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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is proteinuria first detected?

A

On the urine dipstick!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What protein are dipsticks most sensitive to?

A

Albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do we quantify proteinuria?

A

Urine protein: creatinine ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does tubular disease occur?

A

Due to DECREASED tubular protein reabsorption

UPC ratio usually

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why does CKD result in proteinuria?

A

Due to adaptive changes within the nephron

Causes low level proteinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

True!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are glomerulonephritis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
When are immunosuppressive therapy contraindicated?
1. pancreatitis 2. bone marrow suppression 3. DM
26
What is the ideal deal for immunosuppressive therapy?
Mycophenolate: recommended as the first choice, rapid onset, low rate of adverse drugs runs
27
If hypertension is present, how do we tx it?
ACE inhibitors or ARBs or Calcium channel blockers (amlodipine)
28
We use ACE inhibitors and ARB to treat proteinuria. Why?
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
How do we tx hyper coagulability?
Aspirin or Clopidogrel DO NOT: drain effusions unless you have difficulty breathing or treat w diuretics unless difficult breathing !!
30
What is the prognosis ?!
Variable depending on underlying cause and severity of dysfxn