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Clinical Pathology > Renal Biochemistry Profile, Pt. 2 > Flashcards

Renal Biochemistry Profile, Pt. 2 Flashcards

1
Q

How is azotemia commonly determined by USG?

A
  • pre-renal = hypersthenuria
  • renal = isothenuria
  • post-renal = variable
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2
Q

How can PE findings and bloodwork confirm pre-renal azotemia?

A

PE = tacky mucous membranes, poor skin turgor

BLOODWORK = increased PCV, increased TP, and increased ALB due to dehydration

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3
Q

Other than dehydration, what can cause pre-renal azotemia? What are 3 of the most common causes?

A

chronic bleeding (HYPOVOLEMIA)

  1. GI ulceration due to prednisone or NSAID therapy
  2. bleeding GI tumor
  3. coagulopathy due to decreased PLTs, DIC, warfarin, or liver failure
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4
Q

What are the 2 hallmark signs of renal disease (until proven otherwise)? What is unique in cats?

A
  1. azotemia
  2. isosthenuria

cats maintain some concentrating ability with renal failure

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5
Q

What is the best clue for determining renal azotemia?

A

USG —> concentrating/diluting ability of the kidney implies functional nephrons

  • if urine is not concentrated or not appropriate for the patient’s hydration status, the cause of azotemia is probably renal
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6
Q

What signalment is most susceptible to post-renal azotemia? What are the 3 most common PE findings?

A

castrated males

  1. straining to urinate
  2. large turgid bladder
  3. distended abdomen (uroabdomen)
    - all due to blockage
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7
Q

What should be considered when an animal’s USG is isosthenuric, but they are not azotemic?

A
  • history, signalment, PE
  • hydration status
  • possible interference with kidney concentration ability (calcium, cortisol, etc.)
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8
Q

Azotemia approach:

A
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9
Q

What are the 2 tiers of evaluating a patient with renal azotemia?

A

FIRST TIER = BUN, creatinine, USG

SECOND TIER = phosphorus, calcium, potassium, sodium, chloride, bicarbonate, anion gap

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10
Q

How should phosphorus levels change with renal azotemia? What is the mechanism? What 2 species show variation?

A

hyperphosphatemia

GFR drops below 25% and phosphorus excretion is impaired, allowing for its accumulation and a risk for mineralization of soft tissues (Ca x P > 70)

  1. HORSES - lose P from the gut
  2. CATTLE - lose P in saliva
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11
Q

What must be measured to get an accurate calcium reading during renal azotemia? Why?

A

ionized calcium

total calcium may be increased, but ionized calcium will be more accurately normal or decreased

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12
Q

How do the calcium levels change with renal azotemia? What is the mechanism? In what animals is this most common?

A

normocalcemic at the early/mild stages that develops into hypocalcemia

renal damage causes decreased renal tubular calcium resorption, which results in renal tubular production of vitamin D and hyperphosphatemia —> physiologic response of decreasing calcium and deposition into tissues

dogs, cats, ruminants

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13
Q

What does the hypocalcemia resulting from renal azotemia commonly result in? What 4 biochemical changes are observed?

A

renal secondary hyperparathyroidism due to decreased calcium causing the stimulation of PTH release

  1. azotemia
  2. increased P
  3. normal to decreased Ca
  4. increased PTH
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14
Q

How does the calcium response in horses with renal azotemia compare? Cats?

A

hypercalcemia - diet and excretion

hypercalcemia - chronic renal failure thought to be caused by receptor abnormalities (tertiary hyperparathyroidism)

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15
Q

How do patients with hypercalcemia and renal failure present on USG? Why?

A

hyposthenuric - calcium interferes with ADH receptors

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16
Q

How are potassium levels commonly altered with chronic renal failure? What is the mechanism in the 2 species this occurs in?

A

hypokalemia

  1. CATS - unknown hypokalemic nephropathy
  2. CATTLE - renal loss, salivary loss, anorexia, metabolic acidosis
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17
Q

What are the 2 mechanisms of hyperkalemia in renal azotemia? When is this life-threatening?

A
  1. oliguria/anuria - kidney unable to excrete potassium in end-stage and acute renal failure
  2. metabolic acidosis - hydrogen ions move intracellularly and potassium ions move extracellulary

acute renal failure and urethral obstructions

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18
Q

Sodium and chloride are most commonly normal in cases of renal failure. How are they altered if observed? In what 2 situations is this most common?

A

hyponatremia and hypochloremia

  1. chronic kidney failure, especially in horses and cattle, causing them to eat less (decreased Na/Cl intake)
  2. always a finding in uroabdomen
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19
Q

How is bicarbonate and the anion gap commonly affected by renal failure? What are the 3 mechanisms?

A

severe renal disease causes metabolic acidosis

  1. increased urinary loss of bicarbonate
  2. decreased tubular secretion of H+ ions
  3. production of sulfates and phosphates

DECREASED bicarb, INCREASED anion gap

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20
Q

What 2 characteristics affect glomerular filtration? What type of proteins pass?

A
  1. size (<68 kDa)
  2. electrical charge (negative charge at podocyte)

small proteins with positive charges —> most resorbed i the proximal tubule and not detected in the urine sample

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21
Q

How is proteinuria measured? What are the 6 levels? What protein is it best at detecting?

A

reagent strip - negative, trace, +, ++, +++, ++++

albumin

22
Q

When is protein (albumin) measurable in the urine? What are the 4 categories of proteinuria?

A

protein either got past the glomerulus or entered after the glomerulus

  1. pre-renal
  2. glomerular
  3. tubular
  4. post-renal
23
Q

What are the 2 main causes of pre-renal proteinuria?

A
  1. physiologic - hypertension, fever, seizure, strenuous exercise
  2. increase in small protein in the blood - hemoglobin, myoglobin, paraproteins (Bence-Jones)
24
Q

What are the 2 types of renal proteinuria? What causes each?

A
  1. glomerulonephritis - damages barrier by antigen-antibody complexes or amyloid
  2. tubular proteinuria - acute renal disease, Fanconi’s syndrome
25
Q

What is Fanconi’s syndrome?

A

defective proximal tubules where filtered proteins are not resorbed, causing renal proteinuria

26
Q

What are 2 causes of post-renal proteinuria?

A
  1. hemorrhage - RBC in urine caused by vessel damage from inflammation, trauma, neoplasia, or coagulopathies
  2. inflammation - WBC in urine caused by UTIs or cystitis
27
Q

How is proteinuria quantified? What type is most severe?

A

urine protein:creatinine ratio (UPCR)

  • normal < 0.5
  • tubular or glomerular > 0.5
  • glomerular > 1.0

GLOMERULAR

28
Q

What is characteristic of glomerular proteinuria?

A

decreased serum albumin (hypoalbuminemia)

29
Q

What are the main 2 signalments to patients with glomerulonephropathy? How do most patients present?

A
  1. familial often manifests young
  2. secondary causes, like chronic infectious disease, noninfectious inflammatory disease, or neoplasms, manifests middle-aged to older

many are asymptomatic, some are sick with underlying disease

30
Q

What is the pathogenesis of glomerulonephropathy? What does this result in?

A

damage to podocytes, most commonly by deposition of antigen-antibody complexes or amyloid, causes the podocytes to retract and allow the filtration of larger, negatively charges proteins

protein loss exceeds protein production, especially albumin and antithrombin —> hypoalbuminemia, hypercoagulability

31
Q

What 3 biochemical markers are observed with glomerulonephropathy?

A
  1. moderate to marked hypoalbuminemia
  2. moderate to marked proteinuria
  3. +/- evidence of renal insufficiency
32
Q

What is nephrotic syndrome? What 5 conditions are characteristic?

A

protein-losing nephropathy that leads to abdominal effusion

  1. proteinuria (glomerular disease)
  2. hypoalbuminemia
  3. abdominal effusion (decreased oncotic pressure)
  4. hypercholesterolemia
  5. hypercoagulable state (antithrombin loss)
33
Q

What differentiates acute from chronic renal failure?

A

speed of development NOT severity

34
Q

What patients are most commonly presenting with acute renal failure?

A

any signalment - acute onset of clinical signs (get sick fast)

35
Q

How will patients with acute renal failure commonly appear? What are the 3 most common signs?

A

good BCS

  1. GI: anorexia, vomiting, diarrhea, halitosis (NH3)
  2. renal: oliguric to anuric
  3. neuro: depressed to obtunded to non-responsive, seizures
36
Q

What are the 3 most common etiologies of acute renal failure? What is the characteristic feature?

A
  1. toxicants - lily toxicity in cats
  2. renal ischemia
  3. infection - leptospirosis
    - (things that damage the kidneys swiftly!)

marked decrease in GFR leading to azotemia

37
Q

What are the 3 most common bloodwork findings with acute renal failure?

A
  1. azotemia (occurs fast, within hours to days)
  2. +/- hyperkalemia
  3. +/- acidemia
38
Q

What are the 4 most common urinalysis findings with acute renal failure?

A
  1. oliguria to anuria due to an abrupt decrease to GFR
  2. variable USG
  3. +/- proteinuria
  4. +/- cellular casts due to tubular epithelial cells
39
Q

How do patients commonly present with chronic kidney failure?

A

extremely common in cats and geriatric animals with a poor BCS and dehydration —> slow onset of clinical signs

40
Q

What is the etiology of chronic kidney disease in cats? What are 4 common clinical signs?

A

irreversible chronic interstitial fibrosis

  1. GI: anorexia, vomiting, diarrhea, halitosis (NH3)
  2. renal: polyuric
  3. neuro: depressed
  4. cardio: hypertension
41
Q

What are the main 2 differences in end-stage chronic kidney failure compared to earlier chronic kidney failure?

A
  1. hyperkalemia
  2. oliguria to anuria
42
Q

What gender most commonly presents with uroabdomen? What are the 2 most common causes? How will these animals present?

A

males

  1. trauma: birth (foals), HBC (dogs)
  2. chronic urethral obstruction

abdominal effusion

43
Q

What are the most common serum electrolyte imbalances with uroabdomen?

A

hyperkalemia and hyponatremia

44
Q

How does the kidney retain and excrete electrolytes and proteins? How is this affected by uroabdomen?

A

HEALTHY: kidney conserves Na and Cl (plasma); excreted CREA, urea, and K (urine)

UROAB: Na and Cl move into urine, causing their decrease in plasma (hyponatremia and hypochloremia); urea and K move into the plasma (azotemia, hyperkalemia); CREA remains in urine since it is a larger molecule and moves slowly

45
Q

What are the 5 common bloodwork findings in uroabdomen?

A
  1. hyponatremia
  2. hyperkalemia
  3. hyphochloremia
  4. azotemia (increased BUN)
  5. +/- increased CREA from previous post-renal disease
46
Q

What is characteristic of the abdominal effusion in uroabdomen? When is it diagnostic?

A

modified transudate (non-inflammatory) with high CREA concentration

when CREA concentration of the effusion is 2x the CREA concentration in the plasma

47
Q

Categorized the azotemia:

A

normal - all within RI

48
Q

Categorize the azotemia:

A

renal azotemia - urine is diluted with increased BUN and CREA

(USG is the best value used to categorize azotemia!)

49
Q

Categorize the azotemia:

A

pre-renal - urine in concentrated

(use USG to categorize azotemia!)

50
Q

How do the values in the renal failure cases prove the bladder is still intact?

A

cases 4 and 5 have azotemia and abdominal effusion CREA is about the same as serum CREA

Clinical Pathology (33 decks)

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