CHEMICAL EXAMINATION OF ● Specimen collected at specific time: Urobilinogen (2-4pm

only) PROTEINS NORMALLY FOUND IN URINE

URINE ○ because urobilinogen is stable at alkaline urine ● Albumin: major serum protein found in normal urine
○ may nakakalusot pero in moderation
○ <10mg/dL
Acid Urine Alkaline Urine
○ pinakamaraming concentration sa plasma, but
pH mostly are repelled
Emphysema Hyperventilation
DETERMINED BY THE CONCENTRATION OF H+ ○ major serum protein
● As H+ increases, pH decreases = Acidic ● Tamm-Horsfall protein (uromodulin)
Diabetes mellitus Vomitting
● As H+ decreases, pH increases = Alkaline ○ Produced in the distal convoluted tubile
● More hydrogen = more acidic = lesser pH ○ Involved in cast formation (forms Matrix of all
Starvation Renal tubular acidosis
types of casts)
CLINICAL SIGNIFICANCE ○ Casts: pathologic except for hyaline cast
Dehydration Presence of
● aid in determining the existence of systemic acid-base ■ affects the tubules, DCT and CD
urease-producing bacteria
disorders ● Other proteins included small amounts of serum and
○ Metabolic or respiratory acidosis = acidic urine Diarrhea Vegetarian diet tubular microglobulins
○ Tubular acidosis = alkaline urine ○ Belongs to post renal
● Important in the identification of crystals Presence of acid-producing Old specimens ● Proteins from prostatic, seminal, and vaginal secretions
○ precipitate, cyrstals, and calculi bacteria (E. coli) ○ Belongs to post renal
○ Calculi = renal stones
● treatment of UTI High protein diet **after meals — alkaline tide NORMAL URINE PROTEIN: <10mg/dL or 100mg/24 hours
○ Cranberry juice = hippuric acid
● determination of unsatisfactory specimen Cranberry juice
Produce hippuric acid
NORMAL pH: CLINICAL PROTEINURIA
● Random: 4.5-8.0 Medications (methenamine ● Increased protein in urine
● First Morning: 5.0-6.0 mandelate [Mandelamine], ● >/= 30 mg/dL (300mg/L)
UNPRESERVED URINE pH: 9.0 fosfomycin tromethamine ● Causes are grouped into 4 categories
[Monurol]) 1. Prerenal or overflow proteinuria
ACID URINE 2. Renal (Glomerular proteinuria, Tabular
● prevents stone formation by alkaline-precipitating solutes proteinuria)
(calcium carbonate and calcium phosphate)
● inhibits the development of UTI
Protein 3. Postrenal proteinuria

● Most indicative of renal dxe PRERENAL OR OVERFLOW PROTEINURIA

ALKALINE URINE
● prevents the precipitation of and enhances the excretion
of various drugs (sulfonamides, streptomycin and
salicylate)
● prevents stone formation (calcium oxalate, uric acid, and
cystine crystals
● Alkaline tide: happened 2hrs after a meal
○ bc the H+ ay pupunta sa stomach to create
hydrochloric acid
○ Parietal cells will create bicarbonate
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○ Proteins are high molecular weight, thus, it
should not be present in urine
○ Renal: overflow of urine
○ Post renal: problems in the ureter, urethra, and
urinary blader
● Produces stable white foam when shaken
● not indicative of actual renal disease
● results from increased quantities of plasma proteins (low
molecular weight) in the blood readily passing the
glomerular filtration barriers into the urine
● Conditions Associated:
○ Hemolytic dxe (Hemoglobin)
○ Infection and inflammation (Acute Phase
Reactants)
○ Other abnormal proteins—immunoglobulin
paraproteins (Kappa and gamma light chains)
 abnormally produced in multiple myeloma and ● Orthostatic / Cadet / Postural proteinuria (functional
macroglobulinemia proteinuria)
■ Bence Jones Protein ○ Proteinuria when standing due to increased MICROALBUMINURIA
pressure on renal veins (causes renal ● 30-300 mg/day
BENCE JONES PROTEIN congestion and glomerular changes) ● nawawala ang shield of negativity
● Multiple Myeloma: proliferative disorder of the ○ Once in lying position, mawawala din ● moderate increase in the level of albumin in urine
immunoglobulin ● associated with hypertension, diabetes mellitus, and
● Screening test: Unique solubility characteristics cardiovascular dxe
Orthostatic Clinical
● Urine: ● signifies onset of renal complications of Diabetes
Proteinuria Proteinuria
○ Coagulates at 40C-60C (Cloudy) mellitus (Diabetic nephropathy)
○ Dissolves at 100C (Clear ● Micral Test
First Morning urine ( - ) Protein (+) protein
● Interference due to other precipitated proteins can be
removed by filtering the specimen at 100C and TUBULAR PROTEINURIA
2 hours after (+) protein (+) protein
observing the specimen turbidity as it cools between ● normal tubular reabsorptive function is impaired
standing transient
40C and 60C ● failure or defective in reabsorption
● Causes: toxic substances/ heavy metals, severe viral
RENAL infections, Fanconi’s syndrome
Functional Proteinuria-absence of renal disease
● Fanconi’s Syndrome
● true renal dxe ● Strenous exercise
○ proximal tubular dysfunction
● actual indicative of renal dxe ● Fever
■ PCT: major site of reabsorption
● Extreme cold exposure
○ caused by heavy metal poisoning and hereditary
2 TYPES ● Emotional distress
dxe (cystinosis)
● Glomerular proteinuria ● Congestive heart failure
○ aminoaciduria, proteinuria, glycosuria, and
● Tubular proteinuria ● Dehydration
phosphaturia
● Other disease that contribute to occurence of tubular
GLOMERULAR PROTEINURIA proteinuria: acute/ chronic pyelonephritis, interstiitial
● most common type and clinically serious Occur in primary glomerular dxe that cause glomerular nephritis renal tubular acidosis, renal tuberculosis, and
● Involves damage to the glomerular filtration barrier, damage systemic dxe (sarcoidosis, SLE, cystinosis, galactosemia
allowing excretion of almost all proteins ● Glomerulonephritis and Wilson’s dxe)
● about 2.5 g/day and can reach up to 20 g/day ● Glomerulosclerosis
● Albumin: primary protein increased—allows other ● Minimal change disease PRINCIPAL PROTEINS IN GLOMERULAR PROTEINURIA
moderate-molecular weight proteins to be excreted ● shield of negativity ● Albumin
(alpha 1-antitrypsin, alpha-acid glycoprotein, and ● Poststreptococcal ● Transferrin
transferrin) ● Glomerulonephritis ● a1-antitrypsin
○ small amounts lang natatapon due to shield of ● Diabetes mellitus ● a1-acid glycoprotein
negativity ● SLE
● Nephrotic syndrome ● Amyloidosis PRINCIPAL PROTEINS IN TUBULAR PROTEINURIA
○ massive proteinuria (>3.5 g/day) with high ● Sickle cell anemia ● Albumin
amount of lipids ● Kidney transplant rejection ● B2-microglobulin
■ may O so may oval fat bodies ● Infectious dxe (malaria, hepatitis B, and bacterial ● Retinol-binding protein
○ hypoalbuminemia endocarditis ● a2-Microglobulin
○ hyperlipidemia ● Preeclampsia and in cases of leukemia and ● a1-Microglobulin
○ lipiduria lymphoma ● Lysozyme
○ generalized edema

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POSTRENAL PROTEINURA
● proteinuria results from an inflammotory process GLYCOSURIA/GLUCOSURIA
anywhere in the urinary tract (renal pelvis, ureters, ● presence of glucose in urine at a concentration greater
bladder, prostate, urethra, and external genitalia than 20mgdL
● protein can be added to a urine specimen as it passes ● ultrafiltrate concentration of glucose exceeds the
through the structures of the lower urinary tract reabsorptive ability of the tubules
● Causes
LOWER UTI (URETERS, BLADDER, URETHRA, PROSTATE, 1. Prerenal condition (hyperglycemia)
AND VAGINA) ● Diabetes mellitus
● inflammation of bacterial or fungla origin produces ● Gestational diabetes mellitus
secretions containing protein from the interstitial fluid ● Other conditions of nondiabetic origin
○ Acromegaly (up growth hormone)
URINE CONTAMINATION DURING EXCRETION ○ Cushing’s dxe (up cortisol)
● hemorrhage / menstrual contamination ○ Stroke
● prostatic fluid ○ Hyperthyroidism (up thyroxine)
● spermatozoa ○ Liver dxe, pancreatic damage
● vaginal secretions ○ Stress and anxiety
2. Renal condution: defective tubular absorption
***Check summary table for classification of proteinuria
HORMONES THAT INCREASE GLUCOSE
(HYPERGLYCEMIC)
● Glucagon: major hyperglycemic hormone
GLUCOSE ○ produced by the alpha cells of the islets of
Langerhans
● Most frequent chemical analysis performed on urine ○ Target: Liver
○ Promotes lvier glycogenolysis
DETECTION OF DIABETES MELLITUS ○ Increases glucunegenesis
● Mellituria= presence of any sugar (reducing and non ○ Inhibits glycolysis
reducing sugar) in urine ● Cortisol: produced by the adrenal gland (adrenal cortex)
● Glycosuria: presence of any reducing sugar in urine ○ increases gluconeogenesis
(Glucose, lactose, galactose, fructose, pentose) ○ Decreases glucose uptake and utilization by
extrahepatic tissues
Normal Urine Glucose: 15 mg/dL ● Catecholamines (Epinephrine)
Fasting: 2-20 mg/dL per 100mL urine ○ produced by the adrenal medulla
○ secreted on fight or flight response
○ stimulates glycogenolysis
● Thyroid hormone
Renal threshold for glucose: 160-180 mg/dL ○ produced by the thyroid gland (FT4, FT3, sTSH)
○ Increases glucose absorption in the small
Maximum reabsorptive capacity (Tm) intestine
350 mg/min ● Growth hormone
250 to 360 mg/min in females ○ prodcued by the anterioir pituitary gland
295 to 455 mg/min in males ○ increases lvier gluconeogenesis
○ inhibits glycolysis
**insert table ○ inhibits glucose transport
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HYPERGLYCEMIA WITH GLUCOSURIA
● diabetes mellitus
● gestational diabetes mellitus (GDM)
● other conditions of nondiabetic origin
○ Acromegaly
○ Hyperthyroidism
○ Cushing’s dxe
○ liver dxe
○ pancreatic damage
○ stroke
○ stress
○ anxiety
HYPERGLYCEMIA WITHOUT GLUCOSURIA
● glomerular barriers are compromised because of a dxe =
glomerular filtration rate can be decreased
● renal arteriosclerosis or low cardiac output
GLUCOSURIA WITHOUT HYPERGLYCEMIA
● reabsorption of glucose by the renal tubules in
compromised
GLYCOSURIA/ GLUCOSURIA
● Pre-renal condition (hyperglycemia)
1. Diabetes mellitus: ineffective glucose utilization caused
by inadequte insluin secretion or abnormal insulin action
2. Galactosemia
● inherited disorder characterized by an inability to
metabolize galactose to glucose
● due to the reduction or absence of an enzyme required
for galactose metabolism
● Galactose I-phosphate uridyl transferase (GALT):
enzyme that converts galactose to glucose
● Galactonate: vomiting and diarrhea: the infant fails to
thrive; hepatomegaly and jaundice
● Galactitol: formed which causes catarct formation
● Both may cause: irreversible brain damage
● Lactose: may found on urine of pregnant women or of
premature infants
● Fructose: result of excessive fruit or hone ingestion or
from a rare genetic defect (fructosuria) involving hepatic
fructokinase deficiency
● Pentose (xylose and arabinose)
○ excessive fruit ingestion (plums and cherries)
 ○ rare genetic defect involving deficiency of
L-xylulose reductase (or L-xylitol
dehydrogenase)

KETONE
● result from increased fat metabolism due to inability to
metabolize carbohydrate
○ Type 1 diabetes mellitus
○ Vomiting
○ Starvation
○ Malabsorption
● Normal urine ketone: normally not in urine

KETONE BODIES

78% B-hydroxybutyric Major ketone but not detected in

acid reagent strip

20% acetoacetic acid/ Parent ketone because it is where

diacetic acid other ketones are derived; detected
by reagent strip

2% acetone

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 - Hypertension
- Postural (orthostatic)
CLASSIFICATION OF PROTEINURIA proteinuria
- Postpartum period
CLASSIFIC PROTEINURIA PROTEINS PRESENT CAUSES - Extreme cold exposure
ATION DESCRIPTION
Tubular Increase in the low MW - Acute/ chronic
Pre-Renal Overflow Normal Proteins: - Muscle injury proteinuria: proteins normally pyelonephritis
proteinuria: increase - Myoglobin - Intravascular hemolysis defective tubular present in the - Interstitial nephritis
in plasma low MW - Hemoglobin - Infection reabsorption protein ultrafiltrate includig - Renal tubular acidosis
proteins leads to - Acute Phase - Inflammation albumin - Renal tuberculosis
increased excretion reactants - Multiple myeloma - Fanconni’s syndrome
in urine - Systemic dxe—
Abnormal Proteins sarcoidosis, SLE,
- Ig light chains cystinosis, galactosemia,
(Bence Jones Wilson’s dxe
Protein) - Hemoglobinuria—hemoly
tic disorders
Renal Glomerular Selective: increase in Primary glomerular dxe: - Myoglobinuria—muscle
proteinuria: GFB is albumin and moderate - Glomerulonephritis injury
defective allowing MW plasma proteins - Glomerulosclerosis - Drugs (aminoglycosides,
plasma proteins to - Minimal change dxe sulfonamides, penicillins,
enter ultrafiltrate Nonselective: increase cephalosporins)
in all proteins, including Glomerular damage due to: - Toxins and poisons
high MW plasma - Poststreptococcal (heavy metals)
proteins glomerulo nephritis - Strenuous exercise
- Diabetes mellitus
- Lupus erythematosus Post-Renal Urine includes - Pus - Inflammation
- Amyloidosis proteins produced - Menstrual and - Malignancy
- Sickle cell anemia by the urinary tract hemorrhoidal - Injury/trauma
- Transplant rejection or the urine is blood - Contamination during
- Infectious dxe (malaria, contaminated with - vaginal urination
hepatitis B, bacterial proteins during secretions
endocarditis) excretion - prostatic
- Preeclampsia secretions
- Cancers (leukemia,
lymphoma)
- Drugs (penicillamine,
lithium) and toxins
(heavy metals)

Transitory glomerular changes

- Strenuous exercise
- Fever, dehydration

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