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Kidney functions (5)
- 1 clearance of waste products
- 2 H20 balance (hydration)
- 3 concentration of macromolecules
- 4 electrolyte/acid-base balance
- 5 endocrine functions
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Primary Kidney Tests (3)
- 1. BUN
- 2. Creatinine
- 3. Urinalysis
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BUN basics
- Formed in liver by conversion of ammonia to urea by the urea cycle
- Freely filtered through renal glomerulus -> renal glomerular function is primary mechanism of clearance
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CREA basics
- Produced at a constant rate by breakdown of phosphocreatine in muscle tissue
- Cleared primarily by kidneys - change dependent on renal glomerular filtration rate
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Secondary Kidney Tests (11)
- 1. PCV
- 2. RBC
- 3. HGB
- 4. RETIC
- 5. Phos
- 6. Ca
- 7. Na
- 8. K
- 9. tCO2 (Bicarb)
- 10. Anion Gap
- 11. CHOL
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Azotemia is ___________
- Increased concentration of non-protein, nitrogenous waste products (creatinine or BUN) in blood
- May be due to renal or nonrenal causes
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Uremia is _____________
- Azotemia + extrarenal clinical signs
- Arises from presence of retained waste products due to azotemia
- No extrarenal signs = NOT uremic
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Clinical signs of Uremia (4)
- 1. Nausea
- 2. Vomiting
- 3. Oral ulceration
- 4. Lethargy
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Chronic muscle wasting can cause (increased/decreased) levels of creatinine
Decreased
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____________ is preferred analyte to characterize GFR because ___________
- Creatinine
- Does not reabsorb by renal tubules
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BUN variable due to (3)
- 1. Diet (^)
- 2. GI bleed (^)
- 3. Hepatic function (v)
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Urea (is/is NOT) reabsorbed by renal tubules
is
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Ammonia is largely from ______________
Digestion of proteins
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^ BUN causes (3)
- 1. ^ protein in diet
- 2. GI bleed
- 3. metabolic states causing ^ muscle breakdown
-
^ ammonia, v BUN cause
Hepatic insufficiency
-
(^/v) unrine flow = (^/v) BUN reabsorbed
- v, ^
- BUN reabsorption indirectly linked to rate of urine flow
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Types of azotemia (3)
- 1. Pre-renal
- 2. Renal
- 3. Post-renal
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Pre-renal azotemia basics
- Renal function is normal
- All causes besides diet -> reduced renal perfusion (v bloodflow to kidneys)
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USG with pre-renal azotemia
- Concentrated urine
- >/= 1.030 dogs
- >/= 1.035 cats
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Causes for v bloodflow to kidneys (3)
- 1. mod-severe dehydration
- 2. hypotension
- 3. v cardiac output (cardiac insufficiency)
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Exceptions to concentrated urine with pre-renal azotemia (2)
- 1. ^ Protein catabolism (^ protein diets, GI bleed, muscle breakdown)
- 2. ^ formation of UREA
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Renal azotemia basics
- Renal disease/failure
- Due to loss of functioning nephrons
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Azotemia is seen with ___% of renal function lost
75%
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Isosthenuria due to renal disease is seen with ___% renal function lost
66%
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Difference between renal and pre-renal azotemia
USG
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Conditions outside of renal failure that cause urine concentration loss (4)
- 1. IVF Therapy
- 2. Certain drugs (Diuretics, glucocorticoids)
- 3. Cushing's
- 4. Electrolyte abnormalities
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How does pyometra cause decreased urine concentration?
Endo toxin inhibiting ADH (anti-diuretic hormone)
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Maximum urine concentration is achieved when __________ (3)
- 1. Clinically dehydrated
- 2. Azotemic
- 3. ^ albumin
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Post-renal azotemia basics
- Adequate # of functioning nephrons
- Secondary to urinary tract obstruction or rupture, resulting in inability to eliminate waste products
- Backup continues until pressure in glomerulus equalizes with blood pressure and filtration stops
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Hydronephrosis
- Swelling of kidney due to backup of urine
- Unilateral or partial long term blockage can cause (complete blockage results in death)
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Uroabdomen
- Urine accumulates in abdomen, BUN & CREA reabsorb to attempt to equilibrate
- CREA equilibrates slower, CREA in peritoneal fluid will be >2X CREA in peripheral blood
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Post-obstructive diureses
- Lasts for 2-3 days following relief of obstruction
- ^ solute load, poor ADH response
- Concentrating ability returns over time if no renal damage
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Secondary renal tests (12)
- 1. PCV
- 2. RBC
- 3. HGB
- 4. Retic
- 5. Phos
- 6. Ca
- 7. Na
- 8. K
- 9. tCO2 (Bicarb)
- 10. Anion Gap
- 11. Chol
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Azotemia
- Increased concentration of non-protein, nitrogenous waste product (Creatinine or BUN) in blood
- May be due to renal or nonrenal causes
-
Uremia
- Azotemia + extrarenal clinical signs
- -Nausea, vomiting, oral ulceration, lethargy
- Arises from presence of retained waste products due to azotemia
-
Clearance by _____ is major variable affecting BUN and Creatinine levels
Glomerular Filtration (GFR)
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CREA (does/does not) reabsorb by renal tubules
does not
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(CREA/BUN) is the preferred anolyte to characterize GFR
CREA - does not reabsorb by renal tubules
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Chronic muscle wasting can cause ___ levels of CREA
decreased
-
BUN is variable due to (3)
- 1. ^ Diet
- 2. ^ GI bleed
- 3. v Hepatic function
-
Prerenal azotemia
- Renal function is normal
- All causes besides diet = reduced renal perfusion
- Concentrated urine
- >1.030 dogs
- >1.035 cats
-
USG should be done _________ fluids
before
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Renal Azotemia
- Renal disease/failure due to loss of functioning nephrons
- >= 75% renal function lost causes azotemia
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Inability to concentrate urine happens with ___% renal function lost
66
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Renal vs. Prerenal azotemia
USG
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Conditions that cause a loss of the ability to concentrate urine (5)
- 1. IVF therapy
- 2. Certain drugs (diuretics, glucocorticoids)
- 3. Cushings
- 4. Electrolyte abnormalities
- 5. Pyometra (E. coli endo toxing inhibiting ADH)
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Electrolyte imbalances that cause decreased urine concentration (3)
- 1. Hyponatremia - Sodium <120 (addisons)
- 2. Hypokalemia - <2
- 3. Hypercalcemia - >2 above normal
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Post-renal azotemia
- Adequate # of functioning nephrons
- Secondary to urinary tract obstruction or rupture, resulting in inability to eliminate waste products
- Backup continues until pressure in glomerulus equalizes with blood pressure and filtration stops
-
_________ Can occur with unilateral or partial long term obstruction
Hydronephrosis
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post-obstructive diuresis
- 2-3 days following relief of obstruction
- Increased solute load, poor ADH response
- Concentrating ability returns over time if no renal damage
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PCV,RBC,HGB, Retic count
- Kidney produces erythropoietin -> normal RBC development
- Chronic renal failure -> normocytic, normochromic, non-regenerative anemia
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Phos
- ^ due to v GFR (cleared by kidneys)
- May remain normal due to active tubular handling
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Ca
- Usually low normal or mildy decreased
- v ca stimulates release of PTH from parathyroid glands
- CRF - renal secondary hyperparathroidism
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