Download Disclaimer

King Saud University
College of Science
Department of Biochemistry
Disclaimer
• The texts, tables, figures and images contained in this course
presentation (BCH 376) are not my own, they can be found on:
• References supplied
• Atlases or
• The web
Chapter 7
Urinalysis-3
Professor A. S. Alhomida
1
Urine Screening for
Metabolic Disorders
1. Urinary Inorganic Constituents
•
•
•
•
•
•
•
Chloride
Phosphates
Sulphur
Sodium
Potassium
Calcium
Magnesium
2
1
Urine Screening for
Metabolic Disorders, Cont’d
2. Urinary Organic Constituents
•
•
•
•
•
•
•
Urea
Ammonia
Uric Acid
Creatine
Creatinine
Oxalic acid
Amino acids
3
Urine Screening for
Metabolic Disorders, Cont’d
3. Abnormal Constituents
•
•
•
Protein
Carbohydrates (Sugar)
Urinary Calculi
4
2
Chloride
•
Most abundant Anion in ECF
•
•
Major contribution to osmolarity
Roles
1. Formation of HCl
2. Chloride shift
•
CO2 Loading/Unloading
3. Regulation of body pH
5
Clinical and Biochemical
Significance
Chloride
Decrease
1. Excessive sweating
2. During fasting
3. Loss through extrarenal channels; diarrhea, vomiting
4. Edema
5. Diabetes insipidus
6. Infections; pneumonia
7. Adrenocortical hyperfuntion; Cashing’s syndrome
6
3
Clinical and Biochemical
Significance, Cont’d
Chloride
Increase
1. Excessive water drinking
2. Addison’s disease
3. Use of diuretics
7
Phosphates
•
•
Relatively Concentrated IN ICF
Roles
1.
2.
3.
4.
5.
Components of bones
Components of DNA and RNA
Components of phospholipids
Activate/deactivate some
Buffer pH of body fluids
8
4
Phosphates, Cont’d
• Components of
•
•
•
•
•
•
•
•
•
Nucleic acids (DNA, RNA)
NTPs AND dNTPs (ATP, dATP, GTP, dGTP, etc)
cAMP
Phospholipids
Various others phosphorylated molecules generated
via ATP hydrolysis, etc
Exist as mixture of three forms
PO43- (phosphate ion)
HPO42- (monohydrogen phosphate ion)
H2PO4- (dihydrogen phosphate ion
9
Phosphate Homeostasis
1. Diet Provides Ample Phosphate
2. Readily Absorbed by Small Intestine
3. Regulation
•
•
•
Renal tubules site of regulation
PTH increases phosphate excretion
Excretion rate affected by urine pH
4. Phosphate Imbalances
•
•
Phosphate Homeostasis NOT Very Critical
Body can Tolerate Wide Variations of Phosphate
Concentration with Little Effect
10
5
Clinical and Biochemical
Significance
Phosphates
Decrease
1. Diarrhea
2. Acute infections
3. Nephritis
4. Parathyroid hypofuntion
5. Pregnancy
6. Insulin administration
7. Certain inherited disorders; galactosemia, fructose intolerance
11
Clinical and Biochemical
Significance, Cont’d
Phosphate
Increase
1. Bone diseases; rickets, osteomalcia, periostosis
2. Addison’s disease
3. Acidosis
12
6
Sulfur
1. Formation of Sulfur Compounds
•
•
•
Inorganic SO4 (80(80-85%)
Ethereal sulfates (organic esters) (5%)
Organic sulfates (Neutral sulfur) (15(15-20%)
2. Sources of Sulfates
•
•
•
Most of urinary sulfates arises from metabolism of
proteins, especially Cys, cystine, Met and GSH
A small amount obtained from S-containing
vitamins, B6, biotin, lipoic acid, coenzyme A
Food proteins that contain on an average of 1% of
sulfur
13
Urinary Excretion of
Sulfates
•
Urinary Sulfate Excretion Varies with
•
•
Protein intake in diet
Rates of tissue protein breakdown
14
7
Clinical and Biochemical
Significance
Inorganic sulfates
Decrease
It is diminished on conditions of renal functional impairment
Increase
1. On high protein diet
2. In excessive tissue protein breakdown
15
Ethereal sulfates
1. Urinary excretion range from 0.060.06-1.2 g/day
2. It consists of Na, K salts of sulfuric acid ester of
phenols, eg indoxal,
indoxal, skatoxyl,
skatoxyl, phenol and cresol
3. These ether sulfates represent of detoxication
compounds of phenols and are formed in liver
4. Some of the phenolic sulfates originate through
• Bacterial action in the gastrointestinal (GI) tract
• Some appears to be formed in tissue metabolism
16
8
Ethereal sulfates, Cont’d
5.
6.
Indoxyl and skatoxyl are formed entirely by
putrefactive decomposition of Trp in the GI tract and
phenol and cresol from Tyr
Formation of indole and skatol from Trp are esterified
with H2SO4 in liver and excreted in urine as Na and K
salts (urinary bile acid sulfates)
17
Clinical and Biochemical
Significance
Ethereal sulfates
Increase
1. In intestinal obstruction due to putrefaction and
absorption of these products in carcinoma, liver cholera,
typhus
2. In cholera and typhus, sufficient indican is excreted to
cause urine to assume a bluish tinge on standing
3. Bacterial decomposition of Trp in pus any where in the
body in pathological conditions increases the excretion
of indican
18
9
Urinary Indican
1. Insufficient gastric HCl,
HCl, insufficient digestive enzymes,
adverse food reactions, parasitic infection, fungal
infection, overgrowth of bacteria that metabolize
specific proteins, hypermotility of the small intestine, or
other gastrointestinal dysfunction can compromise
protein digestion
2. The level of indican is an index of the efficiency of
protein digestion
19
Urinary Indican
3.
4.
Poor protein digestion also can result from the dietary
intake of protein from a group of food proteins called
lectins
The Indican test uses a urine sample to test for the
presence of indole,
indole, a metabolic byproduct of the
action of intestinal bacteria on the amino acid
tryptophan
20
10
Conditions with Elevated
Levels of Urinary Indican
1.
2.
3.
4.
5.
6.
7.
Inflammatory bowel disease
Celiac disease
Hypochlorhydria
Achlorhydria
Gastric ulcer
Biliary and intestinal obstruction
Jejunal diverticulosis
21
Conditions with Elevated
Levels of Urinary Indican,
Cont’d
8.
9.
10.
11.
12.
13.
14.
Scleroderma
Postgastrectomy
Hartnup's disease
Pancreatic insufficiency
Diminished peristalsis
Blue diaper syndrome
Hypermotility of the small intestine
22
11
Urinary Indican Test
• Trp is converted to indole
by intestinal bacterial
cleavage of Trp side chain
• Following absorption,
indole is converted to 33hydroxy indole (indoxyl or
indican)
indican) in the liver, where
it is then conjugated with
potassium sulfate or
glucoronic acid
• It is then transported
through the blood to the
kidneys for excretion in
urine
23
Results of Urinary Indican
Test
Urine Color
0 (normal)
Light Blue
1+ (Low Positive)
Blue
2+ (Medium Positive)
Violet
3+ (High Positive)
Jet Black
4+ (Very high Positive)
24
12
Neutral sulfates
1.
2.
3.
Urinary excretion range from 0.08 – 0.16 g/day
It is composed of heterogeneous mixtures of sulfur
compouds
These includes cystine,
cystine, Met, urochrome,
urochrome, throsulfates,
throsulfates,
oxyproteic acid, thiocyanates,
thiocyanates, bile acids and taurine
and its derivatives
25
Clinical and Biochemical
Significance
Neutral sulfates
Increase
1.
2.
3.
4.
5.
Inherited disorders like cystinuria,
cystinuria, homocystinuria
Melanuria in melanoma
Hepato cellular jandice
Cyanide poisoning as cyanide is converted to
thiocyanates
Chloroform as an anesthesia
26
13
Urinary Bile Acid Sulfate
1. The enterohepatic circulation regulates bile acid levels
2. Under normal conditions, little leaks into the blood and
is converted to sulfate and excreted in the urine
3. Elevated bile acid sulfate levels in the urine are
associated with impaired liver function, hepatocellular
damage, and a high specificity toward hepatobiliary
diseases
4. Urinary bile acid sulfates test uses a urine sample to
provide a direct assessment of liver function
27
Urinary Lipid Peroxides
1. The level of lipid peroxides is an index of cellular
membrane damage caused by the action of free radicals
2. The membranes of the organelles within the cells
(mitochondria, lysosomes,
lysosomes, peroxisomes,
peroxisomes, etc) can also
be damaged
3. Membrane proteins, membrane lipids and cholesterol
can be damaged due to an insufficiency of antioxidants
to deal with the level of oxidative stress and free
radicals
28
14
Urinary Lipid Peroxides,
Cont’d
4. Other associated diseases include coronary artery
disease and cancer
5. Normal urinary lipid peroxide concentrations: 1.0 - 7.5
nmol/mg
nmol/mg creatinine
29
Sodium
•
Principal ECF Cation
•
•
90 – 95% OF OSMOLARITY FROM SODIUM SALTS
Roles
•
Depolarization
•
•
•
•
Muscles, nerves
Affect total body water
Affect water distribution
Cotransport
•
Glucose, amino acids, calcium, etc
30
15
Sodium Homeostasis
1.
2.
3.
4.
0.5 g/day Dietary Requirement
Receive 3 – 7 g/day from Our Diet
Kidneys excrete excess (~5 g/day)
Excretion regulated by three hormones
•
•
•
Aldosterone
Antidiuretic hormone (ADH)
Atrial natriurtic factor (ANF)
31
Sodium Homeostasis,
Cont’d
•
Regulation by Aldosterone
•
•
“SaltSalt-retaining hormone
Steroid Hormone
•
Aldosterone secretion stimulated by:
•
•
•
Hyponatremia
Hperkalemia
Hypotension
32
16
Sodium Homeostasis,
Cont’d
•
Regulated by Aldosterone
•
Target Cells
•
•
Distal convoluted tubule
Colleting duct
Transcribe gene for Na+-K+ pump
•
•
•
•
Sodium reabsortion increases
H+ and K + secretion increases
Urine pH drops
33
Sodium Homeostasis,
Cont’d
•
Regulation by Aldosterone
•
•
•
•
•
Average Na+ excretion 5 g/day
Aldosterone reduces to ~ 0
Water reabsorbed proportionally
Sodium concentration in body unchanged
Inhibited by Hypertension
•
•
Kidneys then Reabsorb little Na+
Excretion increased to ~30 g/day
34
17
Action of Aldosterone
35
Sodium Homeostasis,
Cont’d
• Regulation by ADH
• Independently modifies sodium and water
excretion
• Can Change sodium concentration
• High blood [Na+] ADH secretion
• Increases water reabsorption
• Sodium concentration decreased
• ADH also stimulates thirst
• Also happens in reverse
36
18
Sodium Homeostasis,
Cont’d
• Regulation by ANF
• Hypertension ANF secretion
• Inhibits ADH and renin secretion
• Inhibits sodium and water reabsorption
• More sodium and water excreted
• Blood pressure decreased
37
Sodium Homeostasis,
Cont’d
• Regulation by Other Hormones
• Estrogens mimic aldosterone
• Water retention during pregnancy
• Menstrual water retention
• Progesterone
• Reduces sodium reabsorption
• Glucocorticoids
• Promote sodium reabsorpiton,
reabsorpiton, Edema
38
19
Sodium Homeostasis
Imbalances
•
•
Relatively Rare
Hypernatremia
•
•
•
Can result from IV saline
Causes water retention, hypertension, edema
Hyponatremia
•
•
•
Generally from water excess
Hypotonic hydration
Corrected by excretion of excess of water
39
Potassium
•
•
•
Principal intracellular cation
Affects intracellular osmolarity
Affects cell volume
• Roles
•
•
•
•
Produces resting and action potentials
Cotransport
Thermogenesis
Cofactor for protein synthesis
40
20
Potassium Homeostasis
•
Homeostasis Linked to that of Na+
K+ and Na+ noregulated by aldosterone
•
•
90% of K+ Reabsorbed in PCT
•
•
Remainder excreted in urine
Control Imparted in DCT and Collecting Duct
(CD)
High [K+] Secrete more into filtrate
Low [K+] Secrete less into filtrate
Exchanged for Na+
•
•
•
41
Potassium Homeostasis,
Cont’d
•
Regulation by Aldosterone
•
High [K+] Aldosterone production
•
•
•
•
Na+-K+ pump produced
Na+ and K+ coregulated
Increase K+ secretion
Decrease Na+ secretion
42
21
Potassium Homeostasis
Imbalances
•
•
Most Dangerous Electrolyte Imbalances
Hyperkalemia
1.
Effects depend on speed of concentration raise
2.
3.
Quick Rise Nerve/muscle cells very excitable
Cardiac arrest
• E.G., K+ Released from injured cells
• E.G., Transfusion with old blood
• E.G., Euthanasia, capital punishment lethal injection
• K+ has leaked from erythrocytes
4. Slow Rise Nerve/muscle cells less excitable
5. (Na+ channels inactivated)
• E.G., Aldosterone hyposecretion,
hyposecretion, renal failure, acidosis
• E.G., Supplemental K+ to relieve muscle cramps
43
Potassium Homeostasis
Imbalances, Cont’d
•
Hypokalemia
1. Nerve/muscle cells less excitable
2. Muscle weakness, loss of muscle tone, depressed
reflexes, irregular heart activity
3. E.G., Heavy sweating, chronic vomiting or diarrhea,
excessive laxatives, aldosterone hypersecretion,
hypersecretion,
alkalosis
4. E.G., Depressed appetite, but rarely from dietary
insufficiency
44
22
Potassium and Membrane
Potentials
45
Clinical and Biochemical
Significance
Sodium and Potassium
1. Fasting or inadequate protein intake, in excessive tissue protein
catabolism, with liberation of ICF resulting in an increase in
urinary K and a change in Na : K ratio (in fasting, there is lack
of NaCl intake
2. Mineralocorticoid, aldosterone, increases the reabsorption of
Na and excretion of K
3. K excretion increases during alkalosis or ingestion of alkaline
diet
4. K excretion decreases during acidosis or ingestion of acid diet
5. Decrease urinary excretion of both Na and K Through
extrarenal channels; excessive sweating, vomiting, diarrhea
46
23
Calcium
•
Roles
1.
2.
3.
4.
5.
Strengthens bone
Muscle contraction
Second messenger for hormones
Activated exocytosis
Blood clotting
47
Calcium, Cont’d
•
Binds to Phosphate Ion
1. Can form Ca3(PO4)2
2. High concentrations of both ions will form
precipitate crystals
3. Intracellular [Ca2+] must be kept low
4. Ca2+ pumped out and into endoplasmic
reticulum
48
24
Calcium Homeostasis
•
Regulated by PTH and Calcitrol
•
•
Also by calcitonin in children
Blood [Ca2+] Regulated via:
1.
2.
3.
Bone deposition and reabsorption
Intestinal absorption
Urinary excretion
49
Calcium Homeostasis
Imbalances
•
Hypercalcemia
1.
2.
3.
4.
Reduces membrane permeability to Na+
Inhibits depolarization of nerve/muscles
Muscular weakness, cardiac arrhythmi,
arrhythmi, etc
Results from
•
•
•
Alkalosis
Hyperparathyroidism
Hypothyroidism
50
25
Calcium Homeostasis
Imbalances, Cont’d
•
Hypocalcemia
1.
2.
3.
4.
Increases membrane permeability to Na+
Nerves/muscles overly excitable
Tetanus if concentration drops to low
Results from
•
•
•
•
•
•
Acidosis
Vitamin D deficiency
Diarrhea
Pregnancy or lactation
Hypoparathyroidism
Hyperthyroidism
51
Urinary Organic
Constituents
Urea Formation
1. Principal method for removing ammonia
2. Occurs primarily in liver; excreted by kidney
3. Hyperammonemia
•
•
Defects in urea cycle enzymes (CPS, OTC, etc.)
Severe neurological defects in neonates
4. Treatment
•
•
•
Stop protein intake
Dialysis
Increase ammonia excretion: Na benzoate, Na
phenylbutyrate,
phenylbutyrate, LL-arginine,
arginine, LL-citrulline
52
26
The Urea Cycle
Asp
+
NH 3 -CHCH 2CO 2 -
NH 3 +
NH 2 CONH CH 2 CH 2 CH 2 CHCO
Citrulline
2
-
CO 2 -
NH 3 +
+
H 2 N=C-HN CH 2 CH 2 CH 2 CHCO
CO 2 - Arginosuccinate
Ornithine
Transcarbamoylase
(mitochondria)
2
-
CO 2 -
H
Fumarate
Urea
H2NCONH2
-
Arginosuccinase
Ornithine
Arginase
-
NH-CHCH 2 CO 2-
Arginosuccinate
synthase
NH 3 +
+
H 3 NCH 2 CH 2 CH 2 CHCO
2
NH 2
H
O2C
TCA Cycle
+
NH 3
+
H 2 N=C-HN CH 2 CH 2 CH 2 CHCO
2
-
Arginine
53
Clinical and Biochemical
Significance
Urea
Decrease
1. In certain liver diseases; cirrhosis, acute yellow atrophy
2. In cases of severe acidosis
3. Nephritis
Increase
Whenever protein catabolism is increased as in fever, diabetes
mellitus, excess of adrenocortical activity
54
27
Clinical and Biochemical
Significance
Ammonia
Decrease
1. In alkalosis
2. Administration of alkalis or base forming foods
3. Nephritis
Increase
1. In cases of severe diabetic acidosis
2. Administration of acid forming foods
3. Copious water drinking
4. Bacterial infection of bladder as in cystitis
55
Clinical and Biochemical
Significance
Uric acid
Diet
On a purine free diet uric acid excretion may fall to 0.1
g/day, while on a high purine diet the excretion may
raise to 2 g/day
Pathophysiolgical Variations
1. Urinary excretion of UA increase during gout
2. In leukemia where breakdown of large amount of nuclear
materials
3. Administration of cortisone of ACTH
56
4. In Wilson’s disease
28
Creatine and Creatinine
Formation
NH 2
NH 3 +
+
H 2 N=C-HN CH 2 CH 2 CH 2 CHCO
Arginine-glycine
transamidinase
(Kidney)
2
-
Glycine
Arginine
NH 2
+
H 2 N=C-HN CH 2 CO 2 -
Ornithine
Guanidoacetate
SAM + ATP
H
N
Creatinine
(Urine)
O
(Liver)
HN
NH 2
NHPO 3 -2
+
H 2 N=C-N CH 2 CO 2 -
Creatine kinase
(Muscle)
+
H 2 N=C-N CH 2 CO 2 CH 3
S-Adenosylhomocysteine
+ ADP
Non-enzymatic
(Muscle)
N
CH 3
Creatine
Guanidoacetate
Methyltransferase
ATP
CH 3
ADP
+ Pi
Phosphocreatine
57
Clinical and Biochemical
Significance
Creatine
Excretion of creatine in urine is called creatinuria
for these causes:
1. In children; reason probably lack of ability to
convert creatine into creatinine
2. In pregnancy
3. In febrile conditions
58
29
Clinical and Biochemical
Significance, Cont’d
Creatine
4. In hypotoxicosis; probably associated with
myopathies
5. In muscular dystrophyies
6. Lack of carbohydrates in diets in diabetes mellitus
7. In Wasting diseases; eg molignancies
8. In starvation
59
Clinical and Biochemical
Significance
Oxalic acid
1. Oxalic acid separates from urine as insoluble Caoxalate crystals which can be seen
microscopically in centrifuged deposit urine. If
passed in excessive amounts can form urinary
calculus in urinary tract
60
30
Clinical and Biochemical
Significance, Cont’d
Oxalic acid
2. Increase:
• Diabetes mellitus
• Certain liver diseases
• In various conditions involving deficient tissue
oxidation
3. Primary hyeroxaluria
• Oxaluric acid; a combination of oxalic acid and urea
occasionally present in traces in normal urine
61
Clinical and Biochemical
Significance
Amino acids
Excretion of amino acids in urine is called
aminoaciduria
Over Flow Aminoaciduria
• There is some metabolic defects; as a result
there occurs an increase in plasma level of one or
more of amino acids which exceeds the capacity
of normal renal tubules to reabsorb them. It
found in:
62
31
Over Flow Aminoaciduria,
Cont’d
1. Severe liver diseases; acute yellow atrophy,
cirrhosis, etc
2. Wasting diseases
3. Metabolic amino acid disorders:
•
•
•
•
•
Phenylkeptonuria
Tyrosyluria
Alkaptonuria
Melanuria
Maple syrup urine diseases
63
Renal Aminoaciduria
•
Plasma level of amino acids is normal, but
because of defects in renal tubular
reabsorption of amino acids, an increase
amount of one or several or all amino acids
escape in urine. The defect may be:
1. Specific to one reabsortion mechanism as in
cystinuria in which there is failure to
reabsorb Cys, Lys, Arg and Orn (a common
transport defect)
64
32
Renal aminoaciduria, Cont’d
2. Nonspecific mechanism as seen in:
•
•
•
•
Fanconi syndrome; in which there is failure to
reabsorb glucose, phosphates, ammonia and other
organic acids, eg lactic acid
Wilson’s disease; in which in addition to
aminoaciduria (Ala, Asp, Glu) there is associated
glycosuria, uric acid and phosphate excretion.
Muscular dystrophies; Met, Val, Ile or Leu.
Heavy metal intoxication; Pb, Hg, Co, Ur
65
Proteins in “Normal” Urine
Protein
% of Total
Daily Maximum
Albumin
TammTamm-Horsfall
Immunoglobulins
Secretory IgA
Other
40%
40%
12%
3%
5%
60 mg
60 mg
24 mg
6 mg
10 mg
TOTAL
100%
150 mg
66
33
Proteinuria
When protein appears in urine in detectable amounts, it
is called misnomer “albuminuria”. Two types:
Functional proteinuria
It is not related to a diseased organ.
67
Functional Proteinuria,
Cont’d
Causes
1.
2.
3.
4.
5.
Violent exercise
Cold bathing
Alimentary of protein ingestion
Pregnancy
Orthastatic or postural; in children or in
adolescents usually in age of 14 to 18 years
68
34
Organic Proteinuria
• It is classified into three major groups:
1. Prerenal
2. Renal
3. Postrenal protienuria
69
Prerenal Proteinuria
It is not related to kidneys
Causes
1.
2.
3.
4.
5.
Cardiac diseases
Any abdominal tumors
Fever and hypoxia conditions
Cancers
Collagen diseases
70
35
Renal Proteinuria
It is related to kidney diseases.
Causes
1. Acute glomerulophritis
2. Chronic glomerulophritis
3. Nephrosclerosis
4. Nephrotic syndrome
5. Renal tumor or infection
71
Postrenal Proteinuria
It is sometimes called “false proteinuria” because
protein don’t pass through kidneys.
Causes
1. Urethritis or prostatitis
2. Bleeding in genito urinary tract
3. Cystitis
4. Contamination with vaginal
secretions
72
36
Glucosuria
When sugar (glucose) appears in urine in
detectable amounts.
Two Types
1. Hyperglycemic glucosuria
• It is NOT related to kidney diseases
2. Renal glucosuria
•
It is related to kidney diseases
73
Hyperglycemic Glucosuria
Causes
1. Alimentary of ingestion of carbohydrates
2. Nervous or emotional conditions; (increases
glycogenolysis)
3. Endocrine disorders:
•
Insulin, diabetes mellitus
•
Hyperthyroidism
•
Epinephrine
•
Hyperactivity of anterior pituitary gland
•
Adrenal cortex
•
Glucagon
74
37
Renal Glucosuria
Causes
1. Hereditary
2. Acquired:
• Renal tubule diseases
• Heavy metal poisoning
• Lowering of renal threshold
• Renal tubular transport defects
• Renal tubular acidosis
• Hyperphosphaturia as in Fanconi syndrome
75
Classification of Urinary
Calculi
1. Calcium oxalate
It is the most commonly formed constituent of urinary
calculi. It precipices at acid or neutral pH
2. Calcium phosphate
It forms calculi at the normal urinary pH 6 – 6.5
3. Magnesium ammonium phosphate
It forms calculi in an alkaline urine probably associated
with bacterial infections
76
38
Classification of Urinary
Calculi, Cont’d
4. Mixed calcium oxalate and calcium phosphate
It is the most common constituents (80 – 84%)
5. Mixed calcium phosphate, magnesium ammonium
phosphate and uric acid
It is about 3 – 10%
77
Classification of Urinary
Calculi, Cont’d
6. Uric acid, cystine and xanthine
It precipitates in acid urine at pH < 6
7. Cystine
It is about 1 – 2%
78
39
Classification of Urinary
Calculi, Cont’d
8. Carbonate
It is frequently detected in chemical analysis and probably results
from absorption of carbon dioxide to the calcium phosphate
crystals
9. Organic matrix
It appears to be the one essential component of all urinary calculi.
This mixture is mucoid containing about 65% protein, 14%
carbohydrates, 12% inorganic ash and 1% bound water
79
Causes of Urinary Calculi
1. Consumption of animal proteins
2. Hyperparathyroidism
3. Hypervitaminosis D
4. Avitaminosis A (Deficiency)
5. Avitaminosis B6
6. Kidney stones
80
40
Reporting Results
1. Most urinalysis reports have a standardized
form
1. Key to reporting is to be consistent
2. Documentatio
81
Laboratory Report:
Urinalysis
82
41
Urinalysis Automation
• Several automated instruments are
currently available to standardize:
•
•
•
•
Sample processing
Biochemical test strips analysis
Microscopy analysis
Report results
83
Urinalysis Automation
• Automation Urinalysis Features:
1.
2.
3.
4.
5.
OnOn-line computer capability
Bar coding
Manual entry of color
Clarity
Microscopic results
84
42
Urinalysis Automation,
Cont’d
• Automation Urinalysis Features:
6.
7.
8.
9.
10.
Flagging of abnormal results
Sorting of patients and control results
Minimal calibration
Cleaning
Maintenance
85
Major Automated Biochemistry
Urine Analyzers
• Semiautomation
• It depends on an operator
for specimen mixing
• Test strip dipping
• InIn-putting physical and
microscopic results
• Fully automation
• Add urine to reagent strips
• Workstations
• Complete urinalysis
86
43
Clinitek 50/100 Reagent
Strips
• It suited for small Lab
• Reagent strips are
manually dipped and
placed into the strip
reader
• Results are displayed or
printed
• Patients ID, specimen
color, clarity are
manually entered
• Abnormal results are
flagged
87
Multistix 10 SG Reagent
Strips
Distinguishes between
hemolyzed and intact
RBCs
Biochemistries
leukocytes, glucose,
Bilirubin,
Bilirubin, Ketone,
Ketone, specific
gravity, nitrite, phosphate,
protein, Urobilinogen,
Urobilinogen,
blood
Automatic urine color
determination
88
44
Clinitek 500 Reagent Strips
• Distinguishes between
hemolyzed and nonhemolyzed
specimen
• Determine low SG and pH
• Rapid entry
• Specimen ID
• Color
• Clarity
• Automatic features
•
•
•
•
•
Color determination
Strips detection
Calibration
Confirmatory
Microscopic analysis
89
Clinitek Microalbumin
Reagent Strips
• Provide albumin,
creatinine and albuminalbumintoto-creatinine ratio results
in one minute
• useful to test for
microalbuminuria in
patients with diabetes or
hypertension in order to
detect early kidney
disease
90
45
Clinitek Atlas
• It designed for large Lab
• Performs >12 tests
automatically
• WalkWalk-away capability (> 225
specimen/hr)
• > 2 mL urine specimen
required
• Flagging abnormal specimen
• Automatic features
•
•
•
•
•
•
Color determination
Strips detection
Calibration
Confirmatory
Microscopic analysis
etc
91
Clinitek Status Analyzer
• Provides important
markers to detect early
stages of many disease
states, such as kidney
disease and urinary tract
infections
• SemiSemi-quantitative results
have proven to be costcosteffective and virtually
immediate
• Its readings eliminate
the subjectivity of color
interpretation
92
46
Intended Use of Clinitek
Status Analyzer
• The Analyzer is for in vitro use in the semisemi-quantitative
detection of
• Albumin, bilirubin,
bilirubin, blood (occult), creatinine,
creatinine, glucose, ketone
(acetoacetic acid), leukocytes, nitrite, pH, protein, specific
gravity and urobilinogen in urine samples
• The calculation of albuminalbumin-toto-creatinine and proteinprotein-totocreatinine ratios in urine samples, when Clinitek®
Clinitek®
Microalbumin and Multistix PRO®
PRO® Reagent Strips for
Urinalysis are used
• The detection of human Chorionic Gonadotropin (hCG)
hCG)
in urine samples, when Clinitest®
Clinitest® hCG cassettes are
used
93
94
47
Urinalysis Workstations
• Automatic analysis (6
mL)
mL) at room
temperature
• Biochemistry strip
tests
• Urine specific gravity
(2 mL)
mL)
• Microscopy (4 mL
uncentrifuged urine
specimen)
95
Urinalysis Workstations,
Cont’d
• Operator makes the final
ID by touching on
monitor screen of touch
buttons:
• An appropriate area
• Category
• Contains body fluids:
• Cerebrospinal fluid
• Serous fluid (pleural,
pericardial, peritoneal
fluid)
• Seminal fluid
• Synovial fluid
96
48
Urine Pathology System
• Complete routine
urinalysis automation
• Fully automated
biochemistry test strip
results
• Urine SG, color, clarity
• Microscopic analysis
(uncentrifuged specimen)
• Automatically counts
• RBC, WBC, bateria,
bateria, yeasts,
squamous epithelial cells,
hyaline, nonhyaline casts,
sperm, mucus, etc
97
Urine Pathology System,
Cont’d
• Operator interacts
with the monitor to
• Review and confirm
analyte images
• Edit the results
• Flag the abnormal
results
• Final report can be
printed
98
49
IRIS Flow Videomicroscopy
• Urine is drawn through a
flat chamber
• Video snaps are sorted
by computer
• Technician scans images
and deletes dud ones
Computer then adds up
#/cmm
#/cmm
• These are RBCs
99
IRIS Flow Videomicroscopy
• Squamous epithelial
cells
100
50
THE END
Any questions?
101
51