This document provides information about urine analysis (urinalysis). It discusses the purpose of urine analysis in diagnosing kidney, urinary tract, and other systemic diseases. It covers proper urine collection and storage. The key components of a urinalysis that are examined are described in detail, including physical characteristics, chemical constituents, and microscopic examination of urine sediment. Urine culture is also discussed as a way to confirm bacterial infection and determine appropriate treatment. The document provides guidance on interpreting urinalysis results and what they may indicate about a patient's health conditions.

1. Urine R/E &C/S
Urea&Creat
Dr.farman ullah ktk
PGR 4
Urology LRH.

2. Urine R/E
 Urine R/E also known as urine analysis or urinalysis
 One of the fundamental test in kidneys or urinary tract
diseases
 Diagnosis of other systemic disease that affect kidney
functions
 Monitoring of patients with diabetes
 Screening for drug abuse (eg Sulfonamide or
aminoglycosides)

3. Urine collection
 Containers for collection of urine should be wide mouthed,
clean and dry.
 Analysed within 1 hours of collection else requires
refrigeration at 5 degree centigrade.

4. Urinalysis ;What to look for?
Urinalysis consists of the following measurements:
 Macroscopic or physical examination
 Chemical examination
 Microscopic examination of the sediment
 Urine culture

5. Physical examination of urine
Examination of physical characteristics:
 Volume
 Color
 Turbidity
 Odor
 pH and
 Specific gravity
 Osmolality
 The refractometeror a reagent strip is used to measure specific gravity

6. volume
Normal1-1.5 or 2 L/day
 Oliguria
Urine Output < 400ml/day
Seen in Dehydration,Shock
Acute glomerulonephritis
Renal Failure
 Polyuria Urine Output > 2.5 L/day, Seen in
Increased water ingestion
Diabetes mellitus and insipidus
 Anuria
Urine output < 100ml/day Seen in renal shut down

7. Color of urine
Normal pale yellow=due to pigments urochrome, Urobilin and
uroerythrin
 Cloudiness may be caused by excessive cellular material or
protein, crystallization or precipitation of non pathological
salts upon standing at room temperature or in the
refrigerator
 Colour of urine depending upon it’s constituents.

8.  Colorless
Very diluted urine
over hydration
 Cloudy
Phosphaturia
Pyuria
chyluria
 Red
Hematuria
Myo/hemoglobinuria
Anthocynin in beets and blackberries
rifampin
 Orange
Dehydration
sulfasalazine
• Yellow
Normal
Riboflavin
• Green blue
Biliverdin
Methyelene blue
phenols
• Brown
Uroblinogen
Prophyria
Fava beens
metronidazole
• Brown black
Sorbitol
Methyl dopa

9. Turbidity
 Freshly voided urine is clear
 Cloudy urine may be due to
phosphaturia,
pyuria,
Chyluria
Lipiduria
Hyperoxaluria

10. odor
 Normal aromatic due to the volatile fatty acids On long standing
 Ammonical decomposition of urea forming ammonia which gives a
strong ammonical smell)
 Foul, offensive pus or inflammation
 Sweet Diabetes
 Fruity Ketonuria
 Maple Syrup like Maple Syrup Urine Disease
 Rancid Tyrosinaemia
 Characteristic "rotten egg“ odor Cystinuria

11. Urinary PH
Reflects ability of kidney to maintain normal hydrogen ion concentration in
plasma & ECF
 Urine pH ranges from 4.5 to 8
 Normally it is slightly acidic lying between 5- 6.5.
 Tested by
litmus paper
pH paper
Dipsticks
Acidic Urine
 Respiratory&metabolic acidosis urine is acidic
 Respiratory and metabolic alkalosis urine is alkaline
 Exception RTA type I&II serum acidic and urine alkaline.
 Type II severe metabolic acidosis urine is acdic
 Unable to acidify the urine with acidic load diagnostic of RTA

12.  PH Help in Dx nd Rx
 In UTI alkaline urine with PH >7.5 suggest infection with urea splitting
organisms(proteus)
 Urease producing organism convert NH3 into NH4 ion increasing PH
causing precipitatios of Ca+MAP crystals
 PH is acidic in uric acid and cystine stones
 Alkalinization of urine is important feature of therapy in both cases(uric
acid&cystine lithiasis).

13.  It is measure the ratio of urine density compared with water
density, which reflects the ability of the kidney to
concentrate or dilute the urine relative to the plasma from
which it is filtered.
 Measured By urinometer refractometer
 dipsticks

14. Specific Gravity
 Normal 1.001-1.035.
 Increase in Specific Gravity
 Low fluid intake,
 Dehydration due to fever,sweating,vomitting and diarrhea
 Diabetes mellitus(glucosuria),
 SIADH.
 I.v contrast
 Decrease in Specific Gravity
 Increased fluid intake
 Decreasd renal concentrating ability
 Diabetes insipidus
 Absence of ADH,
 Renal Tubular damage.
 Fixed specific gravity (isosthenuria)=1.010Specific gravity

15. Osmolality
 Amount of material dissolved in the urine.
 50-1200 mOsm/L
 Urine osmolality is the better indicator of Renal function but
it can not be measured with dipstick.

16. Chemical analysis of urine
 The chemical analysis of urine us undertaken to evaluate the
levels of the following components
 Blood
 Protein
 Glucose
 Ketones
 Bilirubin
 Urobilinogen
 Wbc’s

17. Hematuria
 When the test strip is dipped in urine the reagents are
activated and a chemical reaction occurs.
 Normal urine having fewer than 3RBCs/HPF
 +ve Dipstick for blood indicates either hematuria,
hemoglobinuria, myoglobinuria.

18. Proteins in urine
 Detected by heat coagulation or dipstickMethod
 Urine proteins come from plasma protein and
TommHorsfall(TH) glycoprotein
 Healthy individuals excrete 80-150 mg/d of total protein and
<30 mg/d of albumin.
 Normal urine protein is 30% albumin 30% globulin 40% tissue
protein
 Plasma cell dyscrasias(multiple myeloma) can be associated
with large amounts of excreted light chains in the urine, which
may not be detected by dipstick. The light chains produced
from these disorders are filtered by the glomerulus.

19.  Cause of proteinuria
 Glomerular: most common type due to inc permeability of G.M to protein
especially albumin e.g in IgA nephropathy and DM
 Tubular: failure to reabsorb normally filtered proteins of LMW such as
Immunoglubulins e.g in fanconi syndrome
 Overflow proteinuria: absence of underlying disease, due to increase
plasma concentration of abnormal immunoglobulins e.g in Multiple
myeloma

20. Glucose&Ketones
 Urine testing for Glucose&Ketones is useful in screening DM.
 Normally glomerular filteration of Glucose=to tubular reabsorption
 Renal threeshold corresponds to serum glucose of about 180mg/dl:
above this level glucose will be detected in urine.
 Ketones not found in urine normally, will appear when body COH
supplies are depleted & body fats breakdown occur.
 Occuring in Diabetic Ketoacidosis, pregnancy, after periods of
starvations/rapid weight reduction.
 Acetoacetic acid, b-hydroxy butyric acid,acetone

21. Bilirubin&uroblinogen
 Bilirubin doesn’t appear in urine
 Uroblinogen in traces amount passes in urine in pathologic
condition of hemolysis and hepatocellular diseases.
 Obstruction of bile ducts or antiboitics that alter intestinal
flora will decrease conversion to uroblinogen and their
urinary excretion.

22. Leukocyte esterase& nitrite tests
 Less important in urologic practice
 LN dipstick
 L.E produced by neutrophils
 Should be done 5 mints after dipstick is immersed in urine
 L.E test may be –ve in presence of infection because not all
pt with bacteriuria may have significant pyuria
 It should be done in conjunction with nitrite test for
bacteriuria

23. False –ve results
1. Inc specific gravity
2. Glycosuria
3. Presence of uroblinogen
4. Medication that alter urine color
5. Ingestion of large amount of ascorbic acid
False +ve results
1. specimen contamination

24.  Nitrite test: many species of gram –ve bacteria convert
nitrate into nitrite
 Higher specifity low sensitivity
 Less accurate in urine specimen having
< 5 organism/ml
 It detects 95% of infected urine specimen and decreases the
need for microscopy by as much as 30%

25. Types of cast seen :
 Acellular cast
Hyaline casts, Granular casts, Waxy casts, Fatty casts, Pigment casts, Crystal casts.
 Cellular cast
Red cell casts, White cell casts, Epithelial cell cast
 The most common type of cast hyaline casts are solidified
TammHorsfallmucoprotein secreted from the tubular epithelial cells
 Red blood cells may stick together and form red blood cell casts. Such
casts are indicative of glomerulonephritis, with leakage of RBC's from
glomeruli, or severe tubular damage
 White blood cell casts are most typical for acute pyelonephritis, but they
may also be present with glomerulonephritis.

26. Microscopic examination of urine
 First morning urine specimen is the specimen of choice and should be
examined within 1 hr.
 A sample of urine (usually 10 -15 ml) is centrifuged in a test tube at
relatively low speed (about 3,000rpm) for 5 minutes which produces a
concentration of sediment (cellular matter) at the bottom of the tube.
 A drop of sediment is poured onto a glass slide, a thin slice of glass (a
coverslip) is place over it and observed under microscope

27. Microscopy
 Microscopic analysis with both low power(100 magnification), high
power(400 magnif)
 Low power: erythrocytes, leukocytes, casts, cystine craystals, oval fat
macrophages & parasites like trichomonas vaginalis & schistosoma
hematobium
 High power: circular from dysmorphic erythrocuytes, types of crystals,
bacteria & yeasts
1.Cells 2.Casts 3.Crystals 4.Bacteria 5.Yeasts 6.parasites

28. Cells
 Erythrocytes identified under low power diagnosed (morphology)under high
power
 Circular(non glomerular) from dysmorphic(glomerular)
 Circular: even distribution of Hb with either a round or crenated contour
 Dysmorphic: irregulary shaped with minimal Hb and irrigular distribution of
cytoplasm

29.  Leukocytes: normal 1-2/HPF in men & upto 5/HPF in women in whom urine
sample may be contaminated e vaginal secretions.
 Greater number indicates infection or inflammation in the Urinary tract
 Old leukocytes: small and wrinkled appearance(vaginal secretions of
normal women)
 Fresh leukocytes: larger and rounder and when the sp.gravity is <1.019 the
granules in cytoplasm demonstrates glitterlike movements so called glitter
cells.

30.  Squamous epi cells: large, central small nucleus about the size of
erthrocytes & irregular cytoplasm with granularity.
frequently detected in female urine derived from lower portion
of urethra, trigone of post pubertal female and vagina
 Transtional epi cells: smaller than squamous cells having large nucleus
& demonstrate promenint cytoplasmic granules near the nucleus
reminder of urinary tract
 Malignant transitional epi cells: altered nuclear size & morphology, can
be identified with either routine papanicolaou staining or automated
flow cytometry

31.  Renal tubular cells: least commonly observed but most significant
because their presence always indicates renal pathology.
 Difficult to distinguish from leukocytes but the are slightly larger

32. Casts
 Is a protein coagulum that is form in the renal tubules and traps any
tubular luminal content within the matrix.
 Tamm-horsfall mucoprotein is the matrix of all renal casts.
 Casts have only mucoprotein they are called hyaline casts,(after exercise or
heat exposure, pyelonephrits or CKD)
 Rbc’s cast: entrapped erythrocytes(glomerular bleeding)
 Wbc’s cast: acute GN, acute PN, acute TIN
 Fatty cast: nephrotic synd, lipiduria, hypothyriodism

33. Crystals
 Cystine crystals=cystinuria
 Acidic urine=Ca oxalate, uric acid, cystine
 Alkaline urine=Ca phosphate, triple(struvite)crystals
 Cholestrole crystals: lipiduria

34. Bacteria
 Each HPF views b/w 1/20,000 – 1/50,000ml
 Each bacterium seen /HPF = bacteria >30,000/ml
 5bacteria/HPF = 100,000/ml
Yeast
• Most common candida albicans
• Biconcave oval shape confused with erythrocytes
and Ca-oxalate crystals but yeast can be
distinguished by charcteristic budding and hyphea
• Diabetes and vaginal candidiasis

35. Parasites
 Trichomonas vaginalis: is a frequent cause of vaginitis in
women and occasionally of urethritis in men
Large cells e rapidly moving flagella that quickly propel
the organism across the microscopic field
 Schistosoma hematobium: extremly common in middle east
and north africa
Charateristic parasitic ova with a terminal spike

36. Expressed prostatic secretions
 Should be examined in pt having prostatis
 Normal prostatic fluid have few if any leukocytes
 Presence of large number or clumps of leukocytes is
indicative of prostatis
 Oval fat macrophages are found in postinfection prostativ
fluid.

37. Urine culture
 Presumptive dx of bacterial infection made by microscopic examination of
urinary sediments be confirmed by urine c/s
 C/s can be used
To estimate the numbers of bacteria
To identify the exact organism present
To predict which drug will be effective to treat the infection
 C/s are particulary important in
 Recurrent infections
 Seriously ill pts
 Persistent infections
 Hospitalised pt with UTI
 Renal insufficency
 Drug allergies

38.  C/s influneced by
 Method used to collect the urine
 Patient hydration status
 Whether patient is taking antimicrobial agent

39. Method
 Plastic culture plate with blood agar on one side and
deoxycholate agar on other side
 A known amount of urine inoculated on agar on each side &
colony counts are determined at 24-48hrs
 Number of bacteria in 1ml of urine is determined by
multiplying the no. of colonies by volume and dilution of the
inoculum if any.

40.  If antiboitic sensitivity is required
 Additional culture plate inoculated and small antibiotic
impregnated disks placed on the agar.
 Zones of growth inhibition seen around the disks at 12-24 hrs
indicate sensitivity

41. Culture for Tuberculosis
 A microscopic examination that show acid fast bacilli can
give a presumptive Dx of T.B
 The rapidity of recovering mycobectrium depend upon pts
bacillary load.
 If smear is highly +ve, culture would become +ve in 1-2
weeks

42. Blood examination
 Done to measure substance in blood that are normally
excreted by kidney.
 Their level in blood increases in kidney dysfunction.
 As markers of renal function creatinine, urea,uric acid and
electrolytes are done for routine analysis

43. Serum creatinine
 Creatinine: breakdown product of creatine phosphate in
skeletal muscle, and is usually produced at a constant rate by
the body depending on muscle mass Creatinine is filtered but
not reabsorbed in kidney.
 0.8-1.2 mg/dl in adults & 0.4-0.8 mg/dl in children.
 Not increased above normal until 50% of renal function has
been lost(GFR<50 ml/min).
 Methods most widely used for serum creatinine are based on
the Jaffe reaction. This reaction occurs between creatinine and
the picrate ion formed in alkaline medium (sodium picrate); a
red-orange solution develops which is read colorimetrically at
520 nm.

44. • Increased serum creatinine:
– Impaired renal function
– Very high protein diet
– Anabolic steroid users
– Vary large muscle mass: body builders, giants, acromegaly patients
 – Rhabdomyolysis/crush injury
 – Athletes taking oral creatine.
 – Drugs:
• Probenecid• Cimetidine• Triamterene• Trimethoprim• Amiloride

45. Blood Urea
 Urea is major nitrogenous end product of protein and amino
acid catabolism, produced by liver and distributed throughout
intra and extracellular fluid.
 Urea is filtered freely by the glomeruli .
 Many renal diseases with various glomerular, tubular,
interstitial or vascular damage can cause an increase in plasma
urea concentration.
 The reference interval for serum urea of healthy adults is 10-40
mg/dl.
 Plasma concentrations also tend to be slightly higher in males
than females. High protein diet causes significant increases in
plasma urea concentrations and urinary excretion.

46.  Measurement of plasma creatinine provides a more accurate
assessment than urea because there are many non renal factors that
affect urea level.
 Nonrenal factors can affect the urea level (normal adults is level 10-
40mg/dl) like:
Mild dehydration,
high protein diet,
increased protein catabolism,
muscle wasting as in starvation,
reabsorption of blood proteins after a GIT haemorrhage,
treatment with cortisol or its synthetic analogous
 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

47.  Blood urea is normally doubled when the GFR is halved.
 Parallel determination of urea and creatinine is performed to
differentiate between pre-renal and post-renal azotemia.
 Pre-renal azotemia leads to increased urea levels, while creatinine values
remain within the reference range. In post-renal azotemias both urea
and creatinine levels rise, but creatinine in a smaller extent.
 Enzymatic Berthelot Method is used for blood urea estimation:
 Principal:
Urea + H2O Urease > Ammonia + CO2
Ammonia + Phenolic Chromogen + Hypochlorite > Green Colored Complex
whoose absorbance is read at 570nm

48. Serum Uric Acid
 In human, uric acid is the major product of the catabolism of
the purine nucleosides, adenosine and guanosine.
 Purines are derived from catabolism of dietary nucleic acid
and from degradation of endogenous nucleic acids.
 Overproduction of uric acid may result from increased
synthesis of purine precursors.
 In humans, approximately 75% of uric acid excreted is lost in
the urine; most of the reminder is secreted into the GIT

49.  Renal handling of uric acid is complex and involves four
sequential steps:
– Glomerular filtration of virtually all the uric acid in capillary
plasma entering the glomerulus.
– Reabsorption in the proximal convoluted tubule of about 98 to
100% of filtered uric acid.
– Subsequent secretion of uric acid into the lumen of the distal
portion of the proximal tubule.
– Further reabsorption in the distal tubule.
 Hyperuricemia is defined by serum or plasma uric acid
concentrations higher than 7.0 mg/dl (0.42mmol/L) in men
or greater than 6.0 mg/dl (0.36mmol/L) in women

50. Glomerular function tests
 The GFR is the best measure of glomerular function.
 Normal GFR is approximately 125 mL/min
 When GFR decreases to 30% of normal moderate renal
insufficiency. Patients remain asymptomatic with only
biochemical evidence of a decline in GFR
 As the GFR decreases further severe renal insufficiency
characterized by profound clinical manifestations of uremia
and biochemical abnormalities, such as acidemia; volume
overload; and neurologic, cardiac, and respiratory
manifestations
 When GFR is 5% to 10% of normal ESRD

51.  Inulin clearance and creatinine clearance are used to measure
the GFR.
 Creatinine Clearance:
A simple, inexpensive bedside estimate of GFR.
GFR= Ccr = {Ucr * Urinary flow rate(ml/min)} / Pcr
Normal 100-120ml/min
Dec.Renal reserve 60-100ml/min
Mild Renal imp 40-60ml/min
Moderate insuff. 25-40ml/min
Renal failure <25ml/min
ESRD <10ml/min

52.  Cockroft Gault Formula
Creatinine Clearance =(140-age)* weight in kg / S.creat.*72
(multiplied by 0.85 for females)
 MDRD Nomogram
GFR(ml/min)=170*S.creat.-0.999 *age-0.176 * BUN-0.170
*albumin0.318 (multiplied by 0.742 if female)