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Examination of urine
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Urine examination

  1. 1. Dr Malini
  2. 2.  Used most frequently - screening test  Can also be utilized - monitoring response to treatment - to note progression of a disease  Suspected urinary tract infection  Suspected acute glomerulonephritis  Suspected acute interstitial nephritis  Unexplained acute or chronic renal failure  Haematuria (with or without proteinuria) on urine dipstick test  Suspected urinary tract malignancy.
  3. 3. 1. First morning, midstream: Preferred for routine urine examination. 2. Random, midstream: Routine urine examination. 3. First morning, midstream, clean catch: Bacteriological 4. examination. 5. Postprandial: Estimation of glucose, urobilinogen 6. 24-hour: Quantitative estimation of proteins or hormones. 7. Catheterised: Bacteriological examination in infants, bedridden patients, and in obstruction of urinary tract. 8. Plastic bag (e.g. colostomy bag) tied around genitals: Infants; incontinent adults. Midstream clean catch early morning sample is preferred for microscopic examination of sediment - most concentrated - highest concentration of cells - high pH and better preservation of cellular architecture.
  4. 4. 1. Midstream specimen: ◦ After voiding initial half of urine , a part of urine is collected in the bottle. ◦ First half of stream serves to flush out contaminating cells and microbes from urethra and perineum. ◦ Subsequent stream is collected which is from the urinary bladder. 2. Clean-catch specimen: ◦ In men, glans penis is sufficiently exposed and cleaned with soap and water. ◦ In women urethral opening should be exposed, washed with soapy cotton balls, rinsed with water-saturated cotton ◦ holding the labia apart, the initial urine is allowed to pass and the remaining is voided into the bottle (amount 20-100 ml). ◦ This method avoids contamination of urine with the vaginal fluids.
  5. 5. 1. Catheter specimen: ◦ This is used for bacteriological study or culture in bedridden, ill patients or in patients with obstruction of urinary tract. ◦ It is usually avoided in ambulatory patients since it carries the risk of introduction of infection. 2. Infants: ◦ In infants, a clean plastic bag can be attached around the baby’s genitalia and left in place for some time. ◦ For bacteriologic examination, urine is aspirated from bladder by passing a needle just abovesymphysis pubis. Collection for routine urinalysis  For routine examination of urine, a wide-mouthed glass bottle of 20- 30 ml capacity, which is dry, chemically clean, leak proof, and with a tight fitting stopper is used.  About 15 ml of midstream sample is cleanly collected.
  6. 6.  Best - immediate, analysis within 2 hours  There is no good substitute for immediate examination. Preservatives should be avoided in- Reagent strip techniques Chemical tests for protein  If delay ---- refrigeration- upto 8hrs(4-6 C).  Preservatives for 24 hr sample: for several days  Formalin- for sediments ; interferes with sugar.  Thymol - for sediments; interferes with sugar, proteins, acetone.inhibits bacteria and fungi  Toluene –forms thin film, used for measurement of chemicals, interferes with protein  Sod azide- research purpose, prevents bacterial growth  Sod fluoride- preserves glucose in 24 hrs urine, xylose is also preserved.  Hydrochloric acid – 24 hr urine sample for adrenaline, noradrenaline, and steroids
  7. 7. 1. Increase in pH due to production of ammonia from urea by urease- producing bacteria. 2. Formation of crystals due to precipitation of phosphates and calcium 3. Loss of ketone bodies, since they are volatile. 4. Decrease in glucose due to glycolysis and utilization of glucose by cells and bacteria. 5. Oxidation of bilirubin to biliverdin causing false negative test for bilirubin 6. Oxidation of urobilinogen to urobilin causing false negative test for urobilinogen 7. Bacterial proliferation 8. Disintegration of cellular elements, especially in alkaline and hypotonic urine.
  8. 8. 1. Volume 2. Color 3. Appearance 4. Odor 5. Specific gravity 6. pH
  9. 9.  The average 24 hr urinary output in adults is 600-2000 ml.  The volume varies with fluid intake, diet and climate.  Polyuria - urinary volume >2000ml/24 hrs ◦ Diabetes mellitus, diabetes insipidus, chronic renal failure and diuretic therapy.  Oliguria – urinary volume <400ml/24 hrs ◦ Febrile states, acute glomerulonephritis, congestive cardiac failure or dehydration.  Anuria – urinary output <100ml/24 hrs or complete cessation of urine output. ◦ Acute tubular necrosis, acute glomerulonephritis and complete urinary tract obstruction
  10. 10.  Normal color in a fresh state is pale yellow or amber due to urochromes.  Depending on state of hydration, urine may be colorless (over hydration) or dark yellow (dehydration)
  11. 11.  Normal freshly voided urine is clear in appearance.  Foamy urine occurs in presence of excess proteins or bilirubin.
  12. 12.  Freshly voided urine has typical aromatic odor due to volatile organic acids.  Abnormal odors ◦ Fruity – ketoacidosis, starvation ◦ Mousy or musty – phenylketonuria ◦ Fishy – UTI with proteus, tyrosinemia ◦ Ammoniacal – UTI with E coli, old standing urine(formation of ammonia occurs when urea is decomposed by bacteria) ◦ Foul – UTI ◦ Sulfurous – cystinuria
  13. 13.  Normal pH range is 4.6 to 8.0 (average 6.0 or slightly acidic).  Urine pH depends on- diet, acid base balance, water balance, and renal tubular function.  On standing, urine becomes alkaline because of loss of carbon dioxide and production of ammonia from urea.  Therefore, for correct estimation of pH, fresh urine should be examined.
  14. 14. 1. Litmus paper test: A small strip of litmus paper is dipped in urine and any color change is noted. If blue litmus paper turns red, it indicates acid urine. If red paper turns blue, it indicates alkaline urine 2. Reagent strip test: The test area contains polyionic polymer bound to H+; on reaction with cations in urine, H+ is released causing change in color of the pH- sensitive dye.
  15. 15. 1. pH indicator paper: ◦ Reagent area (which is impregnated with bromothymol blue and methyl red) of indicator paper strip is dipped in urine sample and the color change is compared with the color guide provided. ◦ Approximate pH is obtained. 2. pH meter: ◦ An electrode of pH meter is dipped in urine sample and pH is read off directly from the digital display.
  16. 16.  Acidic urine 1. Ketosis-diabetes, starvation, fever 2. Systemic acidosis 3. UTI- E.coli 4. Acidification therapy  Alkaline urine 1. Strict vegetarian 2. Systemic alkalosis 3. UTI- Proteus 4. Alkalization therapy
  17. 17.  Relative mass density.  Depends on amount of solutes in solution.  It is basically a comparison of density of urine against the density of distilled water at a particular temperature.  Specific gravity of distilled water is 1.000.  Normal SG of urine is 1.003 to 1.030 and depends on the state of hydration.  SG of urine is a measure of concentrating ability of kidneys and is determined to get information about this tubular function.
  18. 18. 1. Urinometer  Take 2/3 of urinometer container with urine  Allow the urinometer to float into the urine  Read the graduation at the lowest level of urinary meniscus  Correction of temperature & albumin is a must.  Urinometer is calibrated at 15or 200c  So for every 3oc increase/decrease - add/subtract 0.001  For 1gm/dl of albumin/glucose- substract 0.003/0.004
  19. 19. 2. Refractometer method:  Refractometer measures the refractive index of the total soluble solids.  Higher the concentration of total dissolved solids, higher the refractive index.  Extent of refraction of a beam of light passed through urine is a measure of solute concentration, and thus of SG. 3. Reagent strip method:  Reagent strip measures the concentration of ions in urine, which correlates with SG.  Depending on the ionic strength of urine, a polyelectrolyte will ionize in proportion.  This causes a change in color of pH indicator (bromothymol blue).
  20. 20.  High specific gravity (hyperosthenuria)  Diabetes mellitus (glycosuria)  Nephrotic syndrome (proteinuria)  Fever  Dehydration.  Low specific gravity(hyposthenuria)  Diabetes insipidus (SG consistently between 1.002-1.003)  Chronic renal failure (low and fixed SG at 1.010 due to loss of concentrating ability of tubules)  Compulsive water drinking. Fixed specific gravity (isosthenuria)=1.010 Seen in chronic renal disease when kidney has lost the ability to concentrate or dilute
  21. 21.  Proteins  Glucose  Ketones  Bile pigments (Bilirubin)  Bile salts  Urobilinogen  Blood  Hemoglobin  Hemosiderin  Myoglobin  Chemical examination for significant bacteriuria
  22. 22.  Normal urine contains small amount of protein:Usually upto 150mg/24 hrs  These include proteins from ◦ Plasma ( albumin) ◦ Protein from urinary tract (tamm-horsfall protein, secretory IgA, proteins from tubular epithelial cells, leukocytes and other desquamated cells)  Excretion of more than this level >150mg/24hrs causes proteinuria Proteinuria
  23. 23.  Glomerular proteinuria:  Glomerular diseases damage glomerular basement membrane (increased permeability) but tubular function is normal  Two types ◦ selective proteinuria---chiefly albumin ◦ nonselective proteinuria  Causes : acute glomerulonephritis and nephrotic syndrome
  24. 24.  Selective proteinuria ◦ When glomeruli can retain larger molecular weight proteins but allow passage of comparatively lower molecular weight proteins ( albumin and transferrin) ◦ Occurs in early stages of disease  Non selective proteinuria ◦ With further glomerular damage, this selectivity is lost and larger molecular weight proteins (ƴ globulins) are also excreted along with albumin  Both distinguished by urine protein electrophoresis ◦ In selective proteinuria, albumin and transferrin bands are seen. ◦ In non selective – pattern resembles that of serum
  25. 25.  Tubular proteinuria  Normally, glomerular membrane although impermeable to high molecular weight proteins, allows ready passage to low molecular weight proteins like ◦ β2 microglobulin, retinol binding protein, lysozyme, α1- microglobulin and free immunoglobulin light chains.  These low molecular weight proteins are readily reabsorbed by proximal renal tubules.  In diseases involving mainly tubules, these proteins are excreted in urine while albumin excretion is minimal.
  26. 26.  Disease: ◦ Acute and chronic pyelonephritis, Tb of kidney ,Heavy metal poisoning, Interstitial nephritis, Cystinosis, Fanconi syndrome, Rejection of kidney transplant  Purely tubular proteinuria cant be detected by reagent strip test – detected by heat and acetic acid test and sulphosalicylic acid test
  27. 27.  Overflow proteinuria  When concentration of a low molecular weight protein rises in the plasma, it overflows from plasma into the urine.  Such proteins are ◦ immunoglobulin light chains ◦ bence jones proteins (plasma cell dyscrasias) ◦ hemoglobin (intravascular hemolysis ) ◦ myoglobin (skeletal muscle trauma ) ◦ lysozyme ( AML M4 or M5)
  28. 28.  Hemodynamic proteinuria  Alteration of blood flow through glomeruli causes increased filteration of proteins.  Protein excretion is transient  Seen in ◦ High fever ◦ Hypertension ◦ Heavy exercise ◦ CCF ◦ Seizures ◦ Exposure to cold  Post renal proteinuria  Inflammation or neoplastic conditions in renal pelvis, ureter, bladder, prostate or urethra
  29. 29.  Postural ( orthostatic proteinuria)  When subject is standing or ambulatory, but is absent in recumbant position.  Seen in adolescents  Due to lordotic posture that causes inferior venacaval compression between liver and vertebral column.  Amount <1000mg/day  Periodic testing is done to rule out renal diseases.  1st morning urine after rising is negative, while another sample collected after patient performs activities is positive.
  30. 30.  Test – Heat & acetic acid test  Principle-proteins are denatured & coagulated on heating to give white cloud precipitate.  Method-take 2/3 of test tube with urine, heat only the upper part keeping lower part as control. Presence of phosphates, carbonates, proteins gives a white cloud formation. Add acetic acid 1-2 drops, if the cloud persists it indicates it is protein(acetic acid dissolves the carbonates/phosphates)
  31. 31.  Reagent strip test  Principle- the reagent area of the strip is coated with an bromophenol blue indicator and buffered to an acidic pH which changes color in presence of proteins. Called as protein error of indicators.  When dye gets adsorbed to protein, there is change in ionization – change in color of indicator.  Intensity of color directly proportional to concentration of protein  False negative- alkaline urine, gross hematuria, contamination with vaginal secretions
  32. 32.  Sulphosalicylic acid test –  Principle- addition of sulphosalicylic acid to the urine causes formation of a white precipitate if proteins are present (proteins are denatured by organic acids and precipitate out of the solution).  False positive – gross hematuria, highly concentrated urine, radiographic contrast media, excess uric acid, tolbutamide, sulphonamides, salicylates and penicillin.  False negatives- very dilute urine.
  33. 33.  Indications- 1. Diagnosis of nephrotic syndrome 2. Detection of microalbuminuria or early diabetic nephropathy 3. Follow response to therapy in renal diseases  Proteinuria ◦ >1500mg/day – glomerular diseases ◦ >3500mg/day – nephrotic range proteinuria ◦ <1500mg/day- tubular, hemodynamic and post renal diseases.
  34. 34.  Two methods – 1. Quantitative estimation of proteins in a 24 hour urine sample ◦ Esbach’s albuminometer method ◦ Turbidimetric method ◦ Biuret reaction ◦ Immunologic method 2. Estimation of protein/creatinine ratio in a random urine sample. ◦ Normal protein/creatinine ratio - <0.2 ◦ Low grade proteinuria – 0.2-1.0 ◦ Moderate- 1.0- 3.5 ◦ Nephrotic range proteinuria - >3.5
  35. 35.  Defined as urinary excretion of 30- 300mg/24 hrs of albumin in urine  Significance ◦ Earliest sign of renal damage in diabetes mellitus (diabetic nephropathy). ◦ Independent risk factor for cardiovascular disease in diabetes mellitus.
  36. 36.  Detection of microalbuminuria  Cannot be detected by rutine tests for proteinuria. Methods are 1. Measurement of albumin-creatinine ratio in a random urine sample. 2. Measurement of albumin in an early morning or random urine sample 3. Measurement of albumin in 24 hr sample. 4. Test strips 5. Exact quantitation by radioimmunoassay or enzyme linked immunosorbent assay
  37. 37.  Presence of bence jones protein (with unusual thermosolubility) in the urine, usually indicative of a neoplastic process such as multiple myeloma, amyloidosis or Waldenstrom's macroglobulinaemia.  The classic method of identifying bence-jones protein is precipitation from urine in the range of 4o-60 c. It goes into solution at temprature above or below this range.
  38. 38.  Electrophoresis- The presence of B.J protein & clonal production of Ig is indicated by single sharp peak in the globulin region .  Heat test- If albumin & B.J protein are present,boil the urine to 100 degree & filter ppt - albumin will be filtered out , take the rest urine heat it to 45-60 deg - B.J protein will ppt then dissolve on boiling  False positive– other protein e.g globulin are ppted by heat test.  False negative – when B.J protein is too conc - ppt does not resolve on boiling
  39. 39.  All the glucose filtered by the glomeruli is reabsorbed by the proximal renal tubules and returned to circulation.  Normally, very small amount of glucose is excreted in the urine (<500mg/24 hrs or <15md/dl)- cannot be detected by routine tests.  Presence of detectable amount of glucose in urine is called as glucosuria or glycosuria.  Glycosuria results when filtered glucose load exceeds the capacity of renal tubular reabsorption.
  40. 40.  Causes 1. Glycosuria with hyperglycemia ◦ Endocrine diseases- Diabetes mellitus,acromegaly, cushing’s disease, hyperthyroidism, pancreatic disease ◦ Non-endocrine diseases- CNS, liver disorders ◦ Drugs- adrenocorticotropic hormones, corticosteroids, thiazides ◦ Alimentary glycosuria (lag storage glycosuria) 2. Glycosuria without hyperglycemia ◦ Renal glycosuria- benign condition in which renal threshold is set below 180mg/dl but glucose tolerance is normal. ◦ other conditions where glycosuria occurs with blood glucose <180mg/dl –  Renal tubular diseases like fanconi syndrome and toxic trenal tubular damage
  41. 41.  Test- copper reduction methods 1. Benedict’s qualitative test-  Principle-  Cupric ions (blue)+ sugar cuprous oxide(red color) +cuprous hydroxide ( yellow)  Method- take 5ml of benedict’s reagent in a test tube, add 0.5 ml of urine and mix well. Boil over flame for 2 min. allow to cool. Note change in color  Sensitivity – 200 mg/dl of reducing agent in urine Grades Alkali & heat
  42. 42.  This test is not specific for glucose  Positive with ◦ Other carbohydrates like- lactose, fructose, galactose, pentoses ◦ Metabolites like- glucuronic acid, homogentesic acid, uric acid, creatinine ◦ Drugs like ascorbic acid, salicylates, penicillin, streptomycin, isoniazid, para-aminosalicylic acid, nalidixic acid 2. Clinitest tablet method ◦ Modified form of benedict’s test in which reagents are in form of tablet form
  43. 43.  Other test- Reagent strip method (sensitivity – 100mg/dl)  Principle- glucose oxidase- peroxidase reaction  Glucose + oxygen (from air)  gluconic acid + hydrogen peroxide  More sensitive than benedicts as specific for glucose  False positive- presence of oxidizing agents like bleach or hypochlorite  False negative- large amounts of ketones, salicylates, ascorbic acid, several E. coli infections Glucose oxidase + chromogen in presence of peroxidase Oxidised chromogen (blue) + water
  44. 44.  Excretion of ketone bodies (acetoacetic acid,β hydroxy butyric acid and acetone) in urine is called ketonuria  Causes  If energy requirements cannot be met by metabolism of glucose, then energy is derived from breakdown of fats- formation of ketone bodies ◦ Decreased utilization of carbohydrates  Uncontrolled diabetes mellitus with ketoacidosis  Glycogen storage disorders ◦ Decreased availability of carbohydrates in diet  Starvation, persistent vomiting, weight reduction programs ◦ Increased metabolic needs  Fever in children, severe thyrotoxicosis, pregnancy, PEM
  45. 45.  Tests – 1. Rothera’s test – ( classic nitroprusside reaction)  Principle- acetoacetic acid or acetone reacts with nitroprusside in alkaline solution to form purple colored complex.  Method-  Take 5 ml urine in a test tube and saturate with ammonium sulphate. Add a crystal of sodium nitroprusside and mix well. Slowly run along the side of test tube, liquor ammonia to form a layer. False positive- L-dopa in urine and in phenylketonuria Sensitivity- 1-1.5mg/dl of acetoacetate and 10-25mg/dl of acetone
  46. 46. 2. Acetest tablet test- ◦ Rothera’s test in the form of a tablet. ◦ Acetest tablet consist of sodium nitroprusside, glycine and an alkaline buffer. ◦ A purple lavender discoloration of tablet indicates presence of acetoacetate or acetone (>5mg/dl). ◦ More sensitive than reagent strip test 3. Ferric chloride test (gerhadt’s test) ◦ Addition of 10% ferric chloride solution to urine causes solution to become reddish or purplish if acetoacetic acid is present. 4. Reagent strip test ◦ Modification of nitroprusside test ◦ Sensitive for 5-10 mg/dl of acetoacetate
  47. 47.  The presence of abnormal number of intact red cells in urine is called hematuria.  Causes 1. Diseases of urinary tract – 1. Glomerular diseases 2. Non glomerular diseases 2. Hematological conditions-  Coagulation disorders , sickle cell anemia
  48. 48.  Tests for detection 1. Microscopic examination of urinary sediment 2. Chemical tests- ◦ These tests detect both intracellular and extracellular hemoglobin ( intact and lysed red cells) as well as myoglobin. ◦ Principle – ◦ Heme proteins in hemoglobin act as peroxidase , which reduces hydrogen peroxide to water. ◦ This process needs a hydrogen donor (benzidine, orthotoluidine or guaiac). ◦ Oxidation of hydrogen donor leads to development of color. ◦ Intensity of color development is proportional to amount of hemoglobin present
  49. 49.  Benzidine test – ◦ Make saturated solution of benzidine in glacial acetic acid. Mix 1ml of this solution with 1 ml of hydrogen peroxide in a test tube. Add 2ml of urine. If green or blue color develops within 5 min, the test is positive.  Reagent strip test- uses chromogens- o-toluidine.  False positive- contamination of urine by oxidizing agents or microbial peroxidase in UTI  False negative- presence of a reducing agent like ascorbic acid in high concentration, formalin as preservative
  50. 50. •Ammonium sulfate solubility test is used as a screening test for myoglobinuria •Myoglobin is soluble in 80% saturated solution of ammonium sulfate, while hemoglobin is insoluble and is precipitated. •A positive chemical test for blood done on supernatant indicates myoglobinuria
  51. 51. 1. Nitrite test:  Nitrites are not present in normal urine  Gram-negative bacteria (e.g. E.coli, Salmonella, Proteus, Klebsiella, etc.) - reduce the nitrates to nitrites through the action of bacterial enzyme nitrate reductase.  Nitrites are then detected in urine by reagent strip tests.  Some organisms like Staphylococci or Pseudomonas do not reduce nitrate to nitrite - such infections nitrite test is negative.  Urine must be retained in the bladder for minimum of 4 hours for conversion of nitrate to nitrite to occur; therefore, fresh early morning specimen is preferred.
  52. 52. 2. Leucocyte esterase test:  It detects esterase enzyme released in urine from granules of leucocytes.  Thus the test is positive in pyuria.  If this test is positive, urine culture should be done.  The test is not sensitive to leucocytes < 5/HPF.
  53. 53.  Also called as the “liquid biopsy of the urinary tract”.  Urine consists of various microscopic, insoluble, solid elements in suspension - classified as organized or unorganized.  Organized substances ◦ red blood cells, white blood cells, epithelial cells, casts, bacteria, and parasites.  Unorganized substances ◦ are crystalline and amorphous material.  These elements are suspended in urine and on standing they settle down and sediment at the bottom of the container; therefore - known as urinary deposits or urinary sediments.
  54. 54.  Specimen- ◦ The cellular elements are best preserved in acid, hypertonic saline. ◦ A mid-stream, freshly voided, first morning specimen is preferred. ◦ Examined within 2 hrs as casts and cells degenerate upon standing at room temperature. ◦ 1 crystal of thymol or 1 drop of formalin is added to 10 ml of urine for preservation  Method- ◦ Well mixed sample of urine (12ml) is centrifuged in a centrifuge tube for 5 minutes 1500 rpm and supernatant is poured off. ◦ The tube is tapped at the bottom to resuspend the sediment (0.5ml of urine) ◦ A drop of this is placed on a glass slide and covered with a cover slip and is examined
  55. 55.  Hematuria is the presence of abnormal number of red cells in urine  Presence of >3 cells/hpf is considered abnormal  Microscopy: smooth, non-nucleated, biconcave disks measuring approximately 7 μm in diameter .
  56. 56.  In concentrated (hypersthenuric) urine, the cells shrink due to loss of water and may appear crenated or irregularly shaped cells  In dilute (hyposthenuria) urine, the cells absorb water, swell, and lyse rapidly, releasing their hemoglobin and leaving only the cell membrane called ghost cells.  If the specimen is not fresh when it is examined, the cells appear as faint colorless circles or shadow cells because the hemoglobin may dissolve out.
  57. 57.  Dysmorphic - RBCs that vary in size, have cellular protrusions, or are fragmented  Clinical significance: >80% strongly suggestive of renal glomerular bleeding.  “G1 cell,”-doughnut shape with one or more membrane blebs, is more specific than dysmorphic cells for diagnosing glomerular hematuria Dysmorphic RBCs (400).
  58. 58.  Indicative of the extent of the damage to glomerular membrane or injury to genitourinary tract. (1) RENAL DISEASE (2) LOWER URINARY TRACT DISEASE (3) EXTRARENAL DISEASE (4) TOXIC REACTIONS DUE TO DRUGS (5) PHYSIOLOGIC CAUSES including exercise, When increased numbers of erythrocytes are found in the urine in conjunction with erythrocyte casts, bleeding may be assumed to be renal in origin
  59. 59.  Pyuria refers to the presence of abnormal numbers of leukocytes(principally neutrophils- 10-12 μm in diameter) in urine.  Under high power, these cells appear as granular spheres about 12 μm in diameter with multilobated nuclei  Normal: < 5 WBC/hpf WBCs. multilobed nuclei (400).
  60. 60.  When cellular degeneration has begun, neutrophils become difficult to distinguish from renal tubular epithelial cells. Dilute acetic acid may enhance nuclear detail so that definition may still be possible  Supravital staining emphasize nuclear detail.  With crystal-violet safranin, neutrophilic nuclei- reddish purple and cytoplasmic granules violet.  The peroxidase cytochemical reaction-also useful in distinguishing neutrophils from tubular cells WBCs with acetic acid nuclear enhancement (400).
  61. 61.  GLITTER CELLS: when exposed to hypotonic urine - absorb water and swell. Brownian movement of the granules within these larger cells produces a sparkling appearance. Because of the refractility of the moving granules, neutrophils called as glitter cells.  Stain light blue with Sternheimer-Malbin stain, as opposed to voilet of other neutrophils, will show loss of nuclear segmentation ◦ Clinical significance: Inflammation or Infection of urinary tract GLITTER CELLS
  62. 62.  Found in a variety of other urinary tract diseases including -glomerulonephritis, -systemic lupus erythematosus (SLE), and -interstitial nephritis. -Calculous disease. -Bladder tumors, -acute or chronic localized inflammatory processes. Physiological: transiently increased during fevers and following strenuous exercise
  63. 63.  Finding >1% among the leukocyte population is significant  A cytocentrifuge preparation with Wright’s, Diff-Quik, or Papanicolaou stain is commonly used  Preferred - Hansel(methylene blue and eosin-Y in methanol)  Characterstic of acute interstitial nephritis due to drug reaction Hansel-stained eosinophils (400).
  64. 64. ◦ Lymphocytes, monocytes, plasma cells and histiocytes ◦ When constitute 30% or more of a differential count-> chronic inflammation ◦ Lymphocyturia - Causes: Chronic infection  An early marker of acute cellular rejection of renal allograft  In particular, the sequential determination of urinary CD3 positive pan T cells after the first week following kidney transplantation may contribute to the diagnosis of acute allograft rejection earlier than clinical criteria.
  65. 65.  Represent normal sloughing of old cells, unless present in large numbers or in abnormal forms.  3 types: squamous cells, transitional(urothelial), and renal tubular cells. Sediment-containing squamous, caudate transitional, and RTE cells (400x)
  66. 66.  Most frequent epithelial cells seen in normal urine and the least significant  largest cells found in the urine sediment.  Origin: the linings of the vagina and distal one third of the urethra  Microscopy: large flattened cells abundant, irregular cytoplasm & a small round prominent nucleus about the size of an RBC. The cell edge is often folded; occasionally the cell rolled into a cylinder
  67. 67. • Line the urinary tract from the renal pelvis to the lower third of the urethra  Microscopy: Smaller than squamous cells size ranging from 40–200 μm and appear in several forms, including spherical, polyhedral and caudate. Frequently present in the sediment owing to their high turnover
  68. 68.  Round or pear shaped, with a round centrally located nucleus with occasional binucleate forms .  When stained, have dark blue nuclei with variable amounts of pale blue cytoplasm.  Another helpful clue for identification is a characteristic ‘endo–ecto cytoplasmic' rim.  Presence of large clumps or sheets of transitional cells in the absence of instrumentation (i.e. catheterization) is considered significant
  69. 69.  Vary in size and shape depending on the area of the renal tubules from which they originate.  Most significant types of epithelial cells found in urine because increased number indicates tubular damage  Cells from PCT : are larger then other RTE cells, rectangular shape. Resemble casts hence the presence of nucleus has to be appreciated  Cells from DCT : are round to oval, with eccentric nucleus
  70. 70.  Collecting duct cells: cuboidal, with the eccentrically placed nucleus, appear in groups  Presence of >2 RTE cells/hpf indicates tubular injury  Small numbers of tubular cells may be seen in normal urine, reflecting the normal sloughing of aging cells. They may be present in somewhat larger numbers in the urine of normal newborns
  71. 71.  PCT & DCT renal epithelial cells  acute tubular necrosis and  with certain drug or heavy metal toxicities.  collecting duct epithelial cells • renal transplant rejection, • acute tubular necrosis (diuretic phase) • Other ischemic injuries to the kidney • malignant nephrosclerosis • acute glomerulonephritis accompanied by tubular damage • Salicylate intoxication.
  72. 72.  Three or more renal cells of collecting duct origin constitute a renal epithelial fragment  Clinical significance: indicative of ischemic necrosis and are usually found accompanying varying degrees of renal tubular injury with basement membrane disruption and pathologic casts.  Proper identification is essential, to avoid a false-positive diagnosis of low-grade transitional cell carcinoma.
  73. 73.  RTE cells that have absorbed lipoproteins with cholesterol and triglycerides leaked from nephrotic glomeruli, appear highly refractile.  Appears in the urine as free fatty droplets, or within histiocytes as ingested material
  74. 74.  Positive identification of lipid is required before lipiduria is reported.  When free or incorporated droplets contain large amounts of cholesterol, they exhibit Maltese cross formation under polarized light  When they contain large quantities of triglycerides, fat stains (Oil Red O or Sudan III) are required for positive lipid identification.
  75. 75. Clinical significance:  The presence these lipid forms + marked proteinuria is characteristic of the nephrotic syndrome  Also seen with 1. severe tubular necrosis 2. Diabetes mellitus 3. Trauma cases that cause release of bone marrow fat from the long bones.  Bubble cells: In cases of acute tubular necrosis, RTE cells containing large, nonlipid-filled vacuoles may be seen along with normal renal tubular cells and oval fat bodies.
  76. 76. 1. With Hburia or myoglobinuria, heme pigment absorbed into the cells and converted to hemosiderin. The iron-laden cells are found in the urine sediment. The cytoplasmic granules appear yellow-brown and stain for iron with Prussian blue. 2. Melanin granules -rare cases of melanuria. Pigmented tumor cells are also found in cases of melanoma metastasis to the bladder. 3. Bilirubin pigment colors all of the elements of the sediment, including renal tubular epithelial cells and casts.
  77. 77.  Formed within the lumens of the DCTs and CTs  Composition: Tamm-Horsfall protein, albumin and immunoglobulins,
  78. 78.  Casts may be - 1. Short and stubby, or 2. Long and convoluted- appears when diuresis occurs after urinary stasis.  Typically have parallel sides and blunt ends, but with age they may begin to disintegrate and show thinning and irregularities.  Clinical significance –  Increased numbers of casts usually indicate that kidney disease is widespread, and that many nephrons are involved. ◦ Also be seen in healthy persons after strenuous exercise accompanied by proteinuria. Casts are the only elements in the urinary sediment that are specifically of renal origin.
  79. 79. Casts may be classified according to their matrix, inclusions, pigments, and cells present
  80. 80.  Most frequently seen cast  Consists almost entirely of Tamm-Horsfall protein  The presence of 0-2/lpf is considered normal  Microscopy: colorless in unstained sediments and have a refractive index similar to that of urine;  Sternheimer-Malbin stain produces a pink color in hyaline casts Causes – acute glomerulonephritis, pyelonephritis, chronic renal disease, and transiently with exercise, heat exposure, dehydration, fever, congestive heart failure, and diuretic therapy
  81. 81. Increased visualization can be obtained by phase microscopy •The morphology is varied, consisting of normal parallel sides and rounded ends, cylindroid forms, and wrinkled or convoluted shapes that indicate aging of the cast matrix
  82. 82.  Representative of extreme urine stasis, indicating chronic renal failure.  Differ from hyaline casts in that they are easily visualized because of their high refractive index.  Microscopy: homogeneously smooth in appearance with sharp margins, blunted ends, cracks or convolutions frequently seen along the lateral margins, indicating a measure of brittleness often appear fragmented with jagged ends and have notches in their sides  With supravital stains, waxy casts stain a homogenous, dark pink
  83. 83.  Commonly associated with tubular inflammation and degeneration.  Most frequently in patients with chronic renal failure & during acute and chronic renal allograft rejection.  Because time is required for granules to undergo lysis, waxy casts imply localized nephron obstruction and oliguria.  When waxy casts are unusually broad, they are known as renal failure casts, imply advanced tubular atrophy and/or dilation, in turn reflecting end-stage renal disease and extreme stasis of urine flow.
  84. 84.  Indicates bleeding from an area within the genitourinary tract  Microscopy: easily detected under low power by their orange-red color, fragile, have a more irregular shape as the result of tightly packed cells adhering to the protein matrix  Prerequisite for identification is that red blood cell outlines should be sharply defined in at least part of the cast
  85. 85.  Better visualized with  phase-contrast microscopy  supravital staining- casts are colorless or lavender in a pink matrix.  With prolonged stasis, red cell casts may degenerate and appear in the urine as reddish brown, coarsely granular hemoglobin (blood) casts.  Granular, dirty, brown casts representing hemoglobin degradation products such as methemoglobin may also be present
  86. 86.  Acute glomerulonephritides,  IgA nephropathy,  Lupus nephritis,  Subacute bacterial endocarditis  Renal infarction.  Rarely, tubulointerstitial disease may allow transtubular entry of erythrocytes with subsequent incorporation into a cast. This may occur in severe pyelonephritis.  Additionally, erythrocyte and leukocyte -> renal relapse in patients with SLE
  87. 87.  Signifies infection or inflammation within the nephron  Microscopy: appear granular, and, unless disintegration has occurred, multilobed nuclei will be present
  88. 88. Clinical significance:  Reflect tubulointerstitial disease with neutrophilic exudates and interstitial inflammation.  The most common disease of this category is pyelonephritis- primary marker for distinguishing pyelonephritis (upper UTI) from lower UTIs  Also seen in interstitial nephritis, lupus nephritis, and even the nephrotic syndrome  Also present in nonbacterial inflammations such as acute interstitial nephritis and may accompany RBC casts in glomerulonephritis.
  89. 89.  Presence of advanced tubular destruction, producing urinary stasis along with disruption of the tubular linings.  Clinical significance: 1. Acute tubular necrosis 2. Viral disease (e.g., cytomegalovirus disease) 3. Exposure to a variety of chemicals & drugs. 4. Heavy metal poisoning and ethylene glycol 5. Salicylate intoxication 6. Reliable criteria for detecting acute allograft rejection after the third postoperative day 7. Also accompany WBC casts in cases of pyelonephritis
  90. 90.  Owing to the formation of casts in the DCT, the cells visible on the cast matrix are the smaller, round, and oval cells
  91. 91.  Difficult to distinguish from leukocyte casts- The most reliable distinguishing characteristic of renal tubular cells is their singular round nuclei Bilirubin-stained RTE cells are seen in cases of hepatitis, - hepatorenal failure syndrome
  92. 92.  Include leukocyte/renal, erythrocyte/leukocyte, and eosinophil/renal  Frequently encountered include RBC and WBC casts Clinical significance: Glomerulonephritis- predominant RBC casts Pyelonephritis- predominant casts WBC
  93. 93.  May be of pathologic or non-pathologic significance.  May originate from plasma protein aggregates that pass into the tubules from damaged glomeruli, as well as from cellular remnants of leukocytes, erythrocytes, or damaged renal tubular cells.  Components: ◦ Fine salt precipitates and lysosomes ◦ Protein aggregates - fibrinogen, immune complexes, and globulins.
  94. 94.  Clinical significance: 1. Glomerular and tubular diseases 2. Tubulointerstitial disease and 3. Renal allograft rejection. 4. Pyelonephritis 5. viral infections 6. Chronic lead poisoning 7. Renal papillary necrosis- with hematuria 8. Hyperparathyroidism- fine granules represent calcium phosphate precipitants 9. Periods of extreme stress or strenuous exercise
  95. 95.  Seen in conjunction with oval fat bodies and free fat droplets in disorders causing lipiduria  Microscopy: highly refractile under bright-field microscopy.  Clinical significance: commonly seen when heavy proteinuria is present and are a feature of nephrotic syndrome
  96. 96.  Casts containing urates, calcium oxalate, and sulfonamides (sulfamethoxazole) occasionally seen.  A matrix is visible in a true crystal cast, and the crystals may polarize. These casts indicate deposition of crystals in the tubule or collecting duct.  Hematuria, possibly related to tubular damage, regularly accompanies crystal casts.  These casts should be carefully distinguished from clumps of crystals forming at room or refrigerator temperatures.
  97. 97.  Hemoglobin (Blood) Casts: typically appear yellow to red, although sometimes the color is pale . Clinical significance: ◦Most often seen with erythrocyte casts and glomerular disease. ◦Less commonly, with tubular bleeding and rarely with hemoglobinuria.
  98. 98.  Hemosiderin Casts. Hemosiderin granules in casts derived from pigment laden renal tubular cells.  Myoglobin Casts: red-brown in color & occur with myoglobinuria following acute muscle damage.
  99. 99.  Often referred to as renal failure casts  Diameter 2-6 times that of normal casts.  Clinical significance: -indicates destruction (widening) of the tubular walls -indicate tubular dilation and/or stasis in the distal collecting duct.  Most commonly broad casts- granular and waxy & have poor prognosis
  100. 100.  Bile-stained broad, waxy casts are seen as the result of the tubular necrosis caused by -viral hepatitis
  101. 101.  Containing bacilli both within and bound to the protein matrix - seen in pyelonephritis  Confirmation is best made by performing a gram stain on the dried or cytocentrifuged sediment.  “gold standard” -quantifying bacterial counts is culture  Clinical significance: 1. nephrotic syndrome 2. toxic tubular necrosis 3. diabetes mellitus, and 4. crush injuries.
  102. 102.  Appear as true geometrically formed structures or as amorphous material  Clinical significance: represent disorders as 1. Liver disease 2. Inborn errors of metabolism 3. Renal damage caused by crystallization of iatrogenic compounds within the tubules.
  103. 103.  Formed by the precipitation of urine solutes, including inorganic salts, organic compounds, and medications (iatrogenic compounds) when alterations in multiple factors affect their solubilities.  Factors affecting: 1. Changes in temperature 2. Solute concentration, Increased solute concentration is typically responsible for crystal formation 3. pH-determines the type of chemicals precipitated which affect solubility.
  104. 104.  First consideration is the urine pH.  All abnormal crystals are found in acidic urine.  The geometric shape of a crystal determines its birefringence and, therefore, its ability to polarize light
  105. 105. 1. Amorphous Urates (Calcium, Magnesium, Sodium, and Potassium Urates). 2. Crystalline Urates (Sodium, Potassium, and Ammonium) 3. Crystalline Uric Acid 4. Calcium Oxalates.
  106. 106.  Precipitate upon standing in concentrated urine of a slightly acid pH >5.5  Microscopy : yellow brown granules. may occur in clumps, and adhere to fibers and mucous threads  When large quantities are present, the urine sediment may appear pink-orange to reddish brown on macroscopic examination this appearance has been referred to as brick dust due to the accumulation of the pigment, uroerythrin, on the surface of granules
  107. 107.  Seen in conjunction with amorphous urates  Acid urates appear as larger granules and may have spicules similar to the ammonium biurate crystals seen in alkaline urine  Sodium urate crystals are needle-shaped and are seen in synovial fluid during episodes of gout, but do appear in the urine.
  108. 108.  Occur at low pH (5–5.5)  Microscopy : seen in a variety of shapes, including rhombic or four- sided flat plates, prisms, oval forms with pointed ends (lemon- shaped), wedges, rosettes, and irregular plates.  Appear yellow-brown, may be colorless and hexagonal, resembling cystine
  109. 109.  Highly birefringent under polarized light, which aids in distinguishing them from cystine crystals  Clinical significance: 1. Associated with increased levels of purines and nucleic acids in patients with leukemia who are receiving chemotherapy 2. In patients with Lesch-Nyhan syndrome & 3. (sometimes) in patients with gout.
  110. 110.  The most common form is the dihydrate recognized as a colorless, octahedral envelope or as two pyramids joined at their bases.  Dihydrates may appear at pH 6 or in neutral urine  Less frequently seen is the monohydrate form, oval or dumbbell shaped.
  111. 111.  They are soluble in dilute hydrochloric acid.  Ingestion of certain foods like tomatoes, spinach, cabbage, asparagus, and rhubarb causes increase in their numbers  Clinical significance: 1. The finding of clumps in fresh urine may be related to the formation of renal calculi 2. Large numbers may reflect severe chronic renal disease or ethylene glycol or methoxyflurane toxicity. 3. Their increased number in fresh urine (oxaluria) may also suggest oxalate stones.
  112. 112. 1. Amorphous phosphate 2. Triple phosphate and 3. Calcium Carbonate 4. Ammonium Biurate.  Phosphates represent the majority of the crystals seen in alkaline urine cause white precipitate that does not dissolve on warming.
  113. 113.  Microscopy: granular in appearance, similar to amorphous urates unlike the former, they tend to be colorless and will produce a fine or lacy white precipitate macroscopically
  114. 114.  Triple phosphate (ammonium magnesium phosphate)  Microscopy: they are colorless, three to six-sided prisms with oblique ends referred to as coffin lids  Have little if any clinical significance.  They are often seen in infected urine of alkaline pH
  115. 115.  Uncommon crystals are small and colorless, with dumbbell or spherical shapes form pairs, fours, or clumps.  Distinguished from other crystals/amorphous material by their production of carbon dioxide in the presence of acetic acid.  They are also birefringent, which differentiates them from bacteria
  116. 116.  Exhibit the characteristic yellow-brown color  Soluble in acetic acid at 60 degree C.  Microscopy: described as “thorny apples” because of their appearance as spicule-covered spheres
  117. 117.  Found in acidic urine or rarely in neutral urine. 1. Cystine Crystals 2. Tyrosine 3. Leucine 4. Sulfonamide(sulfadiazine) Crystals 5. Ampicillin Crystals 6. Radiographic Dye Crystals 7. Cholesterol Crystals 8. Crystals Associated With Liver Disorders
  118. 118.  Found in the urine of persons who inherit a metabolic disorder that prevents reabsorption of cysteine by the renal tubules (cystinuria).  Microscopy: Cysteine crystals appear as colorless, refractile, hexagonal plates and may be thick or thin  Clinical significance: 1. Among the most important crystals identified in urine sediment. 2. Occur in patients with cystinuria and may be associated with cysteine calculi.
  119. 119.  In acidic urine, tyrosine forms fine silky needles that may be arranged in sheaves or clumps, especially after refrigeration.  These may be colorless or yellow, appearing black as the microscope is focused .  They are soluble in alkali (ammonia and potassium hydroxide) and dil HCL; they are not soluble in alcohol or ether.  Clinical significance: 1. Tyrosinemia 2. Occasionally seen in the urine of patients with severe liver disease
  120. 120.  Microscopy: yellow-brown oily-appearing spheres that demonstrate concentric circles and radial striations  Usually accompanied by tyrosine crystals in severe liver diseases.  Leucine may be precipitated with tyrosine crystals if alcohol is added to the urine
  121. 121.  Microscopy: seen as yellow-brown sheaves of wheat with central bindings, striated sheaves with eccentric bindings, rosettes, arrowheads, petals, needles, and round forms with radial striations.  Clinical significance: seen in the urine of patients on sulfonamide therapy who were inadequately hydrated. This could result in renal tubular damage if crystal formation occurred within the nephron.
  122. 122.  Encountered in massive doses of penicillin compound without adequate hydration.  Microscopy: appear as long, fine colorless needles that tend to form bundles following refrigeration
  123. 123.  Rarely seen  Microscopy: rectangular plate with a notch in one or more corners  Cholesterol crystals are highly birefringent with polarized light  Clinical significance: associated with disorders producing lipiduria, such as the nephrotic syndrome, and in conjunction with fatty casts and oval fat bodies
  124. 124.  Form after radiographic examinations using diatrizoate dyes.  May be found in urine of acid pH shortly after intravenous radiographic studies (particularly if the patient has not been well hydrated),  Microscopy: appearing as flat, clear, colorless, notched rhombic plates, or longer, slender rectangles.  They are easily polarized, showing interference colors  The presence of radiographic crystals should correlate with a high specific gravity (>1.040).
  125. 125.  Bilirubin crystals: present in hepatic disorders producing large amounts of bilirubin in the urine  Microscopy: appear as clumped needles or granules with the characteristic yellow color of bilirubin Clinical significance: In disorders that produce renal tubular damage, such as viral hepatitis, bilirubin crystals may be found incorporated into the matrix of casts.
  126. 126.  May be present in the form of cocci (spherical) or bacilli (rods).  Reported as few, moderate, or many /hpf  If bacteria are identified with Gram's stain in an centrifuged urine specimen under an oil-immersion lens suggests >100 000 organisms/mL are present (i.e. significant bacteriuria).
  127. 127.  Clinical significance: indicative of either lower or upper UTI.  To be considered significant for UTI, bacteria should be accompanied by WBCs.  Bacteria associated : 1. Enterobacteriaceae (referred to as gram- negative rods) 2. Cocci-shaped Staphylococcus & Enterococcus 3. Acid-fast bacilli may be seen, but because the urethral flora may contain nonpathogenic acid-fast organisms, the presence of Tuberculosis in urine must be substantiated by culture and/or polymerase chain reaction (PCR) methodology
  128. 128.  Microscopy: appear in the urine as small, refractile oval structures  In severe infections, they may appear as branched, mycelial forms  Clinical significance: primarily Candida albicans, ◦ urine of diabetic ◦ immunocompromised patients and ◦ women with vaginal moniliasis.  vaginal contamination should be ruled out, which is likely when the background contains numerous squamous cells and bacteria and few neutrophils
  129. 129. 1. Trichomonas vaginalis- Most frequent parasite encountered in urine. ◦ Pearshaped flagellate with an undulating membrane, rapid darting movement The nucleus is small and oval, & the cytoplasm contains fine red granules ◦ Clinical significance: sexually transmitted pathogen associated primarily with vaginal inflammation, but it can cause urethritis and even prostatitis 2. Microfilaria: seen in chyluria of filariasis as long, filamentous structure with an outer sheath .
  130. 130. 3. The ova of the bladder parasite Schistosoma haematobium will appear in the urine accompanied by red cells. 4. Fecal or vaginal contamination of a urine specimen also result in the presence of ova from intestinal parasites in the urine sediment. The most common contaminant is ova from the pinworm Enterobius vermicularis Enterobius vermicularis Schistosoma haematobium
  131. 131. 5. Amoebae are rarely seen in the urine ◦ These may reach the bladder from lymphatics or more likely from fecal contamination of the urethra ◦ Usually accompanied by erythrocytes and leukocytes. Entamoeba histolyitca cyst
  132. 132.  Identified in the urine sediment by their oval, slightly tapered heads and long, flagella like tails  Urine is toxic to spermatozoa; therefore, they rarely exhibit the motility  Clinical significance: in cases of male infertility or retrograde ejaculation in which sperm is expelled into the bladder instead of the urethra. Spermatozoa- 400x
  133. 133.  Protein material produced by the glands and epithelial cells of the lower genitourinary tract and RTE cells.  Tamm-Horsfall protein- glycoprotein excreted by the RTE cells of the distal convoluted tubules and upper collecting duct is a major constituent of mucus  Microscopy: thread-like structures with a low refractive index  no clinical significance Mucus in urine with entrapped WBCs
  134. 134.  Found in specimens collected under improper conditions or in dirty containers  The most frequently encountered artifacts include starch, oil droplets, air bubbles, pollen grains, fibers, and fecal contamination.  often very highly refractile or occur in a different microscopic plane than the true sediment constituents. 1. Partially digested muscle fibers or vegetable cells may be found when fecal contamination occurs
  135. 135. 2. Pollen grains contaminate specimens seasonally, appear as spheres with a cell wall and occasional concentric circles 3. Starch granule contamination: occur when corn starch powder is used in powdered gloves  Microscopy: highly refractile spheres, usually with a dimpled center
  136. 136. 4. Oil droplets may result from contamination by immersion oil or lotions and creams 5. Air bubbles occur when the specimen is placed under a cover slip.
  137. 137. 6. Hair and fibers from clothing and diapers may initially be mistaken for casts, though they are usually much longer and more refractile. ◦ Unlike casts, these fibers polarize brightly. 7. Fecal artifacts may appear as plant and meat fibers or as brown amorphous material in a variety of sizes and shapes
  138. 138.  Casts are reported as the average number per low-power field (lpf) following examination of 10 fields  RBCs and WBCs, as the average number per 10 high-power fields (hpfs).  Epithelial cells, crystals, and other elements are frequently reported in semi quantitative terms such as, rare, few, moderate, and many, or as 1, 2, 3,and 4, following laboratory format as to lpf or hpf use.
  139. 139. Clinical condition Physiochemical Findings(macroscopic findings) Diagnostic urine sediment findings(microscopic findings) Acute glomeurlonephritis Decreased urine volume Haematuria(often gross) Increased turbitiy(smoky) Proteinuria(<2g/24hrs) Erythrocytic & blood casts Erythrocytes Neutrophils Renal epithelial cells Occasional leucocytic &/or renal epithelial casts Chronic glomerulonephritis Proteinuria(>2-3g/24hrs) Occasional lipiduria Hematuria Decreased & fixed specific gravity Granular & waxy casts Broad casts Occasional lipid inclusion cells renal epithelial casts Erythrocytes leucocytes Nephrotic syndrome Marked Proteinuria(>4.5g/24hrs) lipiduria Minimal Hematuria Fatty & waxy casts Doubly refractile oval fat bodies(maltese cross with polarised light) Highly vacuolated or lipid laden renal tubular epithelial cells Renal epithelial casts
  140. 140. Clinical condition Physiochemical Findings (macroscopic findings) Diagnostic urine sediment findings (microscopic findings) Acute pyelonephritis Increased turbidity Occasional `odor` Positive nitrite reaction Minimal proteinuria Numerous neutrophils( many in clumps) Leucocytic casts Granular & waxy casts Bacteria Bacterial casts Renal epithelial cells Renal epithelial casts Lymphocytes, plasma cells, Histiocytes Erythrocytes Chronic pyelonephritis Decreased specific gravity Proteinuria(>2g/24hrs) Granular & waxy casts Broad casts Occasional renal epithelial casts Rare leucocytic casts histiocytes Acute tubular necrosis Decreased specific gravity Decreased urine volume Hematuria Minimal proteinuria Necrotic or degenerated renal epithelial cells renal epithelial casts Granular & waxy casts Broad casts renal epithelial fragments Neutrophils erythrocytes
  141. 141. Necrotising papillitis(papillary necrosis) Occasional decreased urine volume Hematuria Numerous neutrophils( many in clumps) renal epithelial fragments Necroritc or degenerated renal epithelial cells Erythrocytes Nephrosclerosis a. Essential hypertension b. Malignant hypertension Minimal proteinuria Decreased urine volume Minimal & marked proteinuria hematuria Non specific & persistent hyaline & granular casts Granular & waxy casts Broad casts Erythrocytes Renal epithelial cells Renal infarction Haematuria(often gross) Necrotic cellular debris Necrotic or degenerated renal epithelial cells renal epithelial fragments Erythrocytes & Neutrophils Fibrin Granular, waxy & mixed casts Regenerative or reactive epithelial cells Acute allograft rejection Decreased urine volume Hematuria Minimal proteinuria Amorphous background & cellular debris renal epithelial cells renal epithelial casts Granular, blood, waxy & mixed casts Neutrophils Lymphocytes,occasional plasma cells, Erythrocytes
  142. 142. Hypernephroma( renal cell carcinoma) Hematuria Atypical mononuclear cells with enlarged irregular, hyperchromatic nuclei, prominent nucleoli & abundant vacuolated cytoplasm that occur singly or as tissue fragments Viral nephropathy( cytomegalic inclusion disease) Hematuria Minimal proteinuria Enlarged mononuclear cells(occasional giant cell form) with prominent basophilic intranuclear &/ or cytoplasmic inclusions Necrotic or degenerated renal epithelial cells Renal epithelial casts Lead nephropathy Occasional glycosuria Large mono- or binulceated with prominent acid-fast intranuclear inclusion & ``balloning`` degenerated granular cytoplasm Non specific red-orange inclusion bodies or degenerated droplets also present Sickle cell disease Decreased specific gravity(early) Hematuria(often gross) Sickle erythrocytes occasionally present cystinosis Minimal proteinuria Minimal hematuria Cystine crystals
  143. 143. gout Decreased specific gravity(early) Minimal proteinuria(late) Minimal hematuria Numerous uric acid crystals Urate crystal cast Renal epithelial cells renal epithelial casts Granular & waxy casts Giant cell formaton with crystal inclusion Hemachromatosis or urinary siderosis Hematuria Glycosuria ketonuria Pigmented renal epithelial cells prussian blue or iron stain positive) Renal epithelial cells Granular casts myelomatosis Decreased specific gravity Proteinuria(predominantly globulin rather than albumin) Granular & waxy casts Broad casts renal epithelial cells renal epithelial casts Plasma cells(myeloma cells) Systemic lupus erythematosus Proteinuria Erythrocytes Granular & blood casts fatty & waxy casts Renal epithelial cells Neutrophils amyloidosis Proteinuria(predominantly globulin rather than albumin) Granular & waxy casts Erythrocytes & Neutrophils Diaberes mellitus Proteinuria Glycosuria ketonuria renal epithelial cells Leucocytes renal epithelial casts fatty & waxy casts Oval fat bodies
  144. 144.  McPherson RA, Ben-Ezra J. Basic examination of urine. In: McPherson RA, Pincus MR. Henry’s Clinical Diagnosis & management by laboratory methods. 22nd ed : Saunders Elsevier ; 2011. p. 463-74.  Strasinger SK, Lorenzo MSD. Urine analysis and body fluids, 5th ed, Philadelphia: Davis company;2008. p.82-119  Essentials of Clinical Pathology 2010 by Shirish M Kawthalkar