Primary Renal Panel (3 major components)
- BUN
- Creatinine
- UA (with USG)
Factors that can influence BUN values
- GI tract
- Liver dysfunction
- Renal insufficiency
- Polydipsia
GI influence on BUN
Increased BUN
- Enteric hemorrhage (moderte)
- High protein diet (mild)
- TERMINAL starvation (rare, mild)–breakdown all proteins to survive
Decreased BUN
- Anorexia (mild)
- Low protein diet– some Hill’s
-RUMINANTS –bacteria degrade –> keep BUN lower than creatinine
Liver influence on BUN
Decreased liver function –> decreased synth of BUN
Renal influence on BUN
Passive diffusion ONLY
- freely filtered
- 40-60% tubular reabsorption (flow RATE dependent) –> creates medullary gradient
- increased flow rate –> decreased absorption
Polydypsia influence on BUN
Decreased BUN
Increase H2O –>increase GFR–> increased tubular flow rate –> decreased Urea reabsorption –> decreased medullary gradient –> dilute urine formed
3 types of Azotemia (differentiate and MOA)
- Pre-renal
- Azotemia + adequate USG
- 1. decreased blood flow (flow or volume) to kidney
- 2. increased production of nitrogenous waste - Renal
- Azotemia + inadequate USG
- 1. Glomerular damage
- 2. Tubular damage - Post Renal
- Azotemia + variable USG
- obstruction/rupture
What causes lack of concentrating ability, NOT related to tubular destruction?
- Fluid therapy
- ADH deficiency (Central Diabetes insipidus)
- Tubules refractory to ADH (Renal diabetes insipidus)
- Medullary washout –loss of osmotic gradient
What effects creatinine levels
- Muscle mass
- creatinine = degradation product of creatine –> freely diffuses out of muscle cells - Dietary intake
- high meat diet (not significantly) - Renal
- Freely filtered at kidney w/o reabsorption
- EXCEPTION = Goats –> secrete - Sweat (minimal)
What is the source of BUN
Protein catabolism
–> ammonia –> urea
What is Azotemia?
abnormal accumulation of NITROGENOUS wastes in blood
-may be asymptomatic
What is Uremia?
clinical signs assoc.’d w/ renal failure!
- Vomiting / diarrhea
- Tachypnea (acidosis)
- Lethergy
- Petechiae (interfere with clotting factors)
- mineralization
What is Isothenuria?
Urine ~ plasma
1.008 - 1.012
can occur in healthy animal–depending on hydration status
What is Adequate USG
- Dog
- Cat
- other
Minimum USG in the face of NEED for H2O conservation
Dog: >1.030
Cat: >1.035
others: >1.025
Interpret: Extremely high BUN w/ normal creatinine
Creatinine is more specifically reflects GFR
- BUN has many extra renal dz
Consider – GI hemorrhage
Interpret: Mildly low BUN w/ normal creatinine
Creatinine is more specifically reflects GFR
Consider: anorexia, liver
Interpret: Normal BUN w/ increased creatinine
Creatinine –suggests decrease GFR
Bc BUN is not also increased, suggests concurrent process
Consider: Decreased urea production/ conversion
Interpret: Normal BUN w/ low creatinine
Consider:
- Increased GFR w/ increased urea production
- Decreased muscle mass
What are the mechanisms of Primary Renal Azotemia
- Decreased Blood flow
- Decreased blood volumes
- Altered blood flow - Increased production of nitrogenous
- BUN not equal to creatinine
What is Secondary renal azotemia
Renal parenchyma may be relatively unaffected
-Decreased GFR + 2ndary tubular dysfunction
Mechanisms:
- Fluid therapy
- ADH deficiency (primary diabetes insipidus)
- Tubules refractory to ADH
- Medullary washout
Effect of Hypercalcemia (on Renal panel)
–what is the primary cause of hypercalcemia
Primary cause = Lymphoma
- Central effect
- Moderate decrease in release of ADH - Renal Effect
- In ability to assemble AQP’s
Effect of Pyometra and Pyelonephritis (on Renal panel)
Bacterial toxins interfere with ADH funx
- -usually reversible
- important to think about when considering Sx
Effect of Cushing’s (on Renal panel)
Glucocorticoid interferes w/ ADH receptors
2 components associated with Renal Azotemia
- Glomerulus – Azotemia
2. Tubules – Inadequate Concentration
