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Clin Chem > Primary Renal Panel > Flashcards

Primary Renal Panel Flashcards

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1
Q

Primary Renal Panel (3 major components)

A
  1. BUN
  2. Creatinine
  3. UA (with USG)
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2
Q

Factors that can influence BUN values

A
  1. GI tract
  2. Liver dysfunction
  3. Renal insufficiency
  4. Polydipsia
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3
Q

GI influence on BUN

A

Increased BUN

  1. Enteric hemorrhage (moderte)
  2. High protein diet (mild)
  3. TERMINAL starvation (rare, mild)–breakdown all proteins to survive

Decreased BUN

  1. Anorexia (mild)
  2. Low protein diet– some Hill’s

-RUMINANTS –bacteria degrade –> keep BUN lower than creatinine

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4
Q

Liver influence on BUN

A

Decreased liver function –> decreased synth of BUN

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5
Q

Renal influence on BUN

A

Passive diffusion ONLY

  • freely filtered
  • 40-60% tubular reabsorption (flow RATE dependent) –> creates medullary gradient
    - increased flow rate –> decreased absorption
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6
Q

Polydypsia influence on BUN

A

Decreased BUN
Increase H2O –>increase GFR–> increased tubular flow rate –> decreased Urea reabsorption –> decreased medullary gradient –> dilute urine formed

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7
Q

3 types of Azotemia (differentiate and MOA)

A
  1. Pre-renal
    - Azotemia + adequate USG
    - 1. decreased blood flow (flow or volume) to kidney
    - 2. increased production of nitrogenous waste
  2. Renal
    - Azotemia + inadequate USG
    - 1. Glomerular damage
    - 2. Tubular damage
  3. Post Renal
    - Azotemia + variable USG
    - obstruction/rupture
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8
Q

What causes lack of concentrating ability, NOT related to tubular destruction?

A
  1. Fluid therapy
  2. ADH deficiency (Central Diabetes insipidus)
  3. Tubules refractory to ADH (Renal diabetes insipidus)
  4. Medullary washout –loss of osmotic gradient
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9
Q

What effects creatinine levels

A
  1. Muscle mass
    - creatinine = degradation product of creatine –> freely diffuses out of muscle cells
  2. Dietary intake
    - high meat diet (not significantly)
  3. Renal
    - Freely filtered at kidney w/o reabsorption
    - EXCEPTION = Goats –> secrete
  4. Sweat (minimal)
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10
Q

What is the source of BUN

A

Protein catabolism

–> ammonia –> urea

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11
Q

What is Azotemia?

A

abnormal accumulation of NITROGENOUS wastes in blood

-may be asymptomatic

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12
Q

What is Uremia?

A

clinical signs assoc.’d w/ renal failure!

  • Vomiting / diarrhea
  • Tachypnea (acidosis)
  • Lethergy
  • Petechiae (interfere with clotting factors)
  • mineralization
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13
Q

What is Isothenuria?

A

Urine ~ plasma
1.008 - 1.012
can occur in healthy animal–depending on hydration status

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14
Q

What is Adequate USG

  • Dog
  • Cat
  • other
A

Minimum USG in the face of NEED for H2O conservation

Dog: >1.030
Cat: >1.035
others: >1.025

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15
Q

Interpret: Extremely high BUN w/ normal creatinine

A

Creatinine is more specifically reflects GFR
- BUN has many extra renal dz
Consider – GI hemorrhage

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16
Q

Interpret: Mildly low BUN w/ normal creatinine

A

Creatinine is more specifically reflects GFR

Consider: anorexia, liver

17
Q

Interpret: Normal BUN w/ increased creatinine

A

Creatinine –suggests decrease GFR
Bc BUN is not also increased, suggests concurrent process
Consider: Decreased urea production/ conversion

18
Q

Interpret: Normal BUN w/ low creatinine

A

Consider:

  1. Increased GFR w/ increased urea production
  2. Decreased muscle mass
19
Q

What are the mechanisms of Primary Renal Azotemia

A
  1. Decreased Blood flow
    - Decreased blood volumes
    - Altered blood flow
  2. Increased production of nitrogenous
    - BUN not equal to creatinine
20
Q

What is Secondary renal azotemia

A

Renal parenchyma may be relatively unaffected
-Decreased GFR + 2ndary tubular dysfunction

Mechanisms:

  1. Fluid therapy
  2. ADH deficiency (primary diabetes insipidus)
  3. Tubules refractory to ADH
  4. Medullary washout
21
Q

Effect of Hypercalcemia (on Renal panel)

–what is the primary cause of hypercalcemia

A

Primary cause = Lymphoma

  • Central effect
    - Moderate decrease in release of ADH
  • Renal Effect
    - In ability to assemble AQP’s
22
Q

Effect of Pyometra and Pyelonephritis (on Renal panel)

A

Bacterial toxins interfere with ADH funx

  • -usually reversible
  • important to think about when considering Sx
23
Q

Effect of Cushing’s (on Renal panel)

A

Glucocorticoid interferes w/ ADH receptors

24
Q

2 components associated with Renal Azotemia

A
  1. Glomerulus – Azotemia

2. Tubules – Inadequate Concentration

25
Q

Reasons for tubule become insensitive to ADH

A
  1. Hypercalcemia
  2. Pyometra
  3. Pyelonephritis
  4. Hypokalemia (cats w/ CRD)
  5. Cushing’s Dz –can concentrate if H2O deprived
26
Q

Cause of Medullary washout

A
  1. Low sodium
  2. Low Urea
    - -If animal has chronic PU/PD for another condition –> medullary wash out –> continued PU/PD after correction of other condition
27
Q

How do you Dx PostRenal Azotemia

If animal urinates, does is it R/O

A

Azotemia + Variable USG

  • Hx
  • PE
  • imaging
28
Q

Which is more SENSITIVE to GFR?

BUN vs Creatinine

A

EQUALLY SENSITIVE!!

29
Q

Which is more SPECIFIC to changes in GFR?

BUN vs Creatinine

A

Creatinine

-bc it has less other factors influencing it.

30
Q

What is a good way to monitor progression of renal failure? (and predict live expectancy)

A

Graph “1/creatinine” vs TIME = Linear

**creatinine vs GFR is NOT linear

31
Q

Explain why Cholesterol is included in the Secondary Renal Panel
( what is a ddx for this change )

A
  • Protein-losing nephropathy –> decreased oncotic pressure –> stimulates the Liver to synth Lipoproteins (cholesterol)–> hypercholesterolemia

Ddx of hypercholesterolemia

  1. Protein Losing nephropathy
  2. Hepatobiliary dz
  3. Pancreatitis
  4. DM
  5. Cushings
  6. Hypothyroidism

Clin Chem (12 decks)

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