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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2593_Библиотеки_им_академика_М_И_Перельмана
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(Eq. 2-1)
and glucosuria), use of thiazide or loop diuretics (eg,
hydrochlorothiazide, furosemide, respectively), excessive
mineralocorticoid activity, or protracted vomiting. Although the fluid
secreted along most of the upper gastrointestinal (GI) tract contains
only a modest amount of potassium (ie, 5–20 mEq/L), vomiting can
induce hypokalemia because of the combined effect from decreased
food intake, loss of acid, alkalosis, and loss of sodium. The loss of
large amounts of colonic fluid through severe diarrhea and/or
laxative abuse can cause potassium depletion because fluid in the
colon is high in potassium content (ie, 30–40 mEq/L). Insulin and
stimulation of β2-adrenergic receptors can also induce hypokalemia
because both increase the movement of potassium into cells from
the ECF. The magnitude of a potassium deficiency is difficult to
establish because of the limited presence of potassium in the ECF.
Equation 2-1 can be used to estimate the potassium deficit with
hypokalemia:
It is also important to note that hypomagnesemia often
accompanies hypokalemia, because magnesium is necessary for the
shifting of sodium, potassium, and calcium in and out of cells. As a
result, individuals with hypokalemia not responding to potassium
therapy may be refractory to treatment until hypomagnesemia is
corrected. Some laboratories omit magnesium from the general
electrolyte panel, so this test may need to be specially ordered.
HYPERKALEMIA
Hyperkalemia most commonly results from decreased renal
excretion of potassium (eg, renal failure, renal hypoperfusion, and
hypoaldosteronism), excessive exogenous potassium administration,
or excessive cellular breakdown (eg, hemolysis, burns, crush
injuries, surgery, and infections). Drug-induced causes include
angiotensin-converting enzyme (ACE) inhibitors, angiotensin-
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receptor blockers (ARBs), aldosterone antagonists, and nonsteroidal
anti-inflammatory drugs, to name a few. Metabolic acidosis can also
induce hyperkalemia because hydrogen ions move into cells in
exchange for potassium and sodium. Abnormal potassium
concentrations in the serum primarily affect excitability of nerve and
muscle tissue (eg, myocardial tissue). As a result, arrhythmias can
be induced by hyperkalemia or hypokalemia. Potassium also affects
some enzyme systems and acid–base balance, as well as
carbohydrate and protein metabolism.
Carbon Dioxide Content
Reference Range: 21–32 mEq/L or mmol/L
The carbon dioxide (CO2) content in the serum represents the sum
of bicarbonate (HCO
3
−
) and dissolved CO2 concentrations. The
dissolved CO2 represents a relatively small component of total CO
2
content, making CO2 essentially a measure of the serum
bicarbonate. Chloride and bicarbonate are the primary negatively
charged anions that offset the positively charged cations (ie, sodium
and potassium). CO2 is a waste product that is produced after we
burn food for energy. Healthy individuals are able to maintain CO2 in
an appropriate range. A CO2 level below the reference range is
associated with such conditions as diabetic ketoacidosis, Addison
disease, and metabolic acidosis. A CO2 level above the reference
range is associated with dehydration, Cushing syndrome, and
metabolic alkalosis.
Although several buffer systems (eg, hemoglobin [Hgb],
phosphate, and protein) participate in regulating pH within
physiologic limits, the carbonic acid–bicarbonate system is the most
important. From a clinical standpoint, most disturbances of acid–
base balance result from imbalances of the carbonic acid–
bicarbonate system. The importance of bicarbonate in maintaining
physiologic pH is presented in Chapter 26, Acid–Base Disturbances.
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(Eq. 2-2)
Chloride
Reference Range: 95–110 mEq/L or mmol/L
Chloride (Cl−) is the principal inorganic anion of the ECF; changes in
chloride concentration are usually related to sodium concentration in
an effort to maintain a neutral charge. Serum chloride has no real
diagnostic significance. The relationship between serum
concentrations of sodium, bicarbonate, and chloride is described by
Eq. 2-2, where R represents the anion gap (AG):
As with bicarbonate, chloride contributes to maintaining acid–base
balance. A decreased serum chloride often accompanies metabolic
alkalosis, whereas an increased serum chloride may indicate a
hyperchloremic metabolic acidosis. The serum chloride, however,
can also be slightly decreased in acidosis if organic acids or other
acids are the primary cause of the acidosis. Hyperchloremia,
absence of metabolic acidosis, is seldom encountered because
chloride retention is usually accompanied by sodium and water
retention. Hypochloremia can result from excessive GI loss of
chloride-rich fluid (eg, vomiting, diarrhea, gastric suctioning, and
intestinal fistulas). Because chloride ions are excreted with cations
by the kidneys, hypochloremia may also result from significant
diuresis.
Anion Gap
Reference Range: 7–16 mEq/L or mmol/L
The R factor, or AG, represents the contribution of unmeasured
acids, such as lactate, phosphates, sulfates, and proteins. As
displayed in Eq. 2-2, a patient’s AG is determined by subtracting the
primary anions (Cl− and HCO
3
−
) from the primary cation (Na+). Some
clinicians include potassium in this determination and subtract the
anions from both major cations (Na+ and K+). If potassium is not
incorporated in the calculation, a normal AG is typically 5 to 12
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mEq/mL. If potassium is considered, a normal AG would be <16
mEq/mL.
An elevated AG may be indicative of metabolic acidosis caused by
an increase in lactic acids, ketoacids, salicylic acids, methanol, or
ethylene glycol. A low AG may be the result of reduced
concentrations of unmeasured anions (eg, hypoalbuminemia) or
from systematic underestimation of serum sodium (eg,
hyperviscosity of myeloma). See Chapter 26, Acid–Base
Disturbances, for a more detailed discussion of the clinical use of the
AG.
Blood Urea Nitrogen
Reference Range: 8–20 mg/dL or 2.8–7.1 mmol/L
Urea nitrogen is a waste product that comes from protein
breakdown. It is produced solely by the liver, transported in the
blood, and excreted by the kidneys. The serum concentration of urea
nitrogen (ie, blood urea nitrogen [BUN]) is reflective of renal function
because the urea nitrogen in the blood is filtered completely at the
glomerulus of the kidney and then reabsorbed and tubularly secreted
within nephrons. Acute or chronic renal failure is the most common
cause of an elevated BUN. Although the BUN is an excellent
screening test for renal dysfunction, it does not sufficiently quantify
the extent of renal disease. In addition, several nonrenal factors such
as unusually high protein intake, disease states that increase protein
catabolism (or upper GI bleeding), and glucocorticoid therapy can
increase the BUN concentration. Liver disease and a low protein diet
can lead to a lower BUN concentration. A patient’s hydration status
will also influence BUN; a water deficit tends to concentrate the urea
nitrogen, and a water excess dilutes the urea nitrogen. The ratio of
BUN to serum creatinine (SCr) can also be of clinical use. A normal
ratio is roughly 15:1. Ratios >20:1 are observed in patients with
decreased blood flow to the kidney (eg, prerenal disease such as
dehydration or conditions involving reduced cardiac output) or
conditions involving increased protein in the blood (eg, dietary intake
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or an upper GI bleed). Situations in which the BUN:SCr ratio is <15:1
are seen in patients with renal failure, significant malnourishment
(decreased intake of protein), or severe liver disease in which the
liver is no longer able to form urea. It is important to note that BUN
can change independent of the renal function, and, therefore, SCr is
more useful in estimating renal function.
Creatinine
Reference Range: ≤1.5 mg/dL or ≤133 μmol/L
Creatinine is derived from the creatine and phosphocreatine
metabolism in the skeletal muscle. Its rate of formation for a given
individual is remarkably constant and is determined primarily by an
individual’s muscle mass or lean body weight. Therefore, the SCr
concentration is slightly higher in muscular subjects, but, unlike the
BUN, it is less directly affected by exogenous factors or liver
impairment. Once creatinine is released from muscle into plasma, it
is excreted renally almost exclusively by glomerular filtration and is
not reabsorbed or metabolized by the kidney. A decrease in the
glomerular filtration rate (GFR) results in an increase in the SCr
concentration. Thus, careful interpretation of the SCr concentration is
used widely in the clinical evaluation of patients with suspected renal
disease. However, SCr concentration on its own should not be
utilized to assess the level of kidney function in an individual.
A doubling of the SCr level roughly corresponds to a 50%
reduction in the GFR. This general rule of thumb only holds true for
steady-state creatinine levels.
11
Of importance, as patients become older, there is a reduction in
muscle mass and creatinine production is progressively decreased.
Furthermore, the SCr concentration in female patients is generally
0.2 to 0.4 mg/dL (85%–90%) less than that for males because
females have less muscle mass.
Creatinine Clearance
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(Eq. 2-3)
(Eq. 2-4)
Reference Range: 90–130 mL/minute
Because creatinine is cleared almost exclusively through the
glomerulus in the kidney, creatinine clearance (CrCl) can be used as
a clinically useful measure of a patient’s GFR. CrCl serves as a
valuable clinical parameter because many renally eliminated drugs
are dose adjusted based on the patient’s renal function. To
determine actual CrCl, the patient’s urine is collected for a 24-hour
period, and the concentration of urine creatinine (mg/dL), total
volume of urine collected during the 24-hour period (mL/minute), and
SCr (mg/dL) are determined. The patient-specific measured CrCl is
determined using Eq. 2-3:
Unfortunately, urine collections are time-consuming and
expensive, and incomplete collections can substantially
underestimate renal function. In lieu of measuring actual CrCl,
simplistic equations are commonly used to estimate a patient’s CrCl.
The following Cockcroft–Gault formula incorporates age, body
weight, and SCr.12 This formula can be utilized to estimate renal
function when SCr is stable. Typically, clinicians use ideal body
weight (IBW) in the calculation of estimated CrCl; however, actual
body weight (ABW) may be used when ABW is less than IBW. For
obese patients who are >20% to 30% of their IBW, an adjusted body
weight (0.4 [ABW − IBW] + IBW) should be used.13 Equation 2-4 has
the highest correlation and the greatest accuracy in patients with SCr
concentrations <1.5 mg/dL14:
The Cockcroft–Gault formula must be multiplied by 85% to
calculate CrCl for females to account for the fact that females have
less muscle mass.
Another commonly used approach to estimating CrCl is the Jelliffe
method,14 shown in Eq. 2-5:
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(Eq. 2-5)
This Jelliffe formula must be multiplied by 90% to calculate the
CrCl for females. The use of this method substantially
underestimates CrCl for patients with SCr values <1.5 mg/dL,
15
whereas Cockcroft–Gault appears to have the highest correlation
and greatest accuracy in patients with SCr values <1.5 mg/dL.14 For
patients with liver dysfunction, all methods of calculating CrCl from
an SCr value are associated with significant overpredictions of
CrCl.16 Thus, methods for predicting CrCl should be used cautiously
when attempting to adjust drug dosages in patients with liver
disease. These equations should not be utilized in patients with
rapidly changing GFR (eg, acute kidney injury) because they will not
provide accurate estimates of the GFR.
CASE 2-1
QUESTION 1: A 24-hour CrCl determination was ordered for D.B., a 72-year-old,
136.69-pound (62-kg) White male. The following data were returned from the
clinical laboratory (total collection time was 24 hours):
Total urine volume: 1000 mL
Urine creatinine concentration: 42 mg/dL
SCr: 2.0 mg/dL
What are the measured and the estimated CrCl for D.B. based on the given
data?
Using Eq. 2-3, D.B. has a 24-hour measured CrCl of ~15
mL/minute. His estimated CrCl is 29.2 mL/minute using the
Cockcroft–Gault method (Eq. 2-4). Based on both methods, D.B.’s
ability to clear renally eliminated drugs is impaired, and adjustments
to the dose/frequency will need to be made. An incomplete collection
of urine during the 24-hour period or possible mishandling of the
specimen can be explanations for the lower value seen with the
measured CrCl. Because D.B. had an elevated SCr of 2.0 mg/dL,
the accuracy of the Cockcroft–Gault estimation might also be
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(Eq. 2-6)
(Eq. 2-7)
compromised. D.B.’s baseline SCr will need to be established, and if
it is determined that SCr of 2.0 mg/dL is corresponding with his
baseline, then the Cockcroft–Gault estimation will hold true; if SCr of
2.0 mg/dL represents an acute change, then the Cockcroft–Gault
equation should not be used to estimate renal function in D.B.
Estimated Glomerular Filtration Rate
An alternative approach to the Cockcroft–Gault method of estimating
an adult patient’s clearance was developed as part of the
Modification of Diet in Renal Disease (MDRD) study and has been
referred to as the MDRD equation.17 The originally described
equation has been modified into an abbreviated format (Eq. 2-6), as
follows:
where SCr is the serum creatinine in mg/dL, age is in
years, and the appropriate additional components are included for
female or African American patients. Equation 2-6 is applicable to
laboratories reporting SCr values that have not been standardized.
Starting in 2005, laboratories began standardizing their SCr values
using an isotope dilution mass spectrometry to minimize the variation
observed in SCr results from different clinical laboratories. In settings
in which the SCr results have been standardized, the initial
parameter in the MDRD equation is adjusted downward. The
following is used to estimate GFR:
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When compared with the Cockcroft–Gault approach, MDRD
estimations of GFR were more consistent with actual measurements
of GFR. However, because both approaches rely on SCr, the
influence of muscle mass and dietary intake still must be taken into
consideration. In certain patient populations (eg, obese and elderly
patients), use of the MDRD can be less accurate, because the
MDRD study equation was primarily derived from White subjects
with a mean age of 51 years who had nondiabetic renal disease. It is
important to note that recent evidence supports removing the race
multiplier in the MDRD equation because it may overestimate renal
function in patients designated as African American.18 Although this
may increase the prevalence and severity staging of chronic kidney
disease (CKD), removal of the race multiplier can increase access to
specialists, kidney transplant services, and medical nutrition therapy.
It may also promote the early use of pharmacotherapies known to
delay kidney progression (eg, ACE inhibitors, ARBs) and prompt
dose reductions and/or discontinuation of drugs unknown to be
nephrotoxic.19 A more detailed description of the MDRD equation to
estimate GFR is addressed in Chapter 28, Chronic Kidney Disease.
Cystatin C
Reference Range: ≤1.0 mg/L or ≤0.749 mmol/L
Although SCr has long been the gold standard for assessing renal
function, cystatin C is a newer biomarker that has been shown to be
subject to less biologic variability and more sensitive to early
declines in kidney function.20 Reference ranges for cystatin C are
similar to that of SCr (≤1.0 mg/L). But unlike SCr, which is produced
from muscle cells, cystatin C is produced by the blood cells and is
not appreciably influenced by factors such as muscle mass, diet,
age, biologic sex, and race; however, higher levels of cystatin C
have been observed in males and patients with higher height and
weight, and higher lean body mass. It has also been observed that
cystatin C levels are increased with age.21 Cystatin C is cleared
predominantly through the kidneys and is not reabsorbed. Elevated
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levels are observed in patients with declining renal function.
Elevations in serum cystatin C levels tend to occur earlier than do
increases in SCr, which do not tend to rise until ~50% of kidney
function is lost, and make it possible to detect renal insufficiency in
patients at an earlier stage.22 This is particularly desirable in patients
with diabetes, hypertension, or cardiovascular disease who may be
at higher risk for the development of renal disease.
Glucose
Reference Range: 65–115 mg/dL or 3.6–6.3 mmol/L (fasting)
The glucose concentration in the ECF is tightly regulated by
homeostatic mechanisms to provide tissues and cells with a reliable
source of energy. Two endocrine hormones, insulin and glucagon,
work synergistically to maintain normal glucose concentrations.
Insulin is released from pancreatic β cells to lower blood glucose
concentrations, whereas glucagon (released from the pancreatic α
cells), along with the counterregulatory hormones, epinephrine,
cortisol, and growth hormone, raises glucose levels. Because
plasma glucose concentrations fluctuate in response to ingestion of
meals, most glucose concentrations are measured in either the
fasting or the postprandial state, depending on the type of
information desired. Generally, normal glucose values refer to the
plasma glucose concentration in the fasting state. The specific
laboratory assay of blood sugar determinations must also be
considered because different assay methods vary in their specificity
and sensitivity to glucose. Glucose testing using whole blood from
capillary finger sticks (eg, self-monitoring of blood glucose) is used in
conjunction with blood glucose monitoring devices for patients with
diabetes. Because glucometer results rely on enzymatic reactions,
results can potentially be altered by oxygen saturation, temperature,
and interfering substances (eg, acetaminophen, ascorbic acid).
23
Whole blood measurements using these devices are typically 10% to
15% lower than are corresponding plasma glucose levels. Newer
technologies such as continuous glucose monitors (CGMs) measure
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