Renal 1 Flashcards
1
Q
Azotemia
A
- Increase serum urea and/or creatinine due to decreased renal excretion
- Prerenal, renal, postrenal
2
Q
Pre-renal azotemia
A
- Reduced renal blood flow decreases GFR, leading to decreased urea and/or creatinine excretion
- Dogs USG>1.030
- Cats USG>1.035
- Large animals USG>1.025
3
Q
What are the common causes of pre-renal azotemia?
A
- **Dehydration
- Shock, blood loss, decreased CO, etc
4
Q
Renal azotemia
A
- Renal pathology causes decline in GFR, thus decreased urea/creatine excretion
- *need loss of at least 75% of renal mass
- Loss of 2/3rds=concentrating defects
o See inadequate USG before azotemia (cats may be an exception) - *creatine is more reliable than urea in horses and cattle
o Urea can be excreted into GI and broken down to AA - **isothenuria is common (USG: 1.008-1.012=approximate to plasma)
5
Q
What are the common causes of renal azotemia?
A
- Primary renal disease (Ex. glomerulonephritis)
- Secondary renal injury (ex. ischemia)
6
Q
Renal azotemia USG expected
A
- Dogs USG<1.030
- Cats USG<1.035
- Large animals USG<1.025
- *unless there are other diseases or conditions affecting urine concentrating ability independently of renal failure
7
Q
Post-renal azotemia
A
- Pathology distant to nephron
- History and clinical findings
- USG if variable
o Depends on hydration, concurrent renal disease or post-obstructive diuresis
8
Q
What are the common causes of post-renal azotemia?
A
- Urinary tract obstruction leading to uroabodomen
9
Q
How do we differentiate between types of azotemia in clinical patients?
A
- Need USG and hydration status to determine type
o May be more than one
o USG measured on a refractometer
10
Q
What are some lab indicators of renal disease?
A
- Markers of GFT
o Urea/creatinine
o SDMA
o Clearance tests: not often performed - Other common lab findings seen with azotemia
- Urinalysis
11
Q
Creatinine
A
- Derived from creatine phosphate (skeletal muscle)
- Freely filtered and not reabsorbed by kidney
- *high variability
o Sequentially measurements are helpful
12
Q
Elevated creatinine
A
- Decreased GFR from prerenal, renal and/or postrenal azotemia
13
Q
Decreased creatinine
A
- Decreased muscle mass (young or small breed dog, cachexia, starvation)
- Increased GFR (pregnancy)
- Overhydration
14
Q
Urea
A
- Synthesized by hepatocytes from ammonia generated from protein catabolism
- Secreted by kidneys, GI, system and sweat
o 40-60% of filtered urea is reabsorbed in tubules
o Added to many bovine diets
15
Q
Increased urea
A
- Increased protein catabolism
- Increased protein digestion
- Decreased GFR
16
Q
Decreased urea
A
- Decreased protein intake
- Increased excretion: any cause of polyuria (ex. DM)
- Decreased production: liver disease or (rare) urea cycle enzyme deficiencies
17
Q
Increased urea, normal creatine
A
- Upper GI bleeding
- Increased protein catabolism
- Azotemia in a patient with decreased muscle mass
18
Q
Normal urea, increase creatine
A
- Normal finding in heavily muscled animals (greyhouds, draft horses, bulls)
- Azotemia in a patient with liver disease/low protein diet/metabolism of urea by GI flora (horses and cattle)
19
Q
SDMA (symmetric dimethylarginine)
A
- Marked as a sensitive and early marker of GFR declining
o Increases with 40% loss of renal mass
o NOT affected by decreased muscle mass but may be decreased in hyperthyroid cats - Increased azotemia types (NOT pathognomic for renal disease)
- *higher sensitivity but lower specificity than creatinine
20
Q
Interpreting SDMA
A
- Non-renal factors can elevate SDMA
- Mild SDMA elevations should be interpreted cautiously
- Monitoring SDMA from trends can be helpful
- Both creatinine and SDMA are used to stage CKD
21
Q
What are other common lab findings associated with decreased GFR?
A
- Hyperphosphatemia
- High AG metabolic acidosis
o Retention of renal acids and/or lactic acid - Alterations in serum potassium
o Hyperkalemia (acute renal failure, UT obstruction or rupture)
o Hypokalemia (CKD) - Alterations in total calcium
- Evidence of dehydration: hyperalbuminemia, erythrocytosis
- Non-regenerative anemia (CKD)
22
Q
Acute kidney injury (AKI)
A
- Rapid deterioration in renal function over hours to days (48h to 7d)
- May be transient or persistent and progressive
- Can complicate pre-existing CKD
- Can be difficult to differentiate from prerenal azotemia
23
Q
What might acute kidney injury occur from?
A
- Decreased renal perfusion (hypovolemia, low BP)
- Intrinsic renal disease (tubular necrosis or inflammation)
- Postrenal causes: UT obstruction or rupture
24
Q
Acute kidney disease
A
- Renal dysfunction persisting for 7-90days
25
Q
Chronic kidney disease
A
- Slowly progressive, chronic deterioration of kidney function (>90days)
- May or may not be preceded by acute kidney injury
- *different stages
26
Q
What are common causes of chronic kidney disease?
A
- Glomerulonephritis
- Amyloidosis
- Breed-related
- Inherited renal dysplasia
27
Q
Chronic kidney disease in horses
A
- Relatively uncommon (vs. acute kidney injury)
- Chronic interstitial nephritis
- Glomerulonephritis
- Ancillary diagnostics: ultrasound, renal biopsy, evaluate BP
- *treatment focuses on slowing down progression and avoiding additional renal insults
28
Q
Ca/P balance in horses with kidney disease
A
- Horses absorb much larger amounts of Ca from their diet than other species
o No dependent on Vit D metabolism
o Excess is excreted in kidneys
o *why calcium carbonate crystals are in a normal finding - *hypercalcemia is common in equine CKD due to decreased renal excretion
- Often see low or low-normal phosphorus
29
Q
Dogs and cats: CKD
A
- **Tend to see opposite as horses (low Ca and high P)
o High P: decreased GFR leads to decreased P excretion
o May not see high P with mild azotemia or early CKD
30
Q
Renal dysplasia in Shih Tzu dogs
A
- Diagnosis: renal failure (CKD) in young dogs
o Age of onset/rate of progression depends on severity of dysplasia
o Ultrasound
o Definitive diagnosis requires renal biopsy/necropsy (retention of immature glomeruli) - *hereditary but mechanism unclear
- *majority of affected dogs go undetected and can pass the defect on
31
Q
Acute on chronic kidney disease (ACKD)
A
- AKI can occur in animals with CKD
32
Q
AKI: physical exam
A
- Good body and muscle condition
- Normal to enlarged and often painful kidneys
- Lack of signs of chronicity
33
Q
ACKD: physical exam
A
- Poor body condition or muscle wasting
- Small irregular kidneys
- Signs of chronicity
o History of PU/PD, weight loss, pale gums
34
Q
What are some ancillary tests to differentiate between AKI and ACKD?
A
- Imaging
- Renal biopsy
- Renal FNA/cytology
- Region specific test
35
Q
Monitoring of AKI, AKD and CKD
A
- Biochem panel
- Urinalysis
- Blood pressure measurement
- +/- UPC ratio
- +/- urine culture
- *if serially increasing creatinine or increase UPC=disease is progressing
36
Q
Monitoring for AKI
A
- Point of maximal recovery is when creatinine/SDMA plateau +/- increase USG
- Early detection of progression of disease is important
- Typically recheck renal parameters at 1 week, 3 months and than every 6 months
37
Q
Monitoring for CKD
A
- Recommended:
o q6 months (stage ½ or early stage3)
o q3 months (stage 3, early stage 4)
o q1-2 months (late stage 3, stage 4)
38
Q
What may be seen in the urinalysis of a patient with renal tubular injury from AKI?
A
- Glucosuria
- Proteinuria
- Granular casts
- Waxy casts
39
Q
Casts formation
A
- Can form anywhere in tubules
- Appearance depends on composition and length of time it remains in tubules
- Form with degeneration and necrosis of tubular epithelial cells
o Granular and waxy casts reflect LATER stages of degeneration of renal tubular epithelial cells in a cast - *may be present in animals w/o renal disease/tubular injury
o Hyaline casts, low numbers of fine granular casts
