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Y4 SA - Urogenital > Glomerulopathies > Flashcards

Glomerulopathies Flashcards

1
Q

The filtration barrier of the glomeruli has 3 different layers, what are they?

A

Fenestrated endothelial cells
Glomerular basement membrane
Podocytes

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2
Q

What is the function of the filtration barrier in the glomerulus?

A

Together they create a size and charge selective barrier
Prevents most of proteins from leaking into the urine

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3
Q

How is filtration different in renal tubules?

A

Renal tubules excrete or reabsorb
Because they have active and passive transporters

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4
Q

What is the hallmark signs of a glomerulopathy?

A

Proteinuria

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5
Q

Are glomerulopathies more common in dogs or cats?

A

Dogs
Tubulointerstitial lesions more common in cats

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6
Q

Describe protein loss in tubulointerstitial disease

A

A tubulointerstitial disease has an inability to reabsorb what’s gone into the interstitium so only a small amount of protein is lost into urine

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7
Q

Describe the pathogenesis of glomerulopathies

A

Can be immune-mediated (a.k.a. acquired) and non-immune mediated (e.g. amyloidosis)
- Immune mediated mechanism = type 3 hypersensitivity

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8
Q

Describe the pathogenesis of immune mediate glomerulopathies

A
  • Circulating immune complex may become trapped in the glomerulus or may be formed in situ
  • Their presence will lead to inflammation (activation complement, recruitment inflammatory cells) -> further damage to the kidney
  • Any severe, chronic inflammatory responses can result in a glomerulopathy so when these occur you need to think about the underlying pathological cause
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9
Q

List some infective causes of glomerulopathies

A

Leptospira spp
Leishmania spp
Borrelial burgdorferi
Babesia spp
Erlichia spp
Anaplasma spp
Toxoplasma
FIP
FeLV/FIV
Sepsis
Pyometra

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10
Q

List some inflammatory causes of glomerulopathies

A

Severe pancreatitis
SIRS
Chronic inflammation
Hyperglobulinemia - multiple myeloma, B cell lymphoma
Hyperadrenocorticism

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11
Q

What are hereditary glomerulopathies?

A

Breeds that are predisposed to glomerular diseases
These breeds tend to present at a young age, then progress rapidly

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12
Q

Which breed is predisposed to Familial Glomerulopathy - Amyloidosis

A

Shar-pei

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13
Q

Describe familial glomerulopathy amyloidosis in Shar-peis

A
  • Shar-pei’s commonly preceded by episodes of “shar-pei’s fever”: self-limiting hyperthermia, swollen joints
  • Formation and deposit of amyloid plaques in the glomeruli
  • Usually very high UPC (average 9)
  • Usually rapidly progressive
  • Treatment: colchicine and/or DMSO but no evidence that either bring benefit
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14
Q

What factors may lead to the suspicion of a glomerulopathy?

A
  • Unexpected proteinuria on urinalysis
  • Investigating renal disease
  • Hypertension of unknow origin
  • Hypoalbuminemia and/or hypercholesterolemia
  • Thromboembolic events
  • Breed at risk
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15
Q

How can you confirm the proteinuria?

A

Can be easily detect with a dipstick
- Not 100% sensitive because the result can be affected by urine pH and the concentration
- But these are quick and cheap
If positive, the value should be quantified by Urine Protein Creatinine Ratio (UPCR)

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16
Q

What feature of proteinuria should be assessed?

A

Important to evaluate the persistence: proteinuria should be repeatable on at least three urine samples obtained at least 2 weeks apart

17
Q

List 4 causes of a pre-renal proteinuria

A

Fever
Systemic inflammation
Haemoglobinuria
Myoglobinuria

18
Q

List 3 causes of a post-renal proteinuria

A

UTI
Nephrolithiasis
Tumours of the urinary tract

19
Q

What is the gold standard for diagnosis of glomerulopathies?

A

Renal biopsy

20
Q

Describe renal biopsies for glomerulopathies

A
  • When performed, samples have to be manage in a specific way and sent to specialist renal pathologist centres
  • Samples have to be examined by: light microscopy, immunofluorescence and electron-microscopy
  • In absence of biopsy, proteinuria can be used as marker
21
Q

What must be done before glomerulopathies are treated?

A

Quantify by UPCR
Confirm persistent proteinuria
Renal origin (Rule out Pre /Post Proteinuria)

22
Q

How can the magnitude of the proteinuria suggest its origin?

A

If >2 = glomerulopathy
If <2 = tubulointerstitial

23
Q

What is the standard treatment for proteinuria?

A

RAAS blockade: ACE-inhibitors OR angiotensin receptor blockers
Telmisartan licensed only for cat: benazepril should be used as first line, following the cascade

24
Q

How does a RAAS blockade treat proteinuria? Side effects?

A
  • Decrease the pressure in the efferent arteriole more than the afferent so glomerular pressure is reduced
  • Side effect: when glomerular pressure is reduced, this also decreased the GFR
  • Can worsen how they are in the short term as azotaemia is worsened
25
Q

Is immunosuppressive treatment indicated for glomerulopathies?

A
  • About 50% of glomerulopathies are the results of deposition of immunocomplex
  • A proportion of these will respond to immunosuppressive medication
    When to consider the use of immunosuppressive medication: Use if biopsy suggests an immune-mediated disease (rarely done though). If biopsies are not possible (costs, lack of personal trained, contraindicated), you can immunosuppress if the animal is doing badly on standard treatment.
26
Q

What must you be aware of when using steroids?

A

Be aware that as most of the diseases, use of steroids will impact the possibility to have a diagnosis in the future!!!!

27
Q

Name the 5 major complications of glomerulopathy treatment

A
  • Thromboembolism
  • Azotaemia
  • Systemic hypertension
  • Diet
  • Oedema
28
Q

Describe thromboembolisms as a complication of glomerulopathy treatment

A

Patients with glomerulopathies are classified as HIGH RISK of thromboembolism, and it is the main cause of death

29
Q

How can you treat thromboembolisms as a complication of glomerulopathy treatment

A

Recommendation is to start thromboprophylaxis treatment
Antiplatelets: Clopidogrel (especially in cats)
Anti-coagulant: Apixaban or Rivaroxaban (monitor for signs of bleeding)

30
Q

Describe systemic hypertension as a complication of glomerulopathy treatment

A
  • Common consequence in glomerulopathy
  • Patients can be non-azotaemic but hypertensive
  • Hypertension lead to progression kidney disease, glomerulopathy and end-organ damage (eye, heart, CNS, kidney)
  • To be treated if BP > 170mmHg or evidence of target organ damage (TOD)
31
Q

How can you treat hypertension as a complication of glomerulopathy treatment

A

Dog: benazepril, then amlodipine
Cat: amlodipine or telmisartan

32
Q

Describe azotaemia as a complication of glomerulopathy treatment

A
  • 60% of the patients are azotaemic on presentation
  • Once established the patient is azotaemic, treat as per IRIS recommendation (classed as CKD)
  • Need to make sure the azotaemia is persistent and not a one off measurement
33
Q

Describe a suitable diet for a dog with glomerulopathy/being treated

A
  • Renal food recommended as containing highly digestible protein source which reduce proteinuria and progression azotaemia (IRIS guidelines)
  • Omega-3 supplementation reduce glomerular inflammation
  • The animal must eat!! If not eating renal diet, use other diets: starvation increase catabolism of body protein –> increase protein processed by kidney
34
Q

Describe oedema as a complication of glomerulopathy treatment

A
  • Glomerulopathies predispose to nephrotic syndrome
  • Usually associated with renal sodium retention
  • Dogs resistant to formation of oedema (incomplete nephrotic syndrome)
35
Q

What are the signs of nephrotic syndrome?

A

Hypoalbuminemia
Proteinuria
Hypercholesterolemia
Oedema

36
Q

How can you treat oedema as a complication of glomerulopathy treatment

A

Treatment is with diuretics:
- Furosemide: pulmonary oedema/hyperK
- Spironolactone: pleural or abdominal effusion
Presence of nephrotic syndrome carriers a very bad prognosis

Y4 SA - Urogenital (12 decks)

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