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نتيجة التلخيص (94%)

viewed while held up to a light source. Correct cali￾bration is vital for accuracy. Most recently, an indirect
colorimetric reagent strip method for assaying SG has
been added to most dipstick screens. Unlike the refrac￾tometer, dipsticks measure only ionic solutes and do not
take into account glucose or protein.
The normal range for urinary SG is 1.003 to 1.035 g/mL.
SG can vary in pathologic states. Low SG can occur in dia￾betes insipidus, pyelonephritis, and glomerulonephritis,
in which the renal concentrating ability has become
dysfunctional. High SG can be seen in diabetes mellitus,
congestive heart failure, dehydration, adrenal insuffi￾ciency, liver disease, and nephrosis. SG will increase about
0.004 units for every 1% change in glucose concentration
and about 0.003 units for every 1% change in protein.
Fixed SG (isosthenuria) around 1.010 is observed in severe
renal damage, in which the kidney excretes urine that is
iso-osmotic with the plasma. This generally occurs after an
initial period of anuria because the damaged tubules are
unable to concentrate or dilute the glomerular filtrate.16
pH
Determinations of urinary pH must be performed on
fresh specimens because of the significant tendency of
urine to alkalinize on standing. Normal urine pH falls
within the range of 4.7 to 7.8. Acidity in urine (pH < 7.0)
is primarily caused by phosphates, which are excreted
as salts conjugated to Na+, K+, Ca2+, and NH4
+ . Acidity
also reflects the excretion of the nonvolatile metabolic
acids pyruvate, lactate, and citrate. Owing to the Na+/H+
exchange pump mechanism of the renal tubules, pH
(H+ concentration) increases as sodium is retained.
Pathologic states, in which increased acidity is observed,
include systemic acidosis, as seen in diabetes mellitus,
and renal tubular acidosis (RTA). In RTA, the tubules
are unable to excrete excess H+ even though the body is
in metabolic acidosis, and urinary pH remains around 6.
Alkaline urine (pH > 7.0) is observed postprandially
as a normal reaction to the acidity of gastric HCl dumped
into the duodenum and then into the circulation or fol￾lowing ingestion of alkaline food or medications. Urinary
tract infections and bacterial contamination also will
alkalinize pH. Medications such as potassium citrate and
sodium bicarbonate will reduce urine pH. Alkaline urine
is also found in Fanconi syndrome, a congenital gener￾alized aminoaciduria resulting from defective proximal
tubular function.
Chemical Analyses
Routine urine chemical analysis is rapid and easily per￾formed with commercially available reagent strips or
dipsticks. These strips are plastic coated with different
reagent bands directed toward different analytes. When
dipped into urine, a color change signals a d
eviation
from normality. Colors on the dipstick bands are
matched against a color chart provided with the reagents.
Automated and semiautomated instruments that detect
to green color is a result of bile pigment oxidation. Red
and brown after standing are due to porphyrins, whereas
reddish-brown in fresh specimens comes from hemoglo￾bin or red cells. Brownish-black after standing is seen in
alkaptonuria (a result of excreted homogentisic acid) and
in malignant melanoma (in which the precursor mela￾nogen oxidizes in the air to melanin). Drugs and some
foods, such as beets, may also alter urine color.
Odor
Odor ordinarily has little diagnostic significance. The
characteristic pungent odor of fresh urine is due to vola￾tile aromatic acids, in contrast to the typical ammonia
odor of urine that has been allowed to stand. Urinary
tract infections impart a noxious, fecal smell to urine,
whereas the urine of diabetics often smells fruity as a
result of ketones. Certain inborn errors of metabolism,
such as maple sugar urine disease, are associated with
characteristic urine odors.
Turbidity
The cloudiness of an urine specimen depends on pH and
dissolved solids composition. Turbidity generally may
be due to gross bacteriuria, whereas a smoky appearance
is seen in hematuria. Thread-like cloudiness is observed
when the specimen is full of mucus. In alkaline urine,
suspended precipitates of amorphous phosphates and
carbonates may be responsible for turbidity, whereas in
acidic urine, amorphous urates may be the cause.16
Volume
The volume of urine excreted indicates the balance between
fluid ingestion and water lost from the lungs, sweat, and
intestine. Most adults produce from 750 to 2,000 mL every
24 hours, averaging about 1.5 L per person. Polyuria is
observed in diabetes mellitus and insipidus (in insipidus,
as a result of lack of ADH), as well as in chronic renal
disease, acromegaly (overproduction of the growth hor￾mone somatostatin), and myxedema (hypothyroid edema).
Anuria or oliguria (<200 mL/d) is found in nephritis, uri￾nary tract obstruction, AKI, and kidney failure.
Specific Gravity
The specific gravity (SG) of urine is the weight of 1 mL of
urine in grams divided by the weight of 1 mL of water. SG
gives an indication of the density of a fluid that depends on
the concentration of dissolved total solids. SG varies with
the solute load to be excreted (consisting primarily of NaCl
and urea), as well as with the urine volume. It is used to
assess the state of hydration/dehydration of an individual or
as an indicator of the concentrating ability of the kidneys.
The most commonly encountered analytic method
consists of a refractometer, or total solids meter. This
operates on the principle that the refractive index of a
urine specimen will vary directly with the total amount
of dissolved solids in the sample. This instrument mea￾sures the refractive index of the urine as compared with
water on a scale that is calibrated directly into the ocular


النص الأصلي

viewed while held up to a light source. Correct cali￾bration is vital for accuracy. Most recently, an indirect
colorimetric reagent strip method for assaying SG has
been added to most dipstick screens. Unlike the refrac￾tometer, dipsticks measure only ionic solutes and do not
take into account glucose or protein.
The normal range for urinary SG is 1.003 to 1.035 g/mL.
SG can vary in pathologic states. Low SG can occur in dia￾betes insipidus, pyelonephritis, and glomerulonephritis,
in which the renal concentrating ability has become
dysfunctional. High SG can be seen in diabetes mellitus,
congestive heart failure, dehydration, adrenal insuffi￾ciency, liver disease, and nephrosis. SG will increase about
0.004 units for every 1% change in glucose concentration
and about 0.003 units for every 1% change in protein.
Fixed SG (isosthenuria) around 1.010 is observed in severe
renal damage, in which the kidney excretes urine that is
iso-osmotic with the plasma. This generally occurs after an
initial period of anuria because the damaged tubules are
unable to concentrate or dilute the glomerular filtrate.16
pH
Determinations of urinary pH must be performed on
fresh specimens because of the significant tendency of
urine to alkalinize on standing. Normal urine pH falls
within the range of 4.7 to 7.8. Acidity in urine (pH < 7.0)
is primarily caused by phosphates, which are excreted
as salts conjugated to Na+, K+, Ca2+, and NH4



  • . Acidity
    also reflects the excretion of the nonvolatile metabolic
    acids pyruvate, lactate, and citrate. Owing to the Na+/H+
    exchange pump mechanism of the renal tubules, pH
    (H+ concentration) increases as sodium is retained.
    Pathologic states, in which increased acidity is observed,
    include systemic acidosis, as seen in diabetes mellitus,
    and renal tubular acidosis (RTA). In RTA, the tubules
    are unable to excrete excess H+ even though the body is
    in metabolic acidosis, and urinary pH remains around 6.
    Alkaline urine (pH > 7.0) is observed postprandially
    as a normal reaction to the acidity of gastric HCl dumped
    into the duodenum and then into the circulation or fol￾lowing ingestion of alkaline food or medications. Urinary
    tract infections and bacterial contamination also will
    alkalinize pH. Medications such as potassium citrate and
    sodium bicarbonate will reduce urine pH. Alkaline urine
    is also found in Fanconi syndrome, a congenital gener￾alized aminoaciduria resulting from defective proximal
    tubular function.
    Chemical Analyses
    Routine urine chemical analysis is rapid and easily per￾formed with commercially available reagent strips or
    dipsticks. These strips are plastic coated with different
    reagent bands directed toward different analytes. When
    dipped into urine, a color change signals a d
    eviation
    from normality. Colors on the dipstick bands are
    matched against a color chart provided with the reagents.
    Automated and semiautomated instruments that detect
    to green color is a result of bile pigment oxidation. Red
    and brown after standing are due to porphyrins, whereas
    reddish-brown in fresh specimens comes from hemoglo￾bin or red cells. Brownish-black after standing is seen in
    alkaptonuria (a result of excreted homogentisic acid) and
    in malignant melanoma (in which the precursor mela￾nogen oxidizes in the air to melanin). Drugs and some
    foods, such as beets, may also alter urine color.
    Odor
    Odor ordinarily has little diagnostic significance. The
    characteristic pungent odor of fresh urine is due to vola￾tile aromatic acids, in contrast to the typical ammonia
    odor of urine that has been allowed to stand. Urinary
    tract infections impart a noxious, fecal smell to urine,
    whereas the urine of diabetics often smells fruity as a
    result of ketones. Certain inborn errors of metabolism,
    such as maple sugar urine disease, are associated with
    characteristic urine odors.
    Turbidity
    The cloudiness of an urine specimen depends on pH and
    dissolved solids composition. Turbidity generally may
    be due to gross bacteriuria, whereas a smoky appearance
    is seen in hematuria. Thread-like cloudiness is observed
    when the specimen is full of mucus. In alkaline urine,
    suspended precipitates of amorphous phosphates and
    carbonates may be responsible for turbidity, whereas in
    acidic urine, amorphous urates may be the cause.16
    Volume
    The volume of urine excreted indicates the balance between
    fluid ingestion and water lost from the lungs, sweat, and
    intestine. Most adults produce from 750 to 2,000 mL every
    24 hours, averaging about 1.5 L per person. Polyuria is
    observed in diabetes mellitus and insipidus (in insipidus,
    as a result of lack of ADH), as well as in chronic renal
    disease, acromegaly (overproduction of the growth hor￾mone somatostatin), and myxedema (hypothyroid edema).
    Anuria or oliguria (


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