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
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2
Q

What are the different ways to classify proteinuria?

A
  • Pre-renal, renal and post-renal
  • Physiologic/functional vs. pathologic
  • Glomerular, tubular, interstitial
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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
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4
Q

Post-renal proteinuria

A
  • Urinary or reproductive tract inflammation and hemorrhage
  • Leakage of plasma proteins into urine
  • *Always look at sediment findings
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5
Q

What are the different types of renal proteinuria?

A
  • Glomerular (pathologic)
  • Tubular (pathologic)
  • Interstitial (pathologic)
  • Physiologic/functional (non-pathologic)
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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)
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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
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8
Q

Interstitial: renal proteinuria

A
  • Altered vascular permeability, hemorrhage or inflammation within kidney parenchyma
  • Pyelonephritis, leptospirosis, renal neoplasia, nephroliths
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9
Q

Physiologic/functional: renal proteinuria

A
  • Transient, mild proteinuria
  • Heat, stress, seizure, venous congestion, extreme exercise, hyperadrenocorticism
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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
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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
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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!
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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
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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&raquo_space;> globulin)
    o May progress to non-selective
    o Proteinuria will eventually result in tubular damage and interstitial inflammation
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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
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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
Q

What might be present with urinary tract obstruction?

A
  • Hematuria
  • Stranguria
  • Pollakuria
  • Abdominal pain
26
Q

Minimum database: urinary tract obstruction

A
  • AKI: severe azotemia, severe electrolyte imbalances
  • Hyperkalemia >7 mEq/L can induce severe bradycardia
27
Q

What might cause uroabodomen?

A
  • 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
Q

How do you diagnose uroabdomen?

A
  • Appropriate history, PE findings
  • Common findings on minimum database
  • Imaging (abdominal fluid, bladder may appear normal)
  • Abdominal fluid analysis
29
Q

What are the common lab abnormalities seen in urine with uroabdomen?

A
  • higher urea, creatinine, K+
  • lower in Na, Cl, “free water”
30
Q

What are the common lab abnormalities in bloodwork with uroabdomen?

A
  • *hyponatremia, hypochloremia
  • *hyperkalemia
  • *azotemia
  • Hyperphosphatemia
  • Metabolic acidosis
  • Evidence of dehydration
  • +/- inflammation on CBC
31
Q

What does the peritoneal fluid look like in uroabdomen?

A
  • 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
Q

Why don’t we measure urea on a fluid analysis for uroabdomen?

A
  • Urea is much SMALLER and diffuses quickly across peritoneum to equilibrate
33
Q

Lilly toxicity in cats

A
  • 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%