Renal Lab Eval Flashcards

1
Q

Kidney’s fxn?

A
  • excretion of waste products of metabolism
  • regulate excretion of water and solutes (Na, K, and H), through changes in tubular reabsorption or secretion
  • secretes hormones: renin, prostaglandins, and bradykinin
    erythropoietin, Ca2+, phosphorus, (and calcitriol)
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2
Q

Sxs of kidnney disease?

A
  • gross hematuria, flank pain
  • edema, HTN, signs of uremia
  • many pts are asx, only sign is elevated serum creatinine or abnorm uirnalysis
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3
Q

Azotemia?

A
  • elevated BUN and/or creatinine, buildup of abnormally large amounts of nitrogenous waste products in the blood
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4
Q

Oliguria?

A
  • urine output of less than 400 ml a day, or less tahn 20 cc/hr
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5
Q

Anuria?

A
  • hardly any output at all

- less than 100 mL/day

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6
Q

Causes of pre-renal failure?

A
  • volume contraction (dehydration)
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7
Q

Causes of intrinsic renal failure?

A
  • arteriolar damage (acute HTN)
  • glomerulonephritis
  • ATN (acute tubular necrosis)
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8
Q

Causes of post-renal obstruction?

A
  • ureteral obstruction

- bladder outlet obstruction

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9
Q

What does the GFR tell us? normals? influenced by?

A
  • sum filtration rate of all fxning nephrons
  • men norm: 130 mL/min
  • women: 120 mL/min
  • influenced by: age, sex, body size, RBF and HP in glomerulus
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10
Q

How can the GFR be measured?

A
  • CrCl
  • urea clearance
  • inulin clearance - 100% filtered, gold std for GFR
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11
Q

What is CrCl? Normals?

A
  • endogenous substance used to assess GFR
  • men (Up to 40): 107-139 ml/min
  • women: 87-107
  • overestimates true GFR by up to 40% because of active tubular secretion of creatinine
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12
Q

How does GFR correlate with kidney disease?

A
  • level of GFR has prognostic indications but isn’t the exact correlate to loss of nephron mass
  • stable GFR: doesn’t imply stable disease
  • some pts with renal disease may go unrecognized b/c of normal GFR
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13
Q

What is BUN (blood urea nitrogen)

A
  • urea nitrogen is what is formed when protein breaks down
  • normal range: 6-20 mg/dL
  • many drugs can effect the BUN
  • usually measured with creatinine to monitor kidney fxn
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14
Q

What causes an increase in BUN?

A

increases when protein is broken down and more ammonia forms:
- renal disease
- excessive protein breakdown (catabolism - tissue necrosis)
- very high protein diet
- GI bleeding***
- burns
- tetracycline
- fever
- decreased GFR: less BUN presented at glomerulus to be removed from the blood
slower transport time through PCT allows more reabsorption

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15
Q

What causes a decrease in BUN?

A
  • liver disease (liver unavailable to convert ammonia to urea then the BUN will decrease and the ammonia increases)
  • starvation
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16
Q

Where does BUN come from?

A
  • protein is cleaved from the AA and a nitrogen is left behind so it takes up 3 H+ to form ammonia
  • NH3+ is then processed through the liver to become urea
  • when urea enters to blood stream it is called BUN
  • then it is excreted by the kidney
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17
Q

How does decreased GFR lead to increased BUN?

A
  • 2 ways
    1. decreased flow through glomerulus
    2. slower transport time allows more BUN to be resorbed at level of PCT
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18
Q

What is creatinine?

A
  • formed from normal breakdown of muscle
  • more muscle mass the higher creatinine
  • lower the muscle mass the lower the creatinine (normal reduction in creatinine as a person ages and loses muscle mass)
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19
Q

Normal range of creatinine?

A
  • waste product of protein breakdown excreted by the kidneys
  • normal range: men - 0.8-1.4
    women: 0.6-1.2
  • 50% loss of renal fxn is needed to increase serum creatinine from 1-2 mg/dL
  • used in ratio with BUN to determine types of azotemia
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20
Q

In what situations is creatinine increased?

A
  • renal failure
  • diet: increased digestion of meats
  • meds: ACEIs, diuretics, NSAIDs
  • muscle disease/breakdown: muscular dystrophy, rhabdomyolysis
  • blockage at sites in DCT that allow for active secretion
  • decreased GFR as there is less creatinine presented at glomerulus to be filtered out
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21
Q

when would creatinine be decreased?

A
  • pregnancy: normal occurence

- range in pregnancy: 0.4-0.6 mg/dL (increased volume)

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22
Q

What happens to creatinine with a decreased GFR?

A
  • increases
  • instead of creatinine being reabsorbed in the tubules like BUN with a decreased GFR the creatinine is just dumped out
  • in the DCT creatinine is actively secreted from the body to be eliminated by the kidneys
  • this active secretion at the DCT can be blocked by drugs such as cimetidine and trimethoprim therefore increasing serum creatinine
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23
Q

Normal range of BUN/creatinine ratio?

A
  • normal: 10-20.1
  • elevated: greater than 20.1
  • increased ratio in a low flow (low BP) state
  • BUN/serum creatinine
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24
Q

When is BUN/creatinine ratio increased with normal creatinine?

A
  • prerenal disease (decreased renal perfusion)
  • catabolic state with increased tissue breakdown
  • GI hemmorrhage
  • high protein intake
  • certain drugs: tetracycline, steroids
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25
Q

When is BUN/creatinine ratio increased with elevated creatinine?

A
  • postrenal disease (obstructive uropathy)

- prerenal disease superimposed on renal disease

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26
Q

When is decreased BUN/creatinine (less than 10:1) with decreased BUN occur?

A
  • acute tubular necrosis (intrarenal disease)
  • low protein diet, starvation, severe liver disease
  • repeated dialysis
  • SIADH
  • pregnancy
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27
Q

When is BUN/Creatinine decreased with increased creatinine?

A
  • rhabdomyolysis

- muscular pts who develop renal failure

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28
Q

Normal values for Na and K?

A
  • Na+: 135-145 mmol/L

- K+: 3.8-5.5 mmol/L

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29
Q

Normal values for anions?

A
  • chloride: 98-106 mmol/L
  • bicarb: 21-28 mmol/L
  • total CO2: 23-30 mmol/L
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30
Q

substances that are normally reabsorbed in the kidneys?

A
  • Na+
  • K+
  • urate
  • chloride
  • Ca2+
  • phosphate ions
  • glucose
  • AAs
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31
Q

What substances are normally secreted in the kidneys?

A
  • H+
  • K+
  • urate
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32
Q

Sodium reabsorbtion in the kidneys? Impt of Na+?

A
  • freely filtered at glomerulus
  • 60% reabsorbed isotonically in PCT
  • reabsorbed in loop of Henle
  • reabsorbed in DCT, secondary to aldosterone effect
  • normall daily Na excretion balances daily intake (body needs for Na can be met by as little as 500 mg/day)
  • Na+ is extracellular ion, doesn’t move freely across the membrane, impt in cardiac and neuro fxn (too low - seizures)
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33
Q

What is hyponatremia primarily due to? Correction?

A
  • most common electrolyte disorder
  • primarily due to intake of water that can’t be excreted
  • excess Na+ loss relative to water loss occurs via renal or extrarenal routes
  • therapy: correct underlying problem, Na+ and fluid replacement
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34
Q

When does hypernatremia occur?

A
  • occurs when there is an excessive loss of water, relative to Na+
  • causes include renal and extrarenal routes
  • therapy: approp fluid replacement combined with use of diuretics to rid body of excess Na+
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35
Q

Gains and losses of K+?

A
  • major cation in intracellular compartment
  • gains: normally derived from dietary sources
    balance usually maintained in healthy persons by daily intake of 50-100 mEq
  • losses: kidneys are the main source of K loss (80-90% lost in urine, remainder lost in stool or sweat)
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36
Q

Why is it so impt to be efficient at regulating K+?

A
  • small change (1-2% of EC volume) can lead to dangerously high serum levels
  • norm: 3.5-5 mEq/L
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37
Q

What is K+ homeostasis dependent on?

A
  • pH (acid-base disturbance causes K+ shifts b/t fluid compartments, in acidosis K+ levels go up as bringing K+ out of cells into blood - diabetic ketoacidosis)
  • renal fxn including effects of diuretics aldosterone and renal parenchyma
  • GI fluid losses (excessive K+ loss with V/D)
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38
Q

What does hypokalemia result from?

A
  • K+ shifting to ICF w/o change in total amt of K+ in the body
  • depletion of body stores (diuretic therapy w/o K+ replacement)
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39
Q

When does hyperkalemia occur?

A
  • acidosis
  • from cellular damage (fever, hemolysis, rhabdomyoylsis - K+ leaking out of destroyed cells)
  • renal and adrenal diseases
  • meds (ACEIs)
  • artifical hyperkalemia: hemolyzed blood specimens, thrombocytosis or leukocytosis
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40
Q

When does hypochloremia occur?

A
- excessive loss of Cl-:
GI losses
DKA
mineralocorticoid excess
salt-losing renal diseases
high bicarb levels
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41
Q

When does hyperchloremia occur?

A
  • metabolic acidosis
  • lower GI losses (diarrhea)
  • mineralocorticoid deficiency
42
Q

Bicarb filtration?

A
  • filtered freely in glomerulus
  • 85% reabsorbed in proximal tubule
  • 15% reabsorbed in distal tubule
43
Q

Ways that urinalysis can be useful?

A
- detect systemic disturbances:
endocrine abnormalities
metabolic disturbances
- detect intrinsic kidney/urinary system disorders:
kidney disease
UTIs
44
Q

Diff ways a UA can be collected?

A
- fresh voided urine:
first morning specimen
random specimen
post-prandial (after meal)
- clean catch (midstream) urine
- catheterized specimens
- timed urine collections (24 hr)
45
Q

Best method of collecting urine sample?

A
  • first morning void is best (most concentrated)
  • record collection time
  • type of specimen (clean catch)
  • analyzed within 2 hours of collection (for best results: within 1 hr)
  • free of debris or vaginal secretions
  • storage/preservation reqd if not tested within 1 hr: refrigeration - 5 c, preservative tablets for transport
46
Q

When is a supra-pubic needle aspiration indicated?

A
  • when pt is unable to void, or there has been trauma to urethra
47
Q

3 types of examination?

A
  • physical
  • chemical
  • microscopic
48
Q

What are the physical characteristics of the urine specimen?

A

appearance (visual exam):
- color: normal varies (colorless to yellow to amber)
depends on concentration of solute (urochrome and urobilin)
- turbidity: normal=clear, cloudy when crystals or large amts of cells present
- odor
- volume: 750-2500ml in 24 hrs (avg of 1500 mL)
oliguria: output of less than 400ml/day
- anuria: less than 100 ml/day

49
Q

Examples of different odors?

A
  • ammonia like (urea splitting bacteria)
  • foul, offensive: old specimen, pus or inflammation
  • sweet: glucose
  • fruity: ketones
  • maple syrup like: maple syrup urine disease
50
Q

Examples of different colors of urine and what they could mean?

A
  • colorless: diluted urine
  • deep yellow: concentrated urine
  • yellow-green: bilirubin
  • red: blood/hemoglobin
  • brownish/red: acidified blood (Acute GN)
  • brownish-black: homogentisic acid (melanin)
51
Q

Turbidity?

A
  • looking at cells or crystals most likely if turbid
  • cellular elements and bacteria will clear by centrifugation
  • crystals dissolved by a variety of methods (acid or base)
  • microscopic exam will determine which is present
52
Q

what are all of the elements of the chem analysis?

A
  • specific gravity
  • pH
  • protein
  • glucose
  • ketones
  • bilirubin
  • urobilinogen
  • blood
  • leukocyte esterase
  • nitrite
53
Q

How is the chem analysis usually done?

A
  • by a dipstick
  • chemical presence produces color changes
  • have to read at appropriate time interval from when reagent dipstick is dipped into urine
54
Q

What is specific gravity, what does it mean?

A
  • reflects the relative proportions of dissolved solid components to total volume of specimen: degree of concentration or dilution of urine, measures concentrating abilities of the kidney
  • expected values:
    range: 1.003-1.030
    usual results: 1.010-1.025
    highest value is 1st morning specimen: greater than 1.020
55
Q

What does a low specific gravity mean?

High specific gravity?

A
  • low: diabetes insipidus - abnormal ADH
  • tubular damage and renal anomalies
  • well hydrated
56
Q

What does a high SG mean?

A
  • DM (glucose, protein, ketones concentrating the urine)
  • adrenal insufficiency
  • hepatic disease
  • CHF
  • excessive sweating or other loss of water (diarrhea, vomiting, fever)
57
Q

pH values?

A
  • urine acidity due primarily to acid phosphates
  • pH of less than 7= acid urine
  • pH of gerater than 7= alkaline urine
  • expected values: normal kidneys produce urine with pH varying from 4.5-8
  • freshly voided urine: 6
58
Q

Acidic urine?

A
  • high protein diets
  • meds
  • uncontrolled diabetes or other causes of metabolic acidosis
59
Q

Alkaline urine?

A
  • normal, post-prandial physiology
  • diets high in veggies, milk, and other dairy
  • meds
  • UTI
60
Q

What makes up the protein in the urine? Expected results?

A
  • majority is globulins (Lower MW than corresponding serum globulins)
  • 1/3 albumin
  • tamm-horsfall mucoprotein: normal urinary protein not found in plasma (matrix to make casts)
  • up to 2.5 mg/dL
  • expected results:
    avg 40-80 mg protein excreted per day
    100-150 mg/day in WNL therefore concentration in random urine is 2-8 mg/dL

***proteinuria is the single most impt indicator of kidney disease

61
Q

Albumin will show up in urine for what reasons?

A
  • strenous exercise
  • emotional stress
  • pregnancy
  • infections
  • glomerulonephritis
  • neonates (1st week)
62
Q

Globulins will show up in urine for what reasons?

A
  • glomerulonephritis

- tubular dysfunction

63
Q

Hemoglobin will show up in urine for what reasons?

A
  • hematuria

- hemoglobinuria

64
Q

Fibrinogen will show up in urine for what reasons?

A
  • severe renal disease
65
Q

Bence Jones proteins will show up in urine for what reasons?

A
  • myeloma (there will be alot of protein)

- leukemia

66
Q

How is protein detected in the urine?

A
  • microalbuminuria: not detected on normal dipstick
    requires use of special dipstick for microalbuminuria less than 50 mg/dl
  • proteinuria: generally requires 24 hr urine collection for total protein
    start in am with first void and collect for 24 hrs keeping specimen in the refrigerator
  • total amt of protein excreted is measured
67
Q

Causes of benign proteinuria?

A
  • functional changes: (increased metabolic rate) high fever, CHF, strenuous exercise, cold exposure
  • orthostatic: occurs when upright (common in adolescence)
68
Q

What is an early indicator of kidney disease?

A
  • microalbuminuria: 30-100 mg/24 hrs
69
Q

What constitutes proteinuria?

A
  • greater than 100 mg in 24 hrs
70
Q

When does glucosuria occr?

A
  • whenever blood glucose level exceeds the renal threshold
  • ability of renal tubule to reabsorb, only can absorb 180 mg/dl
  • condition may be benign (renal glycosuria) or pathological: DM
  • renal glycosuria occurs after heavy meals and emotional stress
71
Q

What is ketonuria the result of?

A
  • of fatty acid metabolism which occurs when there is:
    inadequate carbs in the diet
    and when there is a defect in carb metabolism
72
Q

Clinical significance of ketonuria?

A

-DKA in DM
- restricted carb diet in assoc with:
fever, anorexia, GI disturbances, fasting/starvation, neuro disorders, anesthesia

73
Q

expected values of bilirubin? clinical significance of bilirubinuria?

A
  • reflects serum levels of conjugated (direct) bilirubin
  • negative urine test is normal
  • concentration in urine is normally less than 0.02 mg/dL
  • clinical significance of bilrubinuria:
    hepatocellular disease, biliary obstruction or any disease that increases the amt of conjugated bilirubin
  • can be an early indicator of disease, even before jaundice is present
74
Q

How is urobilinogen produced?

A
  • bilirubin is conjugated in the liver and secreted into the bile
  • bile enters intestinal tract where bacterial action converts bilirubin to urobilinogen
  • excreted in feces or reabsorbed into portal circulation
  • removed by the liver and/or excreted in the urine
75
Q

Normal urinary excretion rates?

clinical significance of increased urobilinogen?

A
  • normal rate: 1-4 mg/24 hr
  • clinical significance of increased urobilinogen:
    pernicious anemia
    liver disease: hepatitis, cirrhosis, CHF
  • urobilinogen is decreased/absent in obstruction of bile duct
76
Q

What is hematuria? Hemoglobinuria? Normal test?

A
  • hematuria: intact red cells in the urine
  • hemoglobinuria: free hemoglobin in the urine
  • myoglobinuria - also produced positive test
  • normal: neg test for blood
77
Q

Clinical significance of hematuria or hemoglobinuria?

A
  • hematuria: renal disease, infections, neoplasm, trauma
  • hemoglobinuria: any of the above plus transfusion reactions, hemolytic anemia, paroxyysmal nocturnal hemoglobinuria (PNH), severe burns, various poisonings
78
Q

What is leukocyte esterase? Clinical significance?

A
  • neutrophilic granulocytes release esterases into urine when present
  • normals: no WBCs, negative esterase
  • clinical significance of + test:
    pyuria (presence of WBCs in urine)
  • bacteriuria/UTI
79
Q

Nitrites?

A
  • nitrates are normal urinary constituent but nitrites are NOT
  • some gram neg bacteria are nitrate reducers producing nitrites, therefore, the presence of nitrites in the urine indicates bacteriuria
80
Q

What nitrate reducing organisms are most comonly found in urine?

A
  • E. coli - 72%
  • klebsiella/enterobacter - 16%
  • streptococcus faecalis - doesn’t reduce nitrate
81
Q

What are frequently seen elements in microscopic analysis?

A
  • crystals
  • cells
  • infectious agents
  • casts
82
Q

Procedure of examining microscopic elements?

A
  • centrifuge 10-15 ml urine 5-10 min at 1500-2000 rpm
  • decant/discard supernatant urine
  • examine under low (10x) and high (40x) magnifications
83
Q

Causes of acidic urine crystals?

A
  • uric acid (kidney stone, gout)
  • amophous urates
  • bilirubin
  • cystine (rare)
  • cholesterol (rare)
  • leucine (rare)
  • tyrosine (rare
84
Q

Causes of neutral urine crystals?

A
  • calcium oxalate
  • hippuric acid
  • triple phosphate
85
Q

Causes of alkaline urine crystals?

A
  • calcium carbonate
  • ammonium biurate
  • calcium phosphate
86
Q

What are the cellular elements of the UA?

A
  • RBC
  • WBC
  • epithelial cells: renal tubular cells (round, slightly larger than WBC), transitional cells (flat, cuboidal, columnar), squamous (large flat cells)
87
Q

Infectious agents on microscopic exam?

A
  • yeast (urinary moniliasis): haephea (tree branch)
    candida albicans (and others)
    especially in pts with diabetes
  • parasites: trichomonas, schistosoma haematobium
88
Q

How are casts formed?

A
  • decreased urinary flow

- increased concentration of solutes

89
Q

When are RBC casts formed?

A
  • acute inflammatory or vascular disorder in glomerulus causing renal hematuria
  • may be the only manifestation of acute glomerulonephritis
90
Q

When are WBC casts formed?

A

(think infection)

  • these indicate kindey inflammation
  • acute pyelonephritis
  • interstitial nephritis, proliferative glomerulonephritis
91
Q

How do RBC casts appear under microscope?

A
  • muddy brown color
92
Q

When are hyaline casts observed in the urine?

A
  • these are only slightly more refractile than water and have a transparent, empty appearance
  • hyaline casts may be observed with small volumes of concentrated urine or with diuretic therapy and are generally nonspecific
  • clear on microscopic exam
93
Q

When are granular casts seen in the urine?

A
  • these are coarsely and finely granular
  • leakage and aggregation of proteins
  • coarse, deeply-pigmented granular casts are considered characteristic of ATN
94
Q

Waxy casts?

A
  • last stage in degeneration of granular cast

- waxy casts are nonspecific and may be observed in a variety of acute and chronic kidney diseases

95
Q

Significance of cellular casts?

A

getting casts: coming from kidneys - RBC/erythrocyte casts, leukocyte casts, and bacterial casts

  • if you are just getting cells: single erythrocytes, single leukocytes, single bacteria
    this could be coming from kidney down through bladder
96
Q

What are common findings in acute tubular necrosis?

A

dipstick:

  • decreased SG
    • for blood
  • positive for protein
  • microscopic:
    renal tubular epithelial cells
    pathological casts (intra-renal problem)
97
Q

Common findings in acute glomerulonephritis?

A

dipstick:

  • blood: increased
  • protein: increased

microscopic:
erythrocytes (dysmorphic)
erythrocyte casts
mixed cellular casts

98
Q

Common findings in chronic glomerulonephritis?

A

dipstick:
decreased SG
increased blood
incread protein

microscopic:
pathological casts (broad waxy casts, RBCs)
99
Q

Common findings in acute pyelonephritis?

A
  • dipstick:
    trace proteins
    positive nitrites
    positive L.E.
microscopic:
bacteria
leukocytes
leukocyte, granular and waxy casts (intra-renal)
renal tubular epithelial cell casts
100
Q

common findings in nephrotic syndrome?

A
  • a lot of protein (++++)

microscopic:
oval fat bodies (dumping protein)
fatty casts
waxy casts

101
Q

Common findings in eosinophilic cystitis?

A
    • blood
  • microscopic: numerous eosinophils (Hansel’s stain)
  • no significant casts
102
Q

Common findings in urothelial carcinoma?

A
    • blood

microscopic:
malignant cells on urine cytology (urine sample should be submitted separately to cytology, void or 24 hr sample)