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STMR GLXPJWV 8 Oma JC 6 ZMF 8

The document provides an overview of kidney function tests, focusing on the determination of blood urea and creatinine levels, which are critical for diagnosing kidney and liver diseases. It details normal and abnormal urine characteristics, including physical and chemical properties, and outlines the implications of various urine constituents. Additionally, it discusses the analysis of urinary stones, their types, causes, and the procedures for chemical examination.

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0% found this document useful (0 votes)
40 views11 pages

STMR GLXPJWV 8 Oma JC 6 ZMF 8

The document provides an overview of kidney function tests, focusing on the determination of blood urea and creatinine levels, which are critical for diagnosing kidney and liver diseases. It details normal and abnormal urine characteristics, including physical and chemical properties, and outlines the implications of various urine constituents. Additionally, it discusses the analysis of urinary stones, their types, causes, and the procedures for chemical examination.

Uploaded by

alaaessam050605
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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Kidney Function Tests


1- Determination of blood urea
Urea is the main end product of protein (amino acid) metabolism. It is produced in
the liver by urea cycle that converts toxic ammonia into less-toxic urea.

• Urea formation:

1. Liver is the only site for urea formation from ammonia by urea cycle.

2. Then urea is transported in the blood to the kidney to be excreted in


urine (its urinary amount is 20-40g/day)
• Normal Blood urea: is 10 – 50 mg/dl.
• Diagnostic importance of blood urea:
o Measurement of blood urea is one of the kidney function tests.
o In kidney diseases as in renal failure, kidney fails to excrete urea, resulting
in high blood urea level (may reach up to 400 mg/dl).
o In liver diseases, blood urea level decreases, and in turn, ammonia level
increases.
2- Determination of Creatinine in Serum and Urine
Creatine is formed from glycine and parts of arginine and methionine by two
steps (first in the kidney and the second in the liver) and goes to blood to be
extracted by tissues particularly the muscles and nerves. Creatine presents in
muscle (98%), brain (1.3%) and liver. Creatine phosphate is the main store of
high energy in muscles. During muscular contraction, creatine phosphate
regenerates ATP from ADP catalyzed by creatine kinase and during rest ATP
regenerates creatine phosphate catalyzed by ATP-creatine transphosphorylase and
the kinase, also.

On the other hand, 1 - 2% of the total body creatine and creatine phosphate is
spontaneously dephosphorylated, or dehydrated daily into creatinine that

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diffuses to blood and then through the kidney to urine. Creatinine clearance rate
from blood into urine is a kidney function test. Normally, no creatine appears in
urine except in children, pregnancy and after parturition, fevers, thyrotoxicosis,
muscle damage, low carbohydrate diet, diabetes mellitus, wasting diseases and
starvation.

Interpretation:
Normal level:
– Serum creatinine (0.7 – 1.4 mg/dl) related to body size, little higher for men
than for women.
– Daily excretion of creatinine in urine 1-2 g/day
– The main cause of increased level of serum creatinine is renal failure.
– Creatinine is a more specific kidney function test because urea is increased by
other factors as high protein diet, dehydration.
Interfering Factors
1. High levels of ascorbic acid and cephalosporin antibiotics can cause a falsely
increased creatinine level.
2. Drugs that influence kidney function.
3. A diet high in meat can cause increased creatinine levels.

Clinical Implications
1. Increased blood creatinine levels occur in the following conditions:
a. Impaired renal function
b. Chronic nephritis
c. Obstruction of urinary tract
d. Shock
e. Dehydration
f. Rhabdomyolysis (skeletal muscle tissue breakdown)
2. Decreased creatinine levels occur in the following conditions:
a- Small stature
b- Decreased muscle mass

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Report (1)
Name of the patient: Sex: Date:
Diagnosis:
Parameter Values Normal Comment
values
serum urea 360 mg/dl
serum creatinine 8 mg/dl
Creatinine clearance 40 ml/min

Urine report
Urinalysis
1. Physical properties:
a) Colour:
• Normal urine: is amber yellow in colour.
• Abnormal urine:
– It is pale yellow in cases of excess fluid intake and in cold weather since
the amount of urine is inversely proportional to the amount of sweat.
– The colour is orange or deep yellow in hot weather, fevers and severe
muscular exercise.
– The colour is tea-like in case of infective hepatitis.
– It is coca cola or liquorice colored in glomerulonephritis.
– It is reddish in case of bilharziasis and carcinoma of the urinary-bladder.
– It is colourless but blackens on exposure to light in cases of alkaptonuria.
– It accepts the colour of certain drugs.
b) Odour:
• Normal urine: has an aromatic odour.
• Abnormal urine:

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– The odour changes according to the type of food.
– The odour is rotten apple like or acetone in diabetic ketoacidosis.
– It is fishy in case of carcinoma of the urinary bladder.
– It is offensive in case of urinary tract infections.

c) Aspect:
• Normal urine: has a clear aspect.
• Abnormal urine: It is turbid in crystalluria – albuminuria and urinary tract
infections.

d) Reaction:
• Normal urine: is acidic in reaction.
• Abnormal urine:
– The pH is alkaline in urinary tract infections.
– The pH varies according to the type of diet, in high protein diets it is
acidic and in cases of increased intake of citrous fruits it is alkaline.

e) Specific Gravity:
• It reflects amount of total solids in urine.
• It is measured by the urinometer.
• Normally specific gravity is 1015 – 1025.
• Abnormal specific gravity occurs in the following cases:
– It is decreased in excess fluid intake – diabetes insipidus.
– It is increased in high protein diet – diabetes mellitus – crystalluria (due to
increased total solids in urine).
– In chronic renal failure the specific gravity is fixed at 1010.

f) Volume of urine:
Normally the 24 hr urine volume varies from 600 ml to 1600 ml.
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Abnormally: (Polyuria , Oliguria and Anuria)
a- Polyuria (more than 2000 ml/day). It is caused by:
Physiological polyuria as in high fluid intake (water, tea) and high protein diet
(urea causes osmotic diuresis).
Pathological polyuria as in:
- diabetes mellitus (glucose causes osmotic diuresis) and in
- diabetes insipidus (due to lack of ADH) and
- Hypertension: (due to increased glomerular filtration).
b- Oliguria (less than 500 ml/day)
– Physiological oliguria: as in low fluid intake
– Pathological oliguria causes: inflammatory kidney diseases, (acute
nephritis),heart failure, severe oedema, fevers, vomiting, diarrhoea &
obstruction in urine passages.
c- Anuria (less than 125 ml/day): acute tubular necrosis, blood transfusion
reaction, surgical shock, bilateral renal stone and in complete obstruction of
urinary passages – acute renal failure.
7. Sediments or deposits:
Normally, urine contains no visible deposits
Abnormally: Upon centrifugation one or more of the following deposits may
appear which are examined using microscopic examination:
➢ Excess Pus cells which are dead leucocytes (pyuria): It indicates UTI
➢ Excess Red blood cells (hematuria): often occurs with stones, tumors,
infections including TB or acute glomerulonephritis.
➢ Epithelial cells: normal in females.
➢ Parasites and ova: e.g. bilharzial ova.
➢ Crystals as urate, oxalate, phosphate crystals

N.B. Fewer than three RBCs and five WBC/hpf are normally seen.

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2. Chemical properties:

A. Normal constituents of urine:


1. Urea: The main end product of protein metabolism. Normally, it ranges 20 -
40 gm/day. It is formed in the liver and excreted by the kidney.
2. Uric acid: end product of catabolism of purines in man.
3. Ammonia: Ammonia in urine is derived from deamination of amino acids in the
kidney or by glutaminase reaction also in the kidney.
4. Creatinine: Creatinine (anhydrous creatine) is the end product of creatine
metabolism.
5. Creatine: It occurs in very small amounts in the urine of adults.
6. Amino acids.

7. Organic acids including glucuronic acid, Citric acid, lactic acid and oxalic acid
8. Urine Chlorides: Its source is diet.
9. Sulphates in urine: Its presence in urine is principally due to the oxidation of
sulphur present in the sulphur amino acids (cystine, cysteine and
methionine).

10. Phosphates in urine: Derived from the oxidation of phosphoproteins of


diet (as casein of milk and vetillin of egg yolk), phospholipids and
nucleoproteins. Urine pH generally depends on the ratio between acidic and
basic phosphates.
B. Abnormal or Pathological Constituents of Urine:
1. Albumin - proteins:
Detected by Boiling test or heat coagulation test:
Usually both albumin and globulin are present but albumin is generally in excess,
due to its low molecular weight.
Causes of Porteinuria:
a) Normal urine contains very little amount of proteins (less than 30 mg/liter).
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b) Microalbminuria is the excretion of proteins (30-200 mg/liter). It indicates early
affection of kidney as in diabetes mellitus. It can not be detected by ordinary
methods and needs special techniques for its detection.
c) Proteinuria: It is an increase of protein loss in urine (more than 200 mg/liter). It
is a characteristic of all acute and chronic kidney diseases. Proteinuria
(albuminuria) may be classified into:

– Pre-renal proteinuria: as in heart failure due to renal venous congestion.

– Renal proteinuria: due to kidney affection (glomerular as in


glomerulonephritis, or tubular as in pyelonephritis).

– Post-renal proteinuria: due to lower urinary tract affection as inflammation


or tumour of urinary bladder.

2. Glucose and other reducing sugars:


Detected by Fehling’s test & Benedict’s test.
Glycosuria (the appearance of a reducing sugar in urine) may be due to:

1. Glucose: Normally less than 0.1g glucose is excreted per day. Glucosuria is
caused mainly by diabetes mellitus.
2. Fructose: (Fructosuria), galactose (galactosuria) and pentose (pentosuria).
3. Lactose: (Lactosuria): presence of lactose in urine. It may occur in infants
and in mothers during pregnancy, lactation and the weaning period.

3. Bile
Constituents of the bile are found in urine when the bile duct is obstructed
(obstructive jaundice), or when the liver cells are diseased (Hepatic jaundice).
Urine containing bile often has a characteristic dark yellowish green (or brown) in
colour and when it is shaken froth rapidly.

4- Blood and Blood Pigments (hematuria)


It is caused by urinary bilharziasis, glomerulonephritis, traumatic or malignant
diseases.
5. Acetone or ketone bodies (Ketonuria)
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The ketone bodies found in urine in the condition known as ketosis are:
acetone, aceto-acetic acid and B-hydroxybutyric acid. This is caused by conditions
characterized by excessive lipolysis such as prolonged starvation, ketogenic diet
and uncontrolled diabetes mellitus.

6. Indican:
It arises from the bacterial decomposition of tryptophan in the intestine and
its excretion is a measure of the amount of putrefaction occurring, generally in the
intestine but sometimes in a large abscess.

Urine Report
Name of the patient: Sex: Date:
Diagnosis:
Reaction Acidic Sp. gravity at 15 1030
°C
Albumin + Bie pigments Nil
Sugar Nil Bile salts Nil
Acetone Nil Urobilinogen Normal
Microscopic Examination:
RBCs 40-60 / H.P.F Pus cells 15-30 / H.P.F
Ep. cells Few Crystals -
Casts - Ova -
Casts: Hyaline cast (++), red cell casts (+++), epithelial casts (+),
granular casts (+)
Nitrite -
Comment:
………………………………………………………………………………………
………………………………………………………………………………………
………………………………………………………………………………………
………………………………………………………………………………………
…………………………………

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Analysis of urinary stones
Introduction:
Renal calculi occur in about 2-3% of the population with the majority (80-
90%) of the stones containing calcium.
The formation of stone ultimately depends on the formation of
crystalluria which may results from:
1. Metabolic disease, e.g. hypercalciuria, hyperuricaemia.
2. Low urine volume.
3. Variation in urine pH, e.g. calcium precipitates in an alkaline urine,
whereas uric acid and cystine precipitates in an acidic urine.
4. Urinary stasis, e.g. obstruction, malformations.
5. Lack of inhibitors (recent evidence suggests that normal urine
contains a number of inhibitors which preclude stone formation e.g.
mucopolysaccharides, citrate and pyrophosphate).

Types of renal calculi :


1. Calcium stones: Due to hypercalcaemia, hypercalciuria, drugs e.g.
acetazolamide (carbonic anhydrase inhibitor), urinary tract infection or
idiopathic.
2. Magnesium ammonium phosphate stones: Due to urinary tract infections.
3. Uric acid stones: Due to hyperuricosuira (primary or secondary), low urine
output or idiopathic.
4. Oxalate stones: Due to acquired hyperoxaluria e.g. ileal disease or iliostomy,
primary hyperoxaluria (inborn error of glycine metabolism) or idiopathic.
5. Cystine stones: Due to cystinuria.
6. Xarnthine stones: Due to xanthinuria.

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The analysis of renal calculi may be of diagnostic and therapeutic value.
Quantitative tests only yield little information, for this reason qualitative tests will
be sufficient.
Gross characteristics rarely give much information about the probable
chemical composition, except in the case large bladder calculi or “staghorn” calculi
from the renal pelvis which are usually predominately phosphate with some
organic debris. Uric acid stones are usually small, but small stones can be of any
composition. Cystine stones are variable in size, color and consistency.
Procedure for chemical examination of urinary stone:
First wash the stone and dry it. Grind it in a mortar to a fine powder. Proceed
as follows:
Urates or uric acid:
Place powder in a small evaporating dish. Add several drops of conc. HNO 3.
Heat gently and evaporate to dryness. Add 2-3 drops of conc. NH4OH. Deep
yellow, orange-red color develops which turn to purple with more NH4OH.
Carbonate:
Place on a dish. Add 8-10 drops of 10% HCI. Foaming effervescence is
positive.
Oxalate:
Place powder in a test tube. Add equal amount of resorcinol. Add 3 drops of
conc. H2SO4. Dark blue-green color is positive.
Cystine:
Place powder on a dish. Add 1 drop NH 4OH wait for 3 minutes then add 2-3
drops of sodium nitroprusside. Upon standing a red color is formed.

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