Microscopic examination Of Urine Flashcards
Most glomerular disorders are caused by:
Immunologic disorders
Dysmorphic RBC casts would be a significant finding with
Good pasture syndrome
Acute glomerulonephritis
Henoch-Schönlein purpura
Dysmorphic RBC casts would not be a significant finding with
Chronic pyelonephritis
Occasional episodes of macroscopic hematuria over periods of 20 or more years are seen with :
IgA nephropathy
Antiglomerular basement membrane antibody is seen with
Goodpasture syndrome
Antineurophilic cystoplasmic antibody is diagnostic for:
Wegner Granulomatosis
Respiratory and renal symptoms are associated with
IgA nephropathy
Wegener granulomatosis
Henoch-Schönlein purpura
Respiratory and renal symptoms is not associated with
Goodpasture syndrome
The presence of fatty casts is associated with
Nephrotic syndrome
Focal segmental glomerulosclerosis
Minimal change disease
The presence of fatty casts is not associated with
Nephrogenic diabetes insipidus
Highest levels of proteinuria are seen with
Nephrotic syndrome
Ischemia frequently produces
Acute renal tubular necrosis
A disorder associated with polyuria and low specific gravity is:
Nephrogenic diabetes insipidus
An inherited disorder producing a generalized defect in tubular readsorption is:
Fanconi syndrome
A teenage boy who develops gout in his big toe and has a high serum uric acid should be monitored for:
Uromodulin-associated kidney disease
The only protein produced by the kidney is:
Uromodulin
Presence of renal tubular epithelial cells and casts is an indication of:
Acute tubular necrosis
Differentiation between cystitis and pyelonephritis is aided by the presence of
WBC casts
Presence of WBCs and WBC casts with no bacteria is indicative of:
Acute interstitial nephritis
End-stage renal disease is characterized by all of the following except:
Hypersthenuria
Prerenal acute renal failure could be caused by:
Massive hemmorrhage
The most common composition of renal calculi is
Calcium oxalate
Urinalysis on a patient with a severe back pain being evaluated for renal calculi would be most beneficial if it showed:
Miscroscopic hematuria
Warming of urine at 37deg C
Dissolves some crystals
Refrigeration of urine
Precipitation of amorphous urates/phosphates and other non-pathologic crystals
Centrifugation
5 minutes in 4000RCF
LPO detects
General composition of sediment
Casts
HPO indentifies
Urinary sediments
Sternheimer-Malbin stain
Most used in urinalysis
Crystal violet and Safranin O
Sternheimer-Malbin stain
Sedi stain and KOVA stain
Sternheimer-Malbin stain
Confirm.presence of triglycerides, neutral fats, and cholesterol
Lipid stains, Oil red O, Sudan III and Polarizing microscopy
Identification of bacterial casts
Gram stain
Crystal violet, Iodine, Alcohol Safranin
Gram stain
Purple/Violet
Gram(+) bacteria
Red
Gram(-) bacteria
Preferred stain for urinary eosinophils (In cases of drug-induced allergic reaction producing inflammation of the
renal interstitium)
Hansel stain
Methylene blue and Eosin Y
Hansel stain
Prussian blue stain
Stain for iron
Aids in identification of Treponema Pallidum
Dark-Field microscopy
Hyaline casts, mixed cellular casts, mucous threads and Trichomonas
Phase-Contrast microscopy
Cholesterol, oval fat bodies, fatty casts and crystals
Polarizing microscopy
Three dimensional microscopy
Interference contrast
Associated with damage to the glomerular membrane or vascular injury within the genitourinary tract
Red Blood Cell
Frequently associated with advanced glomerular damage but is also seen with damage to the vascular integrity of the urinary tract caused by trauma, acute infection or inflammation, and coagulation disorders.
Macroscopic hematuria
Critical to the early diagnosis of
glomerular disorders and malignancy of the urinary tract and to confirm the presence of renal calculi
Microscopic hematuria
Increased in urinary WBC which indicates the presence
of an infection or inflammation in the genitourinary system.
Pyuria
Drug-induced Interstitial Nephritis, UTI and renal
transplant rejection
Eosinophil
Resembles RBC
Lymphocytes
increased numbers in the early stages of renal transplant rejection
Lymphocytes
Used to enhance nuclear detail
Supravital staining/Addition of Acetic Acid
Largest cells found in urine sediment
Squamous EC
Originate from the lining of the renal pelvis, calyces,
ureters, and bladder, and from the upper portion of the
male urethra
Epithelial Cell
Smaller than squamous cells and appear in several forms, including spherical, polyhedral and caudate.
Epithelial Cell
Lipid containing RTE cells
Oval Fat Bodies
Squamous EC covered with Gardnerella coccobacillus
(Bacterial Vaginosis)
Clue cells
Bacteria accompanied with WBC
Significant UTI
Small Refractile oval structures (may or may not contain bud)
Yeast
most frequent parasite
encountered in the urine. Asymptomatic for male
Trichomonas vaginalis (ST):
bladder parasite (ova). Bladder
Cancer
Schistosoma haematobium
most common fecal contaminant
Enterobius vermicularis
Significant: Male infertility, Retrograde Ejaculation (Sperm is
expelled into bladder instead of urethra)
Spermatozoa
Uromodulin: major constituent
Thread-like structures (Low Refractive Index)
Frequently seen in Females
Mucus
Presence of urinary cast
Cylinduria
: True geometrically structure or amorphous
materials
Crystals
appear as spheres with a cell wall and occasional concentric circles
Artifacts
Pathologically increased in: Acute glomerulonephritis,
Pyelonephritis, Chronic Renal Disease, CHF
Hyaline
Glomerular damage (glomerulonephritis) is associated with proteinuria and dysmorphic erythrocytes
RBC Casts
Non-Bacterial inflammation
Acute Interstitial Nephritis
Bacterial inflammation
Pyelonephritis
May resemble granular cast
Bacterial Casts
Frequently Associated with: Nephrotic syndrome
Fatty Casts
Significantly increased in: Gout, Lesch-Nyhan Syndrome
Uric Acid
Prism shape, resembles “COFFIN-LID”
Triple Phosphate/Ammonium Magnesium Phosphate
Most often encountered in: OLD SPECIMEN associated with
ammonia produced by ammonia spitting bacteria
Ammonium Biurate
Formation of kidneys stones at an early stage
Cystine
Inadequate px hydration which is the primary cause of
Sulfonamide crystalization
Sulfonamides
Immune-mediated
Glomerular
INCREASED permeability of the GLOMERULI to the passage of plasma proteins (ALBUMIN)
Heavy PROTEINURIA (3.5g/day)
HYPOPROTEINEMIA (Plasma albumin usually <3g/dL – LIVER SYNTHESIS unable to compensate for the large amount of protein EXCERETED in the urine
HYPERLIPIDEMIA (INCREASED plasma levels of TRIGLYCERIDES, CHOLESTEROL, PHOSPHOLIPIDS & VLDL)
Nephrotic Syndrome
One cause: Post-Streptococcal Infection → known as: ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS (Group A βhemolytic Streptococci – those with M PROTEIN in their cell wall induces this type of nephritis)
Blood: ELEVATED ASO Titer
NON-AGN: non-streptococcal agent (bacteria:pneumococci, viruses:mumps,Hepa B, parasitic infection:malaria)
Acute Glomerulonephritis
SCLEROSIS of the GLOMERULI
FOCAL (Occurring in some glomeruli); SEGMENTAL (Affecting a
specific area of the glomerulus)
Predominant Feature: PROTEINURIA
Focal Segmental Glomerulonephritis
Cellular Proliferation of the MESANGIUM along with LEUKOCYTE INFILTRATION & THICKENING OF THE GLOMERULAR BASEMENT MEMBRANE
Membranoproliferative Glomerulonephritis
Most prevalent type of glomerulonephritis world wide
Deposition of IgA in the GLOMERULAR MESANGIUM
IgA Nephropathy
Development: Slow and Silent
80%: have previously some form of glomerulonephritis
20%: form of glomerulonephritis that has been unrecognized
Chronic Glomerulonephritis
Follows a HYPOTENSIVE event that result in decrease
perfusion of the kidneys followed by renal tissue ischemia
3 Principal Cause:
1.Sepsis
2.Shock
3.Trauma
Acute Tubular Necrosis: ISCHEMIC ATN
exposure to NEPHROTOXIC AGENTS
Acute Tubular Necrosis: TOXIC ATN
normal solutes or substances that become toxic when their concentration in the bloodstream is excessive:
a. hemoglobin – hemoglobinuria – severe hemolytic events
b. myoglobin – myoglobinuria - rhabdomyolyis
c. uric acid
d. immunoglobulin light chain
ENDOGENOUS NEPHROTOXIN
substances ingested or absorbed
a. therapeutic agents
b. anesthetics
c. radiographic contrast media
d. chemotherapeutic drugs
e. recreational drugs
f. industrial chemicals
EXCOGENOUS NEPHROTOXIN
Impaired ability to REABSORBED GLUCOSE
Renal Glucosuria
Impaired ability to REABSORBED SPECIFIC AMINO ACIDS
Cystinuria (Cystine
and Dibasic AA)
Hartnup Disease (Monoamino – Monocarboxylic AA)
Impaired ability to REABSORB SODIUM
Bartter’s Syndrome
Impaired ability to REABSORB BICARBONATE
Renal Tubular Acidosis Type II
Impaired ability to REABSORB CALCIUM
Idiopathic Hypercalciuria
Excessive REABSORPTION of CALCIUM
Hypocalciuric Familial Hypercalcemia
Excessive REABSORPTION of SODIUM
Gordon’s Syndrome
EXCESSIVE REABSORPTION of PHOSPHATE
Pseudohypo parathyroidism
Generalized LOSS OF PROXIMAL TUBULAR FUNCTION NOT REABSORBED form the ULTRAFILTRATE & EXCRETED in the URINE: (AA, Glucose, Water, Phosphorous, Potassium, & Calcium)
Fanconi Syndrome
Impaired ability to REABSORB PHOSPHATE
Familial Hypophosphatemia
(Vitamin D Resistant Rickets)
Impaired ability to REABSORB CALCIUM
Idiopathic Hypercalciuria
Impaired ability to ACIDIFY URINE
Renal Tubular Acidosis, Types I and IV
Impaired ability to RETAIN SODIUM
Renal Salt-Losing Disorder
Impaired ability to CONCENTRATE URINE
Nephrogenic Diabetes
Excessive reabsorption of SODIUM
Liddle’s Syndrome
Inability to REABSORB INORGANIC PHOSPHATES
Renal Phosphaturia
Urethra (Urethritis)
Bladder (Cystitis)
Painful Urination (Dysuria)
Burning Sensation
Frequent urge to urinate
LOWER UTI
Renal Pelvis Alone (Pyelitis)
Renal Pelvis including Interstitium (Pyelonephritis)
Upper UTI
Bacterial infection that involves the renal tubules,
interstitium, & renal pelvis
Mechanism:
1. Movement of bacteria from the lower urinary tract to the kidney
- Localization of the bacteria from the bloodstream in the kidneys
(hematogenous infection)
Acute Pyelonephritis
Develops when permanent inflammation of
renal tissue causes permanent scarring that involves the renal calyces
and pelvis
Chronic Pyelonephritis
Allergic response to the interstitium of the kidney
Most common cause: Acute Allograft Rejection of a transplanted kidney
Acute Interstitial Nephritis
Candida species (e.g. Candida albicans) – normal
flora of GIT & vagina
Proliferation of yeasts due to: changes in pH, adversely disrupted by antibiotics
Yeast Infections
URINE SODIUM CONCENTRATION IS LOW – INCREASED AMOUNT OF SODIUM BEING REABSORBED
pre-renal
INCRASED URINARY EXCRETION OF SODIUM
Renal
Progressive LOSS of RENAL FUNCTION
“END-STAGE RENAL DISEASE” / “END-STAGE KIDNEYS”
Chronic Renal Failure
Alkaptonuria (Homogentesic Acid)
MSUD
Melanoma (Melanin)
PKU
Ferric Chloride test
Alkaptonuria (Homogentesic Acid)
Ammoniacal Silver Nitrite/Benedict’s Test
Tyrosinuria
Nitrosonaphthol Test
Porphyria (Porphobilinogen)
Hoesch Test/Watson-Schartz Test
Inborn errors of metabolism Result from: INHERITED DEFECT
Primary Aminoaciduria
SEVERE LIVER DISEASE or GENERALIZED TUBULAR
DYSFUNCTION
Secondary Aminoaciduria
DEPOSITION OF CYSTINE in the LYSOSOMES of cells throughout the body
Cystinosis
Most common & SEVERE FORM of Cystinosis
Nephropathic Cystinosis
RARE FORM of Cystinosis
Intermediate Cystinosis/Ocular Cystinosis
Autosomal Recessive
Cystinuria
Deficient Enzyme: Branched-Chain α-Keto Acid Dehydrogenase (BCKD)
Maple Syrup Urine Disease
INCREASED urinary excretion of PHENYLPYRUVIC ACID (a ketone) and its metabolites
Urine, Sweat & Breath: Characteristic MOUSY/MUSTY ODOR
Phenylketonuria
Excretion of large amount of HOMOGENTISIC ACID (HGA) in the urine
Alkaptonuria
Excretion of large amount of HOMOGENTISIC ACID (HGA) in the urine
Alkaptonuria
Increased amount of TYROSINE in the urine → occurs when → tyrosine levels in PLASMA is abnormally high
Tyrosinuria
Increased excretion of urinary melanin
Melanuria
Defective melanin production
Hypomelanosis / Albinism