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Renal > Proteinuria > Flashcards

Proteinuria Flashcards

1
Q

How can proteinuria be quantified?

A
  • dip stick
  • sulphosalicylic acid test
  • 24hr protin loss
  • UPC
  • protein electrophoresis
  • albumin quantification methods
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2
Q

Is dipstick measurement reliable? Pros and cons

A 
\+ cheap 
\+ convenient
\+ qualitative
- trace 1+ usually normal 
- must consider with USG 
- only useful in identifying severe proteinuria
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3
Q

What is UPC?

A
  • urine protein creatinine ratio adjust level of protein for concetnratino of urine (^ conc = ^ creatinine)
  • practice for routine clinical use
  • high day-today variability so ideally measure several times OR pool samples (cheaper)
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4
Q

How is UPC used for IRIS staging?

A

0.4 (caats) or 0.5 (dogs) = proteinuric

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5
Q

Where can protein be lost within the kidney?

A 
> pre-glomerular
- ^ amount low molecular weight proteins presented to filter
- cannot all be reabsorbed
> renal 
- glomerular
- tubular 
> post-glomerular/renal 
- addition of protein to  urine after formation in the kidney
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6
Q

Which proteins specifically are commonlyl lost in the urine d/t pre-renal causes?

A

> bencejones proteins : IG light chains

- plasma cell tuymours (or serious inflam?? maybes)

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7
Q

Causes of post-renal proteinuria

A

> LUT
- haemorrhage
- inflam/infection
- neoplasia
* importance of blood contamination over-emphasised - urine must be grossly contaminated before this casues proteinuria)
UTI
- effect highly variable and difficult to predict
- should be r/o before proceding with work up for glomerular causes of proteinuria

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8
Q

Is any protein usually excreted by the kidney?

A

YES small amount always

  • mild increases may be d/t glomerular hypertension or tubular dysfunction
  • serious pathological increases likely d/t 1* glomerular dz
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9
Q

How id gross proteinuria defined?

A

UPC >3 (by hattie, no actual definition)

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10
Q

What is PLN

A

> Protein losign nephropathy

  • clinical syndrome of severe gross proteinuria
  • may -> hypoproteinaemia
  • caused by glomerular disease
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11
Q

What is the glomerular barrier made up of?

A
  • fenestrated endothelial cells
  • basement membrane
  • epithelial cell foot processes/slit pores (modified adherent junction)
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12
Q

When should you suspect PLN?

A
  • routine screening UA
  • hypoalbumenaemia (specifically disopproportionate albumen v cf. pan hypoproteinaemia)
  • breeds at risk
  • associated diseases
  • r enal failre
  • clinical signs of PLN
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13
Q

Ddx for panhypoproteinamiea and hypoalbumenaemia

A 
> v albumen 
- PLN
- hypoadenocorticism (?)
- liver failure 
> v protein in general 
- PLE
- haemorrhage
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14
Q

What is nephrotic syndrome?

A
  • proteinuria
  • hypoalbumenaemia
  • hyperlipidaemia
  • oedema/fluid accumulation in body cavities
    > NOT necessarily always azotaemic
    > may occour in 1/3 glomerular disease dogs
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15
Q

Clinical signs of PLN

A
  • nephrotic syndrome e
  • muscle wasting/weight loss/malaise
  • azotaemix CKD (sometimes)
  • Azotaemic AKI (rarely)
  • signs of underlying dz
  • hypertension
  • thromboembolism
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16
Q

Why do PLN pateitns get thromboemboli?

A
  • loss of anti-thrombin (same size as albumen)
  • frequently fatal
  • only part of the explanation
17
Q

Diagnostic plan for PLN patietns

A 
>  in all proteinuric patients 
- urea/creatinine/USG 
- albumin/cholesterol 
- urine culture
- blood pressur
- fundic exam 
> to ID a underlying cause 
- CBC/chemistry 
- imaging 
- serology
- CSF/joint taps 
- FeLV fiv 
- specific tests
18
Q

What needs to be attempted in PLN cases?

A

> identify underlying cause

  • NIN (neoplastic, infectious or non, inflammatory)
  • many patients cannot identify underlying cause
19
Q

What are the different causes of glomerular disease and how can these be dx?

A 
> amyloidosis 
> immune-complex glomerulonephritis
- ICGN
- many different types 
> minimal change dz
- lesions only visible with electron microscopy 
> glomerulosclerosis 
- scarring of glomeruli 
- many types 
> familial glomerulopathy 
- check pure breeds 
- consider in young dogs 
- look up PDF
- no specifics Tx 
- breeding programmes 
*can only be distinguished on biopsy*
20
Q

How may travel history assist with dx of PLN

A
  • leishmania
  • heartworm (dirofilaria)
  • Lyme dz (borrelia burgderfori)
21
Q

How may drug Hx assist with dx of PLN?

A 
> steroids 
- ^ proteinuria 
- glomerulosclerosis 
> sulphonamides
- esp dobermans 
> tyrosine kinase inhibitors (MCT chemo) 
- freq -> proteinuria 
- minimal change dz
22
Q

Outline non-specific Tx options for PLN

A

> glomerular haemodynamics
- v glomerular pressure hence GFR -> v proteinuria
- slows dz progression
- v inflam response
diet
- mild protein restriction (counterintuitive)
- reduce proteinuria
- protein high biological value
- omega 3 fatty acid (DHA/EPA)supplements
- sodium restriction
ACEI
- proven benefit (idiopathic and familial glomerular disease)
- indicated in all patients with GROSS proteinuria
- angiotensin receptor blockers (ARBs) reasonable alternative
anti-thrombotic Tx
- aspirin (low dose 0.5-1mg/kg)
- reduced thromboembolism
- clopidogrel an alternative
- delay starting this if potential renal biopsy
antihypertensive Tx
- guided by BP measurement
- ACEI or ARB
- combo with amlodipine if BP remains high
Tx oedema /ascites
- sodium restriction
- thoracocentesis
- abdomenocentesis (only if significant abdo discomfort)
- diuretics (avoid if poss)
- colloids if necessary prior to biopsy

23
Q

Pros and cons of renal biopsy

A 
*PROS*
> specific Tx
- immunosuppression
- aim to induce remission 
> breed management 
> prognostication 
*CONS*
> risks
- haemorrhage 
- renal injury 
> complications 10% dogs 20% cats 
> expensive
24
Q

Outline practical technique of renal biopsy

A 
> US guided or surgical wedge biopsy 
> cortical tissue 
> specialist fixative 
- formalin (H&E, Congo red, PAS) 
- Michels (IHC)
- gluteraldehyde (electron microscopy)
25
Q

Why are specialist nephropathy labs needed to analyse renal tissue ?

A
  • amyloidosis can be reliably distinguished on light microscopy
  • requires very thin sections, multiple stains and interpretation by a specialist
  • definitive ID of immunoglobulin deposits often only poss with ELECTRON microscopy
26
Q

Which species and PDF most commonly get immune complex glomerulonephritis?

A 
> dogs 
- more common 
- broad age range 
- M=F
> cats
- uncommon
- young adults 
- M>F
27
Q

Tx immune complex nephritis?

A

> remove inciting cause
-eliminate antigenic source
- often no cause can be identified
- removal may not be possible (eg, hard to remove tumour)
immunosuppression
- uncertain benefit
- proteinuria may worsen with steroids
- ONLY INDICATED IF BIOPSY SHOWS IMMUNE-COMPLEXES
- consult with specialist first
- many drug protocols
amyloidosis
- extra-cellular deposition insoluble fibrillar proteins in tissue
- compromise organ function
- if deposited in medulla will not be proteinuric

28
Q

Pathophysiology of reactive systemic amyloidosis

A
  • inflam tissue unhurt -> SAA protein -> insoluble AA amyloid and soluble peptides
  • chronic inflammation and familial disease decreases soluble peptide fraction
29
Q

Specific Tx of amyloidosis

A
  • no identified Tx to solubilise amyloid fibrils once formed
    > colchicine
  • consider in high risk animals (esp. sharpeis with recurrent hock swelling)
  • unproven benefit
  • may cause GI upset
  • not advised once patient azotaemic
30
Q

Monitoring Tx of proteinuria

A
  • sequential evaluation UPC
  • in combination with serum creatinine conc
  • as no functioning nephrons declines UPC may decline
31
Q

Px proteinuria

A
  • variable
  • often progressive
  • remission and recovery occasionally reported
  • worse if azotaemic
  • poor if have nephrotic syndrome
32
Q

What usually maintians low urine protein conc?

A
  • glomerular filtration barrier sorts by charge and prticle size (-ve charge barrier facilitates passage of ctions, impedes anions - most proteins are anions)
  • reabsoprtion in PCT of low molecular weight proteins
33
Q

What is the protein normally present in urine made from?

A
  • low molecular wt proteins freely filtered and not reabosorbed
  • 25-70% urine protein larger (
34
Q

Why may quantification of urinary proteini loss be undertaken?

A
  • abnormal protein on urine dipstick
  • isolated hypoalbumenaemia (globulins much bigger so rarely lost in urine, PLN should not cause panhypoproteinaemia)
  • high suspicion familial renal dz
  • paraproteinuria or bence-jones proteinuria d/t hyperglobulinaemia
35
Q

How does iris staging scheme relate to proteinuria in 1* glomerular dz?

A
  • useful for deescribing severity of proteinuria in patients with CKD BUT
    > severity of proteinuria in 1* glomerulardz ORDERS OF MAGNITUDE GREATER than this
  • UPCs 5, 10 , 20 with 1* glomerular dz
  • only at this sort of level systemic hypoalbumenaemia occours (and even then inconsistent in severity)
    > fluctuations naturally occour so small changes in UPC should not be over-interpretted
  • also if renal function severely imparied UPC may fall d/t v no. functioning nephrons
36
Q

Caues of med/severe UPC >2

A

> glomerular origin

  • glomerulonephritis (deposition AgAb complexes)
  • amyloidosis (insoluble depositioon of fibrillar protein, not limited to renal tissue but clinical signs usually d/t renal failure or nephrotic syndrome)
  • familial glomerulopathies
37
Q

What is amyloid

A

fragmment of an acute phase protein only produced in response to CHRONIC INFLAM or NEOPLASIA

38
Q

Which breeds have a familial orm of amyloidosis?

A
  • sharpei

- abyssinian cat

39
Q

Do all dogs with PLN develop nephorotic syndrome?

A

NOT NECESSARILY

- may not be azotaemic but may develop as dz progresses

Renal (23 decks)

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