Glomerular Disease Flashcards

1
Q

What causes proteinuria?

A

Physiological: strenuous exercise, fever, stress

Pre-renal: abnormal concentrations of proteins being presented to the kidneys (multiple myeloma: Bence-Jones proteins)

Renal: defective renal fxn or inflammation of renal tissue (glomerular or tubular)

Post-renal: inflammation in the ureter, bladder, urethra or prostate

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2
Q

How is proteinuria first detected?

A

On the urine dipstick!

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3
Q

What protein are dipsticks most sensitive to?

A

Albumin

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4
Q

If you suspect multiple myeloma but the dipstick comes back as normal, should you rule out MM?

A

No! Bence jones proteins which are monoclonal protein produced by plasma cells and usually occurs w MM and don’t get picked up on dipstick

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5
Q

What is the gold standard method to quantifying proteinuria?

A

24 hour urine protein measurement but it’s difficult to do so not used clinically

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6
Q

How do we quantify proteinuria?

A

Urine protein: creatinine ratio

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7
Q

If sediment is negative, what UPC ratios in cats and dogs are considered non proteinuric, borderline proteinuric and proteinuric?

A

Dogs Cats

0.5 >0.4 Proteinuric

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8
Q

What are the ways renal proteinuria can occur?

A
Defective renal fxn: 
   1. Glomerular pathology 
   2. Tubular pathology 
Inflammation of renal parenchyma: 
   1. Pyelonephritis 
   2. Acute tubular necrosis
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9
Q

How does glomerular disease occur?

A

Due to INCREASED glomerular permeability

Leads to greater protein loss (UPC ratio >2.0)
If UPC ratio >8 consider amyloidosis

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10
Q

How does tubular disease occur?

A

Due to DECREASED tubular protein reabsorption

UPC ratio usually

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11
Q

Why does CKD result in proteinuria?

A

Due to adaptive changes within the nephron

Causes low level proteinuria

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12
Q

T/F CKD can be caused by primary glomerular pathology (especially dogs) . . . causing a significant proteinuria.

A

True!

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13
Q

What is the most significant proteinuria?

A

Protein Losing Nephropathy (PLN)

Term used for condition causing severe proteinuria due to primary glomerular dz

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14
Q

What are glomerulonephritis?

A

Group of conditions where immune complexes are deposited in the glomeruli. More common in dogs than cats.

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15
Q

What causes glomerulonephritis?

A
  1. Chronic antigenic stimulation: inflammation (immune mediated dz, chronic inflammatory dz); infectious (endocarditis, leishmania, erlichia); neoplasia
  2. Idiopathic 50%
  3. Familial Nephropathy basement membrane: X linked hereditary PLN of Samoyeds or Alport syndrome of English Cocker Spaniels (type IV collagen dz)
  4. Glomerulonephritis may be d/t immune complex deposition in glomerulus
  5. Immune complex glomerulonephritis (ICGN)
  6. Amyloid deposits in glomeruli: Familial in Shar pei, Beagle, Abyssinian and Siamese
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16
Q

How do we screen for neoplasia?

A

Thoracic radiographs and abdominal ultrasound

17
Q

How many times should we test for BP?

A

five times!

18
Q

Regarding blood pressure, what organs would show of evidence of end organ damage?

A

Kidneys, brain, eyes, heart. Especially eyes!

19
Q

How do we measure hyper coagulability?

A

Thromboelastography

20
Q

What are the clinical signs of glomerulonephritis?

A
Early Signs: 
  - may have no clinical abnormalities 
  -loss of body condition 
  -lethargy, anorexia 
Later: nephrotic syndrome 
Very Late: uremic syndrome
21
Q

What characterizes nephrotic syndrome?

A

kidney dz characterized by edema and loss of protein from the plasma into the urine d/t increased glomerular permeability

  • abdominal and pleural fluid
  • subcu pitting edema
  • acute onset blindness (hypertensive retinopathy)
  • thromboembolic dz
22
Q

When are kidney biopsies contraindicated?

A

IRIS stage IV or coagulopathies

23
Q

What are common findings in nephrotic syndrome?

A
  1. proteinuria
  2. hypoALB
  3. ascites/edema
  4. hypercholesterolemia
  5. often have systemic hypertension and hyper coagulability
24
Q

How do we tx glomerulonephritis?

A

Immunosuppressive therapy

  • provided proteinuria has been confirmed to be glomerular in origin
  • provided a biopsy confirms ICGN (immune complex glom nephritis)
25
Q

When are immunosuppressive therapy contraindicated?

A
  1. pancreatitis
  2. bone marrow suppression
  3. DM
26
Q

What is the ideal deal for immunosuppressive therapy?

A

Mycophenolate: recommended as the first choice, rapid onset, low rate of adverse drugs runs

27
Q

If hypertension is present, how do we tx it?

A

ACE inhibitors or ARBs or Calcium channel blockers (amlodipine)

28
Q

We use ACE inhibitors and ARB to treat proteinuria. Why?

A

ACEi: inhibit RAAS

  • reduce intraglomerular BP
  • contraindicated in IRIS Stage IV
  • monitor creatinine-discontinue if increased >30%
  • titrate dose

ARB

  • more complete blockade
  • may be used in combination
29
Q

How do we tx hyper coagulability?

A

Aspirin or Clopidogrel

DO NOT: drain effusions unless you have difficulty breathing or treat w diuretics unless difficult breathing !!

30
Q

What is the prognosis ?!

A

Variable depending on underlying cause and severity of dysfxn