intravenous pyelogram (IVP) Intravenous injection of contrast with radiography; allows visualization of internal kidney tissues
Angiography Injection of contrast into arterial blood perfusing the kidneys; allows visualization of renal blood flow; may also visualize stenosis, cysts, clots, trauma, and infarctions
Computed tomography (CT) Radioisotope is administered by intravenous route and absorbed by the kidneys; scintillation photography is then performed in several planes; spiral or helical CT allows rapid imaging; density of the image helps evaluate kidney vessels, perfusion, tumors, cysts, stones/calculi, hemorrhage, necrosis, and trauma
Ultrasound High-frequency sound waves are transmitted to the kidneys and urinary tract, and the image is viewed on an oscilloscope; noninvasive; identifies fluid accumulation or obstruction, cysts, stones/calculi, and masses; useful for evaluating kidney before biopsy
Magnetic resonance imaging (MRI) A scanner produces three-dimensional images in response to the application of high-energy radiofrequency waves to the tissues; produces clear images; density of the image may indicate trauma, cysts, masses, malformation of the vessels or tubules stones/calculi, and necrosis

Some radiologic studies require the use of contrast or injection of a radiopaque dye. Because many of the dyes used in radiology are potentially nephrotoxic, they must be used carefully in patients with AKI or chronic kidney disease.17,18 To prevent contrast induced nephrotoxicity (CIN), adequate hydration before and after the test and careful monitoring of kidney function are always indicated.17,18

Kidney Biopsy

Kidney biopsy is the definitive tool for diagnosing disease processes involving the parenchyma of the kidney. Percutaneous needle biopsy involves inserting a needle through the flank to obtain a specimen of cortical and medullary kidney tissue.19,20 An open biopsy is a surgical procedure and is rarely done in critically ill patients. In either case, biopsy is the last choice for diagnostic assessment in the critically ill patient because of the periprocedural risks of bleeding, hematoma, and infection.19,20

Summary

Clinical Assessment

Laboratory Studies

Related posts:

Ethical Issues Sedation, Agitation, Delirium: Assessment and Management Shock, Sepsis, and Multiple Organ Dysfunction Syndrome Gastrointestinal Disorders and Therapeutic Management Pulmonary Diagnostic Procedures Cardiovascular Diagnostic Procedures