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UREA

FORMATION OF UREA

Liver is the main organ involved in urea formation, and kidneys are involved in its
excretion.

Recently it has been shown that brain and mammary glands can also synthesize urea to
some extent.

Normal range:

In blood: 0.20 g/l ---0.40 g/l or 20--40mg/dl

In urine: 170—600mmol/24 h

10.2—36 g/24 h

2.5-6.6 mmol/l

UREMIA

• UREMIA is a term used to loosely describe the illness accompanying kidney


failure (also called renal failure).
• Uremia is a clinical syndrome associated with fluid, electrolyte, and hormone
imbalances and metabolic abnormalities, which develop in parallel with
deterioration of renal function.
• In kidney failure, urea and other waste products, which are normally excreted into
the urine, are retained in the blood.
• Early symptoms include anorexia and lethargy, and late symptoms can include
decreased mental acuity and coma.
• It is usually diagnosed in renal failure patients when the glomerular filtration rate,
a measure of kidney function, is below 50% of normal
• There are many dysfunctions caused by uremia affecting many systems of the
body, such as blood (lower levels of erythropoietin), sexual (lower levels of
testosterone/estrogen) and bones (osteoporosis and metastatic calcifications).

AZOTEMIA

Azotemia is another word that refers to high levels of urea, but is used primarily
when the abnormality can be measured chemically but is not yet so severe as to produce
symptoms.
PATHOPHYSIOLOGY

• Normally, the kidney is the site of hormone production and secretion, acid-base
homeostasis, fluid and electrolyte regulation, and waste-product elimination.
• In the presence of renal failure, these functions are not performed adequately and
metabolic abnormalities, such as anemia, acidemia, hyperkalemia,
hyperparathyroidism, malnutrition, and hypertension, can occur.
• Uremia usually develops only after the creatinine clearance falls to less than 10
mL/min, although some patients may be symptomatic at higher clearance levels,
especially if renal failure acutely develops
• The syndrome may be heralded by the clinical onset of nausea, vomiting, fatigue,
anorexia, weight loss, muscle cramps, pruritis, and change in mental status.

CAUSES OF RENAL FAILURE

A) Pre renal

Prerenal azotemia is the most common form of kidney failure in hospitalized patients.
Any condition that reduces blood flow to the kidney may cause it, including:

• Burns
• Conditions that allow fluid to escape from the bloodstream
• Loss of blood volume (such as with dehydration)
• Prolonged vomiting or diarrhea, bleeding
• Accelerated production of nitrogenous waste products because of enhanced
catabolism of tissues in association with infection, fever, trauma, corticosteroid
excess, or burns.
• Increased gastro- intestinal digestion and absorption of protein sources (diet or
gastrointestinal hemorrhage

Conditions in which blood volume is not lost, but the heart cannot pump enough blood or
the blood is pumped at low volume, also increase the risk for prerenal azotemia. These
conditions include:

• Heart failure
• Shock (such as septic shock)

It also can be caused by conditions where the blood flow to the kidney is interrupted,
such as:

• Certain types of surgery


• Renal artery embolism
• Renal artery occlusion
• Trauma to the kidney
B) Renal

• Acute or chronic renal failure


• Primary renal disease affecting glomeruli, renal tubules, renal interstitium, or
renal vasculature that impairs renal function by at least 75%)
• Malignant hypertension
• Nephrotoxic drugs
• Renal cortical necrosis
• Chronic renal diseases such as
o Glomerulonephritis
o Pyelonephritis
o Diabetes mellitus
o Arteriosclerosis
o Amyloidosis
o Collagen vascular diseases

C) Post renal

• Bilateral Urinary obstruction by stones, tumor, inflammation, surgical procedure


• Enlarged prostate
• Rupture of the excretory pathway.

DECREASED LEVEL OF UREA:


• Low intake
anorexia
malnutrition
• Low production
liver failure
• Increased excretion

High urine flow (reduced tubular reabsorption)

Medical uses

Drug use :

• Urea is used in topical dermatological products to promote rehydration of the


skin.
• If covered by an occlusive dressing, 40% urea preparations may also be used for
nonsurgical debridement of nails.
• This drug is also used as an earwax removal aid.
Clinical diagnosis :
Blood urea nitrogen (BUN).

The blood urea nitrogen (BUN) test is a measure of the amount of nitrogen in the blood
that comes from urea. It is used as a marker of renal function.

Other diagnostic use :

• Isotopically-labeled urea is used in the urea breath test, which is used to detect the
presence of the bacteria Helicobacter pylori (H. pylori) in the stomach and
duodenum of humans.
• The test detects the characteristic enzyme urease, produced by H. pylori, by a
reaction that produces ammonia from urea. This increases the pH (reduces
acidity) of the stomach environment around the bacteria.

Hazards

• Urea can be irritating to skin and eyes.


• Too high concentrations in the blood can cause damage to organs of the body.
• Repeated or prolonged contact with urea in fertilizer form on the skin may cause
dermatitis.
• The substance also irritates the respiratory tract.
• The substance decomposes on heating above melting point, producing toxic gases,
and reacts violently with strong oxidants, nitrites, inorganic chlorides, chlorites and
perchlorates, causing fire and explosion hazard.
SERUM UREA ESTIMATION

PRINCIPLE:
Urease specifically decomposes urea producing, carbondioxide and ammonia. The
latter reacts with phenol and hypochlorite in alkaline medium, producing indophenol
blue, which is colorimetrically measured.

PROVIDED REAGENTS:
 Reagent 1: Dried reagent containing phenol and sodium nitroferricyanide.
 Reagent 2: Concentrated reagent containing sodium hypochlorite and in sodium
hydroxide.
 Standard: 60 mg/dl urea solution.

NON-PROVIDED REAGENT:
 Distilled water.
 Urease: Stabilized and buffered solution, provided separately by Wiener lab.

WARNINGS:
Reagents are for “in vitro” use. Phenol is toxic and irritating.

SAMPLE:
Serum, plasma or urine.

a) Collection: Obtain serum in usual way


b) Known interfering substances:
 Anticoagulants containing fluorides inhibit urease activity.
 Strong hemolysis may produce falsely high results up to 5%. This
interference can be corrected with a serum blank.
 No interference is observed from light or moderate hemolysis or bilirubin
up to 400 mg/l.
c) Stability and storage instructions: serum urea is stable several days in refrigerator
or 6 months in freezer without preservatives.

REQUIRED MATERIAL:
 Spectrophotometer.
 Micropipettes.
 Water bath at 37 0C.
 Stop watch.

ASSAY CONDITIONS:
 Wave-length: 540 nm.
 Reaction temperature: 37 0C.
 Reaction time: 20 min.
 Reaction volume: 12 ml.
 Sample volume: 10 µl.

PROCEDURE:
In three colorimeter test tubes labeled B (Blank), S (Standard), and U (Unknown),
place 1 or 2 water drops. Then add:
B S U
Standard - 10 µl -
Serum or plasma - - 10 µl
Urease 1 drop 1 drop 1 drop
Mix by gently shaking and incubate for 5 minutes at 37 0C. Then add:
Reagent 1 0.5 ml 0.5 ml 0.5 ml
Reagent 2 0.5 ml 0.5 ml 0.5 ml
Mix by gently shaking and incubate for 5 minutes at 37 0C. Then add:
Distilled water 5 ml 5 ml 5 ml
Mix by inversion and remove from bath. After 10 minutes read in photocolorimeter with
green filter (501-550nm), setting the instrument to zero O.D. with Blank.

STABILITY OF FINAL REACTION:


Final reaction color is stable for 12 hours; therefore readings may be performed within
this period.

CALCULATIONS & OBSERVATIONS:

Urea (mg/dl) = O.D of unknown


-------------------- multiply by conc. of stand (S60 mg/dl)
O.D of standard

BUN (mg/dl)= O.D of unknown


-------------------- multiply by conc. of stand (28 mg/dl)
O.D of standard