Renal 2 Flashcards
1
Q
Why is proteinuria important?
A
- Can be an early indicator of kidney disease
- May lead to progression of CKD
- When treated, can slow CKD progression and improve survival
2
Q
What are the different ways to classify proteinuria?
A
- Pre-renal, renal and post-renal
- Physiologic/functional vs. pathologic
- Glomerular, tubular, interstitial
3
Q
Pre-renal proteinuria
A
- Overabundance of low molecular weight (LMW) proteins (hemoglobin, myoglobin, Bence-Jones)
- Overwhelm resorptive capacity of proximal tubule (“overload proteinuria”)
- Usually mild, may NOT be detected on dipstick
4
Q
Post-renal proteinuria
A
- Urinary or reproductive tract inflammation and hemorrhage
- Leakage of plasma proteins into urine
- *Always look at sediment findings
5
Q
What are the different types of renal proteinuria?
A
- Glomerular (pathologic)
- Tubular (pathologic)
- Interstitial (pathologic)
- Physiologic/functional (non-pathologic)
6
Q
Glomerular: renal proteinuria
A
- Renal disease increases glomerular permeability (selective or non-selective)
- Amyloidosis, glomerulonephritis
- Can be severe: urine protein to creatinine ratio variable but supported when >2
- May develop significant hypoalbuminemia (chem panel)
7
Q
Tubular: renal proteinuria
A
- Tubular malfunction or damage leads to decreased reabsorption/increased leakage
- Fanconi syndrome, renal ischemia, nephrotoxins (aminoglycosides)
- Usually mild, urine protein to creatinine ratio <2
8
Q
Interstitial: renal proteinuria
A
- Altered vascular permeability, hemorrhage or inflammation within kidney parenchyma
- Pyelonephritis, leptospirosis, renal neoplasia, nephroliths
9
Q
Physiologic/functional: renal proteinuria
A
- Transient, mild proteinuria
- Heat, stress, seizure, venous congestion, extreme exercise, hyperadrenocorticism
10
Q
Urine dipstick to evaluate proteinuria
A
- More sensitive to albumin than other proteins
- Need to interpret relative to urine specific gravity
- *pre-renal and post-renal need to be ruled out to diagnose renal proteinuria
11
Q
When might false negative results occur on a urine dipstick to evaluate proteinuria?
A
- Low molecular weight proteins
- Low [albumin]
- Dilute urine
- *false positives are also possible
12
Q
Urine protein to creatinine ratio
A
- Gold standard test for proteinuria (quantitative test)
- Eliminates the variability caused by differences in the USG
- Monitoring can be helpful to assess response and trends
- **only run samples with quiet urine sediment!
13
Q
What are some guidelines for interpreting urine protein to creatine (UPC) ratio?
A
- Ideally: evaluate UPC on 2 samples, 2 weeks apart
- If persistently borderline proteinuric=reassess in 2 months
- Proteinuria may decline as renal dysfunction worsens
14
Q
What is protein-losing nephropathy (PLN)
A
- Glomerular disease alters the glomerular function barrier allowing protein to ESCAPE into the urine
o Initially, proteinuria is selective (albumin»_space;> globulin)
o May progress to non-selective
o Proteinuria will eventually result in tubular damage and interstitial inflammation
15
Q
What is the most common cause of protein-losing nephropathy?
A
- **Immune-complex glomerulonephritis
- Renal amyloidosis
- *mean age of onset in dogs is 5-8 years
16
Q
What are the common lab findings of protein-losing nephropathy?
A
- Proteinuria in excess of USG
- Not azotemic and able to concentrate urine
o Renal tubules are functional until LATE in the disease - May see selective hypoalbuminemia on chem panel
17
Q
What are possible sequelae to protein-losing nephropathy?
A
- **Hypertension
- Hypercoagulability and thromboembolism
o due to loss of antithrombin III and platelet hyperresponsiveness (many treated with low dose aspirin) - edema/ascites: severe albuminemia (<10-12 g/dL)
- nephrotic syndrome
18
Q
Amyloidosis
A
- most commonly from misfolding of APP serum amyloid A resulting in AA amyloidosis
- persistence, long term high SAA can result in accumulation of AA amyloid in tissues
- secondary amyloidosis occurs from chronic inflammatory disease
- hereditary amyloidosis occurs in some breeds (shar-pei)
19
Q
Membranous glomerulonephropathy
A
- immune complexes (immunoglobin and antigen) deposited on glomerular basement membrane and can activate the complement system
- often associated with infections (Leishmania, Lyme disease)
o could be neoplasia, inflammatory disease, sulpha drugs and unknow causes
20
Q
What is seen with nephrotic syndrome? (4)
A
- Hypoalbuminemia
- Proteinuria (due to albuminuria)
- Hypercholesterolemia
o Due to increased synthesis and impaired catabolism/clearance of lipoproteins - Edema/ascites
21
Q
How do you diagnosis protein-losing nephrotic syndrome?
A
- Significant, persistent PROTEINURIA (UPC >0.5 dogs, >0.4 cats)
o If UPC >2 = supports glomerular (rather than tubular) disease
o Perform paired urine evaluations 3-4 weeks apart
o Rule out other causes of proteinuria (sediment exam) - Standard tests
- Imaging studies (ultrasound)
- Renal biopsy needed for definitive diagnosis
- DNA test for PLN-associated variant genes in dogs (Airedales, Wheatons)
22
Q
What are some standard tests to uncover a potentially treatable cause of PLN?
A
- Minimum database
- Titers for common tick-borne disease
- Heartworm testing (dogs)
- FeLV testing (cats)
23
Q
What are some examples of things that cause urinary tract obstruction?
A
- Urethral calculi (dogs)
- Matrix-crystalline plugs (young male cats)
- Ureter uroliths (geriatric cats)
- *imaging can help to localize
- *beware of post-obstructive diuresis that can last 1-5 days
24
Q
Post-obstructive diuresis
A
- Response by kidneys to remove accumulated volume and solute after bladder outlet obstruction is relieved
- Massive polyuria can result in significant dehydration and hypokalemia and low USG
25
What might be present with urinary tract obstruction?
- Hematuria
- Stranguria
- Pollakuria
- Abdominal pain
26
Minimum database: urinary tract obstruction
- AKI: severe azotemia, severe electrolyte imbalances
- Hyperkalemia >7 mEq/L can induce severe bradycardia
27
What might cause uroabodomen?
- Trauma
- Inflammation/infection
- Neoplasia
- Calculi obstruction
- Iatrogenic injury
- *early clinical signs may be non-specific and many still have normal urination
o May develop fluid wave, abdominal pain, uremia
28
How do you diagnose uroabdomen?
- Appropriate history, PE findings
- Common findings on minimum database
- Imaging (abdominal fluid, bladder may appear normal)
- Abdominal fluid analysis
29
What are the common lab abnormalities seen in urine with uroabdomen?
- higher urea, creatinine, K+
- lower in Na, Cl, “free water”
30
What are the common lab abnormalities in bloodwork with uroabdomen?
- *hyponatremia, hypochloremia
- *hyperkalemia
- *azotemia
- Hyperphosphatemia
- Metabolic acidosis
- Evidence of dehydration
- +/- inflammation on CBC
31
What does the peritoneal fluid look like in uroabdomen?
- Usually pale yellow
- Initially low cell count, low protein concentration (transudate)
- Will become exudative with time (see increased proportion of neutrophils)
- Rarely can see urine crystals
- *confirm by measuring creatinine
o Fluid creatinine >2x serum creatinine
32
Why don’t we measure urea on a fluid analysis for uroabdomen?
- Urea is much SMALLER and diffuses quickly across peritoneum to equilibrate
33
Lilly toxicity in cats
- all parts are very nephrotoxic to cats
o acute tubular necrosis
o vomiting and hypersalivation may occur within several hours (acute kidney injury develops within 24hrs)
o if treatment is delayed=mortality from acute RF is 50-100%
