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Kidney Function Test


Functions of the kidney Regulation e.g. homeostasis ,water, acid/base Excretion e.g. uric acid, urea, creatinine Endocrine e.g. renin, erythropoietin, Calcitriol or ... – PowerPoint PPT presentation

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Title: Kidney Function Test

Kidney Function Test
Functions of the kidney
  • Regulation e.g. homeostasis ,water, acid/base
  • Excretion e.g. uric acid, urea, creatinine
  • Endocrine e.g. renin, erythropoietin, Calcitriol
    or (1,25-dihydroxyvitamin D3 )- conversion only
    in kidney!

When should you assess renal function?
  • Older age
  • Family history of Chronic Kidney disease (CKD)
  • Decreased renal mass
  • Low birth weight
  • Diabetes Mellitus (DM)
  • Hypertension (HTN)
  • Autoimmune disease
  • Systemic infections
  • Urinary tract infections (UTI)
  • Nephrolithiasis
  • Obstruction to the lower urinary tract
  • Drug toxicity

  • Nitrogen containing compounds that are not
    proteins or polypeptides
  • Total NPN can be tested by making a protein-free
  • Useful clinical information is obtained from
    individual components of NPN fraction

Uric Acid
  • Uric acid is formed from the breakdown of nucleic
    acids and is an end product of purine metabolism.
  • Purines are found in some foods and drinks, such
    as liver, anchovies, mackerel, dried beans and
    peas, beer, and wine.
  • Purines are also a part of normal body
    substances, such as DNA.
  • Uric acid is transported by the plasma from the
    liver to the kidney, where it is filtered and
    where about 70 is excreted.
  • The remainder of uric acid is excreted into the
    GI tract.

  • High levels of uric acid in the body is called
  • Normal values fall between 3.0 and 7.0 mg/dL.
  • Note Normal values may vary slightly from
    laboratory to laboratory.
  • It is ordered during
  • when a doctor suspects high levels of uric acid
  • Gout
  • monitoring test when a patient has undergone
    chemotherapy or radiation
  • If a patient appears to have failing kidneys

Greater-than-normal levels of uric acid
(hyperuricemia) may be due to
  • Alcoholism
  • Diabetes
  • Gout
  • Hypoparathyroidism
  • Lead poisoning
  • Leukemia
  • Nephrolithiasis
  • Renal failure
  • Toxemia of pregnancy
  • Purine-rich diet
  • Excessive exercise
  • Chemotherapy-related side effects

Lower-than-normal levels of uric acid may be due
  • Fanconi syndrome
  • Wilson's disease
  • Syndrome of inappropriate antidiuretic hormone
    (SIADH) secretion
  • Multiple Sclerosis
  • Low purine die

  • Gout is a kind of arthritis that occurs when uric
    acid builds up in the joints.
  • In Gout increased serum levels of uric acid lead
    to formation of monosodium urate crystals around
    the joints.
  • Acute gout is a painful condition that typically
    affects one joint.
  • Chronic gout is repeated episodes of pain and
    inflammation, which may involve more than one

Symptoms of acute gouty attacks
  • Symptoms develop suddenly and usually involve
    only one or a few joints. The big toe, knee, or
    ankle joints are most often affected.
  • The pain frequently starts during the night and
    is often described as throbbing, crushing, or
  • The joint appears warm and red. It is usually
    very tender.
  • There may be a fever.
  • The attack may go away in several days, but may
    return from time to time. Additional attacks
    usually last longer.
  • Tophi are lumps below the skin around joints or
    in other places. They may drain chalky material.
    Tophi usually develop only after a patient has
    had the disease for many years.

Clinical Significance
  • Measurement of uric acid is used most commonly in
    the evaluation of renal failure, gout, and
  • In hospitalized patients, renal failure is the
    most common cause of elevated uric acid levels,
    and gout is the least common cause.
  • Hypouricemia is seldom observed and associated
    with rare hereditary metabolic disorders.

  • Serum or plasma may be used slight but
    insignificant positive bias (0.2 mg/dL) has been
    noted in plasma specimens as compared with serum.
  • Stability in serum / plasma
  • 6 months at -20C
  • 7 days at 4-8C
  • 3 days at 20-25C

Possible Complications
  • Chronic gouty arthritis
  • Kidney stones
  • Deposits in the kidneys, leading to chronic
    kidney failure

Enzymatic Colorimetric
  • Uric acid H2O O2 Allantion CO2
  • TBHBA 4- Aminoantipyrine 2H2O2
    Quinoneimine 3 H2O
  • Uric acid is oxidized to allantoin by uricase.
  • The generated hydrogen peroxide reacts with
    4-aminophenazone/ESPT to quinoneimine.

  • Treatments for a sudden attack or flare-up of
  • Your doctor will recommend that you take
    nonsteroidal anti-inflammatory drugs (NSAIDs)
    such as ibuprofen, naproxen, or indomethacin as
    soon as your symptoms begin
  • Your health care provider may occasionally
    prescribe strong painkillers such as codeine
  • Daily use of allopurinol decrease uric acid
    levels in your blood

Some diet and lifestyle changes may help prevent
gouty attacks
  • Avoid alcohol, sardines, oils, organ meat (liver,
    kidney, and sweetbreads(
  • Limit how much meat you eat at each meal.
  • Avoid fatty foods such as salad dressings, ice
    cream, and fried foods
  • Eat enough carbohydrates
  • If you are losing weight, lose it slowly. Quick
    weight loss may cause uric acid kidney stones to

  • Uric acid may also form kidney stones
  • Although uric acid can act as an antioxidant,
    excess serum accumulation is often associated
    with cardiovascular disease.

  • Highest concentration of NPN in blood (45)
  • Major excretory product of protein metabolism
  • Urea is synthesized in the liver, from CO2 and
    ammonia, as the final product of amino acid
  • It is freely filtered at the glomerulus, though
    40 is passively reabsorbed by the proximal
  • The reference interval for serum urea of healthy
    adults is 5-39 mg/dl (slightly higher in males
    than females)
  • BUN (blood urea nitrogen)
  • The real urea concentration is BUN x 2.14

  • Blood urea levels can vary proportionately with
  • the protein content of the diet,
  • rate of protein catabolism during tissue
  • and liver function.
  • Because of its metabolism, urea is a nonspecific
    indicator of renal function.
  • Blood urea levels are usually elevated before
    significant changes in creatinine levels have
  • Monitoring blood urea levels is very useful when
    one is following the course of renal disease.

Clinical Significance
  • States associated with elevated levels of urea in
    blood are referred to as uremia or azotemia.
  • Causes of urea plasma elevations
  • Prerenal renal hypoperfusion
  • Renal acute tubular necrosis
  • Postrenal obstruction of urinary flow

  • Parallel determination of urea and creatinine is
    performed to differentiate between pre-renal and
    post-renal azotemia.
  • Pre-renal azotemia, caused by e.g. dehydration,
    increased protein catabolism or decreased renal
    perfusion, leads to increased urea levels, while
    creatinine values remain within the reference
  • In post-renal azotemias, caused by the
    obstruction of the urinary tract, both urea and
    creatinine levels rise, but creatinine in a
    smaller extent.
  • With obstruction, both plasma urea and creatinine
    increase, but there is greater rise of urea than
    of creatinine because the obstruction of urine
    flow backpressure on the tubule and
    back diffusion of urea into blood from the tubule.

  • Increased protein catabolism
  • Increased dietary protein
  • Severe tress fever, etc
  • Rhabdomyolysis
  • Upper GI bleeding
  • Causes of urea plasma decrease
  • Decreased dietary protein
  • Increased protein synthesis ( Pregnant women ,
    children )
  • severe liver disease
  • Overhydration (IV fluids)

  • Serum and heparinized plasma can be used for the
    urease/GLDH methods.
  • Fluoride will inhibit the urease reaction
    therefore methods employing urease cannot use
    serum preserved with fluoride.
  • Ammonium heparin also cannot be used as an
    anticoagulant for urease methods.
  • Stability in serum or plasma
  • 7 days at 48C
  • 1 year at -20C
  • Because of ureas susceptibility to bacterial
    degradation, serum and urine samples should be
    kept at 4 to 8 C until analysis.

Urease/GLDH Method
  • The method is optimized for 2-point kinetic
  • Decrease in absorbance at 340 nm is proportional
    to concentration of urea

Urea / Creatinine Ratio
  • Pre-renal
  • BUN is more susceptible to non-renal factors
  • Post-renal
  • Both BUN and Creat. are elevated

  • Creatinine is a non-protein nitrogen waste
    product formed in muscle.
  • Creatine Phosphate phosphoric acid Creatinine
  • Creatine water Creatinine
  • Creatine is synthesized in liver from some a.a
    (glysine, methionine, arginine)
  • Filtered by kidney and excreted in the urine
  • Creatinine filters easily into the glomerular
    filtrate and is not reabsorbed by the tubule.
  • The plasma levels of creatinine are related to
    the muscle mass.

Clinical Significance
  • Elevated Creatinine is found in
  • Impaired renal function
  • Very high protein diet
  • Vary large muscle mass body builders, giants,
    acromegaly patients
  • Rhabdomyolysis/crush injury
  • Drugs
  • Probenecid
  • Cimetidine
  • Triamterene
  • Trimethoprim
  • Amiloride

Clinical Significance
  • For renal transplant patients, an increase in
    serum creatinine of 2 mg/L has been used as a
    criterion of establishing rejection.
  • In other persons a change in creatinine of 2 mg/L
    would represent a 20 loss in renal function.

  • One can analyze serum, plasma, or diluted urine.
  • The common anticoagulants (fluoride and heparin)
    do not cause interference, though heparin, which
    can be formulated as the ammonium salt, must be
    avoided in enzymatic methods that measure ammonia
  • Storage
  • 7 days at 4-25oC
  • At least 3 months at -20oC

  • Urine should be diluted 1100
  • Bacterial contamination has been found to falsely
    lower creatinine values measured using the Jaffé
  • The mechanism of this interference appears to be
    bacterial production of a substance that retards
    the rate of the Jaffé reaction.

Enzymatic Method
  • Creatinine H2O
  • Creatine ATP
    Creatine-P ADP
  • ADP Phosphoenolpyruvate ATP
  • Pyruvate NADH
    Lactate NAD
  • The difference in absorbance at fixed times
    during conversion is proportional to the
    concentration of creatinine in the sample

Creatinine aminohydrolase
Creatine Kinase
Pyruvate Kinase
Lactate dehydrogenase
Creatinine Clearance
  • Creatinine clearance is used to estimate the
    glomerular filtration rate (GFR).
  • One method of determining GFR from creatinine is
    to collect urine (usually for 24-hours) to
    determine the amount of creatinine that was
    removed from the blood over a given time
  • Clearance is defined as the (hypothetical)
    quantity of blood or plasma completely cleared of
    a substance per unit of time.
  • The most frequently used clearance test is based
    on the measurement of creatinine.
  • Creatinine is chosen because it is freely
    filtered at the glomerulus and is not reabsorbed
    by the tubules.

  • However, a small amount of the creatinine (about
    5) in the final urine of healthy persons is
    derived from tubular secretion.
  • To do the test, one needs a precisely timed urine
    collection and a blood sample taken during the
    collection period.
  • Best results are obtained from a 24-h urine
  • The test is initiated by having patients empty
    their bladder at the beginning of the timed
  • Urine is collected throughout the period, the
    bladder is again emptied at the end of the time

  • The 'clearance' of creatinine from plasma is
    directly related to the GFR if
  • The urine volume is collected accurately
  • There are no ketones or heavy proteinuria present
    to interfere with the creatinine determination.
  • It should be noted that the GFR decline with age
    (to a greater extent in males than in females)
    and this must be taken into account when
    interpreting results.

Creatinine Clearance
  • Creatinine determinations are performed on both
    samples. The creatinine clearance is calculated
    from the following formula
  • A person has a plasma creatinine concentration of
    0.01 mg/ml and in 1 hour produces 60ml of urine
    with a creatinine concentration of 1.25 mg/mL.

  • Creatinine clearance (mL/min) (UV)/P X 1.73/S
  • where U is urinary creatinine (mg/L), V is volume
    of urine (mL/min), P is plasma creatinine (mg/L),
    S is the calculated surface area of the patient,
    and 1.73 is the surface area (m2) of a standard
    70 kg person.
  • The range of creatinine clearance in healthy
    persons corrected to a surface area of 1.73 m2 is
    90 to 120 mL/min.
  • At low filtration rates, the creatinine clearance
    does not parallel true glomerular filtration rate
    because a relatively large portion of the urine
    creatinine is secreted rather than filtered.

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