Urine examination how to approach final.ppt1


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Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.

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Urine examination how to approach final.ppt1

  1. 1. URINE EXAMINATION Dr. Sachin Verma MD, FICM, FCCS, ICFC Fellowship in Intensive Care Medicine Infection Control Fellows Course Consultant Internal Medicine and Critical Care Web:- http://www.medicinedoctorinchandigarh.com Mob:- +91-7508677495 References:1. Brenner’s & Rector’s The Kidney 7th Ed.2. Harrison’s Internal Medicine 16th Ed.3. Oxford Textbook Of Clinical Nephrology4. Manual of nephrology 5th Ed.5. Internet.
  2. 2. COMPOSITION OF URINE Urine composition is affected mainly by 3 factors Nutritional status State of metabolic processes Ability of the kidney to selectively handle the material presented to it.
  4. 4. URINE EXAMINATIONGlomerulus proteinProximal GlucosetubuleLoop of henle Specific gravity OsmolalityCollecting pHtubule
  5. 5. Physicochemical characteristics of urine pH 4.8 -8.0 (mean 6.1) Osmolality 38 – 1400 mOsm/Kg water(Avg =500- 800) Specific gravity 1.003-1.030 Volume 600-2500(Avg 1200ml) Organic comtituents per 24 Hours Nitrogenous – total 25 - 35 gm Urea 15-30 gm Creatinine 1 -1.6 gm Creatine 10- 50mg(children,Excreated in Urine . in adults in hepatic or muscle disorders) Ammonia 0.7(0.3-1) gm Uric acid 0.45 – (0.3 – 0.6) gm Protein < 150 mg
  6. 6.  Inorganic Constituents per 24 Hours Sodium 4 gm on usual diet Phosphate 0.8-1.3 gm on usual diet Chlorides 6(4-10) gm on usual diet Sulphur 2 gm Calcium < 150 mg Cells And Casts RBC 0-2 /high power field WBC 0-2 /high power field Bladder Cells -ve Squamous Cells -ve Tubular cells -ve Hyaline cast 0-5 /low power field Granular ,waxy, Broad casts -ve
  7. 7. Method of urine collection For microscopic analysis fresh mid – stream collection of second urine of the morning under aseptic condition is required. Strenuous activity must be avoided several hours before collection. Sample should ideally be analysed within 1 hr of voiding.
  8. 8. Physical Features Colour pale -dark yellow 1. Normal - 1. Colourless Dilution ,Diabetes mellitus /insipidus,diuretic or alcohol intake 2. Pink-Black Haematuria 3. Red Haemoglobinuria,Myoglobinuria, Haematuria, Phenolphthalein,rifampicin 4. Dark yellow-brown Jaundice.Nitrofurantoin 1. Fresh urine darken up on Porphyria(dark brown), standing Alkaptonuria(Black) 1. Brown-black Levodopa 2. Green-blue green Amtryptyline.phenol poisoning 3. Dark orange Clofazamine 4. Dark blue Hairdye poisoning
  9. 9. Physical FeaturesODOUR Fruity Ketones Launch Internet Explorer Browser.lnkPungent UTIMousy Phenyl ketonuriaMaple syrup Maple syrup urine (sotolone)Sweaty feet Isovaleric acidaemiaRotten fish odour Fish odour syndrome
  10. 10. Physical FeaturesTURBIDITYNORMAL CLEAR/TRANSPARENTCloudy High concentration of Bacteria,Leucocyte,Eryth rocytes,epithelial cellsMilky/Cheese like ChyluriaFresh urine gets cloudy ppt of phosphates &on standing urates
  11. 11. Physical Features Relative density Specific gravity Most commonly used Refractometer Osmolality Most accurate assessment Dry chemistry Specific gravity A function of no & wt of the dissolved solute particles. Measured by URINOMETER (scale 1.000 to 1.060) Needs correction factor for TEMP(+/- 0.001 for each 3◦C above/below standard temp of instrument. Proteins ↑ sp gt by 0.001 for each 0.4 g/dl Glucose ↑ sp gt by 0.001 for each 0.27 g/dl
  12. 12. Physical Features In the absence of proteinuria or glucosuria if sp gt is > 1.040, +ce of abnormal substance must be considered.High Excessive sweating, Glycosuria, Albuminuria, All causes of oliguria Acute nephritisLow(< 1.010) Excessive water intake Diabetes inspidus Chronic nephritis All causes of polyuria except diabetes mellitus.Low & fixed(1.010 to End stage renal disease1.012) ADH deficiency Arteriosclerotic kidney
  13. 13. Chemical Features pH Acidic urine Alkaline urine Normally range from Ketosis Diabetes, Post prandial alkaline 4.5 to 8.0(Avg 6.1) Starvation tide Method: 1.Dipstick Most Systemic acidosis Systemic Alkalosis commonly used Except with impaired Utilizes methyl red& renal tubular function, Renal tubular acidosis bromothymol as Respiratory or indicator covering pH 5 metabolic acidosis to 9 UTI Proteus/ 2.Digital electronic pH UTI E. coli Pseudomonas infection meter Acidification therapy Alkalinization therapy
  14. 14. Chemical Features Haemoglobin Method : Dipstick – Haemoglobin reacts with cumene peroxidase & a orthotolidine(chromogen) to produce a blue colour. Presence of Hb is expressed as Spots in +ce of intact RBC Homogenous pattern in +ce of free Hb. Measure up to as low as 0.1 – 0.6 mg/l Myoglobin & Hb distinguised by 5 ml urine + 2.8 g Ammonium sulfate, followed by centrifugation, HB ppts while myoglobin does not. Spectrophotometry,Electrophoresis,Ultracentrifugation False +ve False -veAscorbic acid, high nitrite conc Myoglobin, large no:of bacteria
  15. 15. Chemical Features Causes of Haemoglobinuria Intracorpuscular Extracorpuscular 1. Abnormalities of RBC interior Extrinsic factor a. Enzyme defect a. Antibody:immune hemolysis b. Haemoglobinopathies b. Microangiopathic hemolysis 2. RBC membrane abnormalities c. Infections, toxins. a. Hereditary spherocytosis b. Paroxysmal nocturnal haemoglobinuria c. Spur cell anemia
  16. 16. Chemical Features PROTEIN Urinary protein excreation does not exceed 150 mg/d for adults & 140 mg/m2 of body surface. Causes Of Proteinuria As Related To Quantity DAILY 0.15 to2.0g 2.0 to 3.5g >3.5 g PROTEIN EXCRETION CAUSE Mild Usually Always Glomerulopathies Glomerular Glomerular Tubular Proteinuria Overflow Proteinuria
  17. 17. Composition Of Urinary Protein 70 mg/d 35 mg/d 15 mg/d 10 mg/d 15 mg/d 5 mg/dTamm Horsfall Protein Blood Group Related AntigensAlbumin MucopolysaccaridesHormones and Enzymes Immunoglobulins
  18. 18. Detection Two methods. 1. Dipsticks: Dipstick analysis is used in most patients in out door setting. Paper strips are impregnated with bromocresol green & salicylate buffer when dipped in urine undergo sequential colour changes from pale green to green & blue. Binding of a protein is pH dependent. Albumin binds at pH 5 – 7, other proteins at lower pH but with a lower affinity, while Bence jones protein does not bind at any pH. The resuts are graded as Negative ( <10 mg /dl ) 2+ ( 100 mg /dl ) Trace ( 10 to 20mg/dl ) 3+ ( 300 mg/dl ) 1+ ( 30mg /dl ) 4+ ( >1000mg/dl ) Detect exclusively albumin. Sensitivity being for conc as low as 250 mg/l Microalbuminuria, globulin, bence jones protein or tubular proteins are not detected. 2. Precipitation methods : Evaluate turbid occuring after proteis are ppt by sulfosalicylic acid, trichloracetic acid,heat or acetic- sodium acetate buffer.
  19. 19. QUANTITATIVE EVALUVATION Detection Method Description limit Comments (mg/l)Patients with persistent proteinuria should undergo 24-hr urine protein estimation. The urinarycreatinine concentration should be included in 24-hr measurement to determine adequacy ofspecimen (normal excretion in men=16 to 26mg/kg/day and in women =12 to24 mg/kg/day as itdepend on muscle mass) Copper reagent, measures peptide Requires precipitation of proteins,Biuret bonds 50 used for 24-h measurement in some laboratories Addition of trichloracetic or Imprecise, different readings for sulfosalicylic acids alters colloid albumin and globulin properties and produces turbidity toTurbidimetric 50–100 be read in densitometer. Benzethomecin also used Indicator changes color in presence Different proteins bind differently; of protein (e.g. Coomassie brilliant several different dyes in use; usedDye-binding blue) 50–100 in many laboratories for 24-h excretion Specific antialbumin antibody used Measures albumin excretion notNephelometric total protein. Does not detect globulins
  20. 20. Quantifying ProteinuriaSpot Urinary Protein To Creatinine Ratio (Upr/Cr) It is an alternative to 24-hr urine protein estimation Recent studies indicates that it is more accurate than 24-hr urine protein estimation The ratio is about the same numerically as number of grams of protein excreted per day
  21. 21. QUALITATIVE EVALUATION Methods Electrophoresis Immunofixation Electrophoresis Causes Measurement of different proteins Diabetic mellitusMicroalbuminuria: defined as presence of High BP albumin in urine above normal range of <30 mg/day but below detectable range Hypertriglyceridaemia with conventional dipstick methodology i.e.30-299 mg/day. OCPMethods : Radioimmunoassay, enzyme HRT immunoassay,nephelometric, & turbidimetric.
  22. 22. Causes Of Proteinuria Primary Secondary Glomerulonephropathyglomerulonephropathy glomerulonephropathy associated with drugs Minimal change disease Diabetes mellitus Heroin Idiopathic membranous Collagen vascular NSAIDs glomerulonephritis disorders (e.g., lupus nephritis) Focal segmental Penicillamine glomerulonephritis Amyloidosis Lithium Membranoproliferative Infection (e.g., HIV, glomerulonephritis hepatitis B and C, poststreptococcal illness, Heavy Metal malaria and IgA nephropathy endocarditis) Lymphoma, chronic renal transplant rejection
  23. 23. Causes Of Proteinuria Tubular Overflow Hypertensive nephrosclerosis HemoglobinuriaTubulointerstitial disease due to Myoglobinuria Uric acid nephropathy Multiple myeloma Acute hypersenstivity Amyloidosis Interstitial nephritis Fanconi syndrome Heavy metals & Drugs Sickle cell disease
  24. 24. Approach to the pt with Protenuria
  25. 25. Chemical Features GLUCOSE Method: 1. Dipsticks: Glucose oxidase + Glucose  Gluconic acid + H2O2 Glycosuria with Glycosuria with H2O2 + orthotoludine  coloured hyperglycemia out product hyperglycemia ENDOCRINE : Renal tubular Highly specific & is sensitive to conc of 1- Diabetis mellitus, dysfuction 20 g/l. Acromegaly. Pancreatic : Carcinoma, severe Pancreatitis, Pregnancy 2. Benidict’s Qualitative & Quantitative test. CNS dysfuction ; Tumours or haemorrhage in hypothalamus False +ve False-ve Drugs : steroids thiazidesAscorbic acid, UTI Oxidising substance (hypochlorite)
  26. 26. Chemical Features KETONE BODIES Nornal value –ve Diabetic Non Diabetic 3 ketone bodies that can be detected are : Diabetes In infant & 1. Acetone (2%) ketoacidosis child 2. Acetoacetic acid (20%) 3. β- Hydroxybutyric acid(78%) Acute febrile states Tests : 1. Dipsticks: contain sodium Toxic states nitroprusside, amino acid & disodium phosphate.+ve test indicated by purple with vomiting colour. & diarrhoea Hyperemesis 2. Rothera’s test grvidarum Starvation 3. Legal’test 4. Diacetic acid test.
  27. 27. Chemical Features BILE PIGMENTS Normal values <0.02 mg% Methods1. Foam test2. Iodine test3. Harrison test4. Diazo test CAUSESOF HYPERBILIRUBINURIA1. Moderate to severe hepatocellular damage2. Obstruction of bile ducyts, extra/ intrahepatic
  28. 28. Chemical Features Rare tests Leucocyte esterase : Based on esterase activity of granulocytes Method is very specific for lysed leucocytes. Thus, in urine with alkaline pH / low sp gt , dipsticks, for esterase may be +ve, while microscopic examination for leucocyte may be –ve. Nitrites : presence of bacteria may be revealed by reduction of nitrates to nitrites, shown by dipsticks containing an aromatic amine that reacts with nitrites to form a coloured diazonium compound. Has low sensitivity & a high specificity. False –ve occur in alkaline urine, or in low / absent nitrate reducers like Pseudomonas, Stap. Albus.
  29. 29. Microscopic examination The formed elements Cells : Erythrocytes Hematuria : defined as 2 -5 cells / high power field. Persistent/Significant hematuria : > 3 RBC’s/HPF on 3 urialyses/ a single urinalysis with >100 RBC’s/ gross hematuria. Hematuria is defined as ‘non glomerular’ when 80% of RBC’s show regular(or isomorphic) appearance. And Glomerular when a similar proportioon of RBC’s are changed (or dysmorphic) or atleast 5% of RBC’s are acanthocytes. RBC morphology is an imp tool in the Mg of pt’s with isolated microscopic hematuria of unknown origin. Appearance of RBC in urine may reflect the appearance they have in the blood.
  30. 30. Microscopic examination (a) Isomorphic erythrocytes (dark cells have lost their haemoglobin content). (b) Different types of dysmorphic erythrocytes. (c) Different types of acanthocytes or G1 cells. (d) Neutrophils with their lobulated nucleus and granular cytoplasm
  31. 31. Microscopic examination
  32. 32. Microscopic examination The formed elements Cells : Leucocytes Most frequently found leucocytes in the urine Neutrophils Urinary tract infections Active proliferative glomerulonephritis, acute or chronic interstitial nephritis, and urological disorders. Lymphocytes Gradual or abrupt appearance of lymphocyturia in renal graft recipients is an early and sensitive marker of acute cellular rejection Eosinophils Marker of acute interstitial nephritis, urinary tract infection, prostatitis, urinary schistosomiasis
  33. 33. Microscopic examination The formed elements CellsRenal tubular round to ovoid mononucleated cellscells acute tubular necrosis (occur in clumps ) acute interstitial nephritis, acute cellular allograft rejection and acute nephritic or nephrotic syndrome.Urothelial cells multilayered epithelium lining the urinary excretory tract Cells of the deep layers, when greater than or equal to 1/high-power field, are typical of conditions such as urolithiasis, bladder cancer, hydronephrosis, or are associated with the presence of ureteric stents or prolonged bladder catheterization . In contrast, the superficial cells are a frequent finding in urinary tract infectionSquamous cells indicate a contamination of urine from vaginal discharge
  34. 34. Microscopic examination (a) Different types of tubular cells. (b) Urothelial cells from the deep cell layers of the urothelium. (c) An aggregate of urothelial cells from the superficial cell layers of the urothelium. (d) Squamous cells surrounded by bacteria (rods)
  35. 35. Microscopic examination Lipids Present in urine mainly as droplets either free—isolated or in aggregates or within casts and cells. In the latter case, they can form the so-called oval fat bodies, which are tubular cells or macrophages gorged with lipids. Typical finding in the urine of patients with nephrotic syndrome or heavy protein. Occasionally found in polycystic kidney disease or with non- glomerular diseases, Fabrys disease
  36. 36. Microscopic examination Casts Elongated elements with a basic cylindrical shape that has some possible variation due to bending, wrinkling, and irregular edges. They form within the distal tubules and the collecting ducts from the aggregation and transformation into a gel of the fibrils of Tamm–Horsfall glycoproteinCast Main clinical associationsHyaline Normal subject ,CHF, Diabetic nephropathy.Hyaline–granular Normal subject ,Glomerulonephritis, PyelonephritisGranular Glomerulonephritis, Pyelonephritis, Nephrotic syndromeWaxy Renal insufficiency either acute or chronicFatty Nephrotic syndromeErythrocyte/haemoglobin Glomerular bleeding,Proliferative/necrotizing glomerulonephritisLeucocyte Acute pyelonephritis, Acute interstitial nephritis, Proliferative glomerulonephritisEpithelial Acute tubular necrosis, Acute interstitial nephritis ,GlomerulonephritisMyoglobin Acute renal failure associated with rhabdomyolysis
  37. 37. Microscopic examination (a) A hyaline cast with a fluffy appearance due to the fibrillary substructure of Tamm–Horsfall glycoprotein (b) A hyaline–granular cast. (c) A finely granular cast. (d) A waxy cast (a) An erythrocyte cast. (b) A leucocyte cast containing packed neutrophils. (c) An epithelial cast. (d) A fatty cast made of packed lipid droplets
  38. 38. Microscopic examination Crystals Uric acid precipitate at a pH less than or equal to 5.4. appear mostly as lozenges Calcium oxalate Two main types of calcium oxalate crystals: the mono- and the bihydrated Mainly found in acidic pH. Monohydrated calcium oxalate crystals are birefringent, while the bihydrated are not.Calcium phosphate In alkaline urine prisms, needles, and star-like aggregates or as plates with a granular surface. While the crystals polarize light, the plates do not. Triple phosphate Precipitate at a pH greater than or equal to 7.0. Have a coffin lid appearance Amorphous urates Appear as granular material, often in clumps, and phosphates urates are found in acid urine and are birefringent, while phosphates precipitate only in alkaline urine and do not polarize light. Cystine Thin, hexagonal, birefringent plates with irregular sides marker of cystinuria, Found mostly in acid urine.Crystals due to drugs sulfonamide sulfadiazine, acyclovir and indinavir ,triamterene, coronary primidone, vitamin C ,amoxycillin
  39. 39. Microscopic examination (a) Uric acid crystals (b). Monohydrated (biconvex disc) and bihydrated(bipyramidal) calcium oxalate crystals. (c) A star-like calcium phosphate crystal Typical triple phosphate crystals (a) Aggregated cystine crystals. (b) 2,8-Dihydroxyadenine crystals (c) Amoxycillin trihydrate crystals. (d) Amoxycillin trihydrate crystals
  40. 40. Microscopic examination Clinical significance of crystals Finding of few crystals of uric acid, calcium oxalate, and calcium phosphate is usually irrelevant Crystalluria may be associated with intratubular precipitation of crystals and acute renal failure(mainly in acute uric acid nephropathy, ethylene glycol poisoning, and after the administration of high dosages of drugs such as sulfadiazine, acyclovir, indinavir, naftidrofuryl oxalate, vitamin C, amoxycillin) To monitor the patients with recurrent metabolic urolithiasis Some crystals are always pathologic cystine which is a marker of cystinuria
  41. 41. MICROORGANISM Bacteria : Frequently seen in urine sediments, either as rods or cocci presence of leucocytes increases the probability of a real infection . Fungi Candida is the most frequent yeast . Most frequent cause of candida in the urine is contamination , can also grow in the urinary tract, mostly in patients with diabetes mellitus, structural abnormalities, indwelling catheters, prolonged antibiotic treatment or immunosuppression. Protozoa : Trichomonas vaginalis -round or pear shaped , has four flagella, found in the urine of both sexes, mostly as a consequence of genital contamination . Parasites : Schistosoma haematobium : adult form lives and lays the eggs in the vesical plexus and veins draining the ureters, is endemic in several geographic areas such as Nile valley, West Africa, Arabia, etc. Responsible for haematuria, chronic renal failure due to obstructive uropathy or bladder cancer
  42. 42. MICROORGANISM (a) A dirty urine background showing many bacteria (rods) and debris. (b) Candida albicans. (c) Trichomonas vaginalis (arrows) (note the flagella). (d) Two eggs of Schistosoma haematobium
  43. 43. Diagnostic Evaluation When proteinuria is found on a dipstick analysis, the urinary sediment should be examined microscopically for- Fatty casts, free fat or oval fat bodies Nephrotic range proteinuria (>3.5 g /24 hours) Leukocytes, leukocyte casts with Urinary tract infection bacteria Leukocytes, leukocyte casts without Renal interstitial disease bacteria Normal-shaped erythrocytes Suggestive of lower urinary tract lesion Dysmorphic erythrocytes Suggestive of upper urinary tract lesion Erythrocyte casts Glomerular disease Waxy, granular or cellular casts Advanced chronic renal disease Eosinophiluria Drug-induced acute interstitial nephritis Hyaline casts No renal disease; present with dehydration
  44. 44. The interpretation of main urine sediment findingsNephrotic characterized by large amounts of lipids and Minimal-change disease, urinary differences may existsediment variable amounts of hyaline, granular, or epithelial casts. Focal segmental Microscopic haematuria is glomerulosclerosis, absent in about 50 %of patients with minimal-change disease, Erythrocytes are absent or only a few, (10/high- while it is almost always Membranous power field). present in membranous nephropathy, nephropathy Diabetic nephropathy, lipiduria is more marked and Neutrophils are also absent frequent in membranous Amyloidosis, nephropathy than in minimal- change diseaseNephritic Distinguishing feature Active proliferative Monitoring the urinarysediment glomerulonephritis sediment in patients with +ce of abundant erythrocyturia associated with proliferative RBC /haemoglobin casts. >/=100 RBC/ hpf is glomerulonephritides is almost invariably important because the associated with sediment reflects to some Extracapillary/necrotizing extent the progressive changes Neutrophils are also frequent in low numbers in the kidneys glomerulonephritis (usually ≤10hpf). Leucocyte casts are possible, but they are rare. Other findings are: tubular cells, hyaline, granular, epithelial, and waxy casts.
  45. 45. The interpretation of main urine sediment findingsNephrotic and Co-existence of lipiduria with abundant Mesangiocapillarynephritic sediment erythrocyturia and cylindruria which also glomerulonephritis, encompasses erythrocyte/ haemoglobin casts. Lupus nephritis with both proliferative and membranous changes, Henoch–Schönlein purpura,Sediment of Characterized by variable amounts of tubular Additional elements depends onacute tubular cells, which often appear damaged the cause of acute tubularnecrosis necrosis. Due to rhabdomyolysis, myoglobin casts may be seen, while RBC may be present in Epithelial and granular casts are another typical finding. acute interstitial nephritis, Crystals in crystalluric forms of acute tubular necrosis (hyperoxaluria or drugs )Sediment of Association of bacteriuria with leucocyturia false negative due to the lysis ofurinary tract leucocytes at alkaline pH,infection false-positive caused by leucocyturia and bacteriuria secondary to urine contamination from genitalia.
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