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Proteinuria Flashcards

1
Q

How do you quanitfy proteinuria?

A

*dip-stick
* protein-creatinine ratio (UPC)
- sulphosalicylic acid test
- 24-hour protein loss
- protein electrophoresis
(albumin quantification methods)

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2
Q

Describe dipstick measurement

A

qualitative
cheap
convenient
trace, 1+, usually normal
must consider with urine specific gravity
only useful in identifying severe proteinuria

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3
Q

Describe protein: creatinine ratio

A
  • widely available

- high day to day variability (ideally measure several times or poor samples)

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4
Q

Where does protein come from that causes proteinuria?

A
  • PRE-GLOMERULAR: increased amounts of low MWt proteins presented to glomerular filter
  • RENAL (glomerular and tubular)
  • POST-RENAL (post-glomerular): addition of protein to urine after formation by the kidney
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5
Q

Causes - post-glomerular proteinuria

A

LOWER URINARY TRACT:

  • haemorrhage
  • inflammation/infection
  • neoplasia
  • (for blood contamination, urine has to be grossly contaminated before this causes proteinuria)
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6
Q

What is the effect of UTI on proteinuria?

A
  • highly variable

- difficult to predict- - UTI should be r/o before proceeding with a work-up for glomerular causes of proteinuria

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7
Q

T/F; a small amount of protein is always excreted

A

true

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8
Q

Causes - small pathological increase in protein excretion

A
  • glomerular hypertension

- tubular dysfunction

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9
Q

Cause - large increase in protein excretion

A

primary glomerular dz

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10
Q

Outline Protein-losing nephropathy (PLN)

A
  • clinical syndrome
  • severe (gross) proteinuria)
  • may result in hypoproteinaemia
  • caused by glomerular dz
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11
Q

Parts of the glomerular barrier

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

When should you suspect PLN?

A
  • Routine screening urinalysis
  • Hypoalbuminaemia
  • Breeds at risk
  • Associated diseases
  • Renal failure
  • Clinical signs of PLN
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13
Q

What should you suspect with low albumin alone?

A
  • liver failure
  • hypoadrenocorticism
  • PLN
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14
Q

What should you suspect with low albumin AND globulin?

A
  • PLE

- haemorrhage

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15
Q

CS and clinical pathology - nephrotic syndrome

A
  • proteinuria
  • hypoalbuminemia
  • hyperlipidemia
  • oedema/fluid accumulation in body cavities
  • not always azotaemic
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16
Q

How common is nephrotic syndrome in dogs with glomerular dz?

A

reported to occur in 5.8-37.5% dogs with glomerular dz

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17
Q

CS - nephrotic syndrome

A
  • Muscle wasting/weight loss/malaise
  • Azotaemic CKD (sometimes)
  • Azotaemic AKI (rarely)
  • signs of underlying disease
  • Hypertension
  • Thromboembolism
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18
Q

What diagnostics should be examined in all proteinuric animals??

A
  • urea/creatinine/ USG
  • albumin/ cholesterol
  • urine culture
  • BP
  • fundic exam
    THEN AS APPROPRIATE TO THE CASE:
  • CBC/chemistry
  • imaging
  • serology
  • CSF/ joint taps
  • FeLV/ FIV
  • specialised tests
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19
Q

Define ‘NIN’

A

Neoplastic, infectious, non-infectious inflammatory disease (i.e. underlying trigger)

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20
Q

Types - glomerular dz

A
  • amyloidosis
  • immune-complex GN (ICGN): many different tyes
  • minimal change dz (lesions only visible with EM)
  • glomerulosclerosis (scarring of glomeruli, many types)
  • familial glomerulopathies
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21
Q

When to consider familial glomerulopathies

A
  • young dogs
  • no specific tx
  • breeding programmes
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22
Q

What is hereditary nephritis?

A
  • defective type 4 collagen
  • english cocker (autosomal recessive) and some other breeds (variable inheritance)
  • genetic test available for cockers
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23
Q

What dz should be considered in light of travel relating to renal problems?

A
  • heartworm (Dirofilaria immitis)
  • leishmania
  • lyme disease (Borrelia burgdorferi)
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24
Q

How do steroids affect kidney?

A
  • increase proteinuria

- glomerulosclerosis

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25
Q

What breed is especially prone to kidney problems d/t sulphonamides?

A

dobermans

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26
Q

How do tyrosine kinase inhibitors affect kidneys?

A
  • frequently induce proteinuria

- minimal change disease

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27
Q

What should you do after thorough investigation and no obvious trigger?

A
  • consider biopsy

- non-specific therapy

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28
Q

How do glomerular haemodynamics affect kidney function?

A

Reduced glomerular pressure, hence GFR –> reduces proteinuria –> slows disease progression –> reduces inflammatory response

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29
Q

Ideal diet for non-specific glomerular dz

A
  • mild-moderate protein restriction, counter-intuitive, reduces proteinuria
  • protein of high biologic value
  • omega-3 fatty acid (DHA/ EPA) supplementation
  • Na restriction
  • phosphate restriction in RF
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30
Q

Outline ACEI in non-specific tx of glomerular dz

A
  • proven benefit: idiopathic GN and familial glomerular dz
  • indicated in all patients with GROSS proteinuria
  • angiotensin receptor blockers (ARBs) likely to be a reasonable alternative
  • cautious introduction + careful monitoring of renal function (a small increase in plasma [creatinine] should not preclude use of this
31
Q

Outline anti-thrombotic tx as non-specific tx of glomerular dz

A
  • aspirin, low dose
  • reduce risk of TE
  • clopidogrel is alternative
  • delay starting though if renal biopsy likely
  • efficacy unknown
32
Q

Describe anti-hypertensive tx in non-specific tx of glomerular dz

A
  • guided by BP measurements
  • ACEI or ARB
  • ACEI preferentially dilate efferent renal arteriole so are the preferred anti-hypertensive agent, but particularly in cats may not decrease BP sufficiently to prevent end-organ damage
  • combine with amlodipine (Ca channel blocker) if BP remains high
33
Q

Tx - oedema/ ascites

A
  • Na restriction
  • thoracocentesis
  • abdominocentesis (only if significant abdominal discomfort)
  • diuretics (avoid if poss)
  • colloids if necessary prior to biopsy
34
Q

Benefits - renal biopsy

A
  • specific tx (immunosuppression, aim to induce remission)
  • breed management
  • prognostication
35
Q

Downsides - renal biopsy

A
  • RISK: haemorrhage, renal injury
  • complications in 13% dogs and 18% cats
  • cost
36
Q

Outline method for renal biosy

A
  • US guided or surgical wedge biopsy
  • cortical tissue
  • specialist fixatives
37
Q

What fixatives are used for renal biopsy?

A
  • FORMALIN
  • Michel’s = immunohistochemistry
  • Glutaraldehyde = EM
38
Q

T/F: amyloidosis can be reliably distinguished on light microscopy

A

true:

  • requires v thin sections, multiple stains and specialist interpretation
  • definitive ID of immunoglobulin deposits often only possible with EM
39
Q

Distinguish immune-complex glomerulonephritis (ICGN) in dogs and cats

A
  • DOGS: more common, broad age range, M+F

- CATS: uncommon, young adults, M>F

40
Q

Tx - ICGN

A
  • eliminate Ag source
  • often no cause can be ID
  • removal may not be possible
41
Q

Outline immunosuppression as tx for PLN

A
  • if I-M dz is suspected
  • uncertain benefit
  • proteinuria may worsen with steroids
  • only recommended if biopsy confirmed immune-complexes
  • consult with specialist first
  • many different drug protocols
42
Q

Outline amyloidosis in relation to proteinuria

A
  • amyloid is a fragment of an APP that is produced in response to chronic inflammatory or neoplastic stimuli
  • only a subset of individuals that produce amyloid will develop systemic amyloidosis
  • extra-celluar deposition of insoluble fibrillar proteins in tissue
  • compromise organ function
  • if deposited in medulla, animal will not be proteinuric
  • depositionnot limited to renal tissue but CS most frequently related to development of RF or nephrotic syndrome
43
Q

Pathophysiology - reactive systemic amyloidosis

A
  • inflammation/tissue injury –> SAA protein (liver) –> insoluble AA amyloid (kidney). Will also be converted from SAA (liver) to AA amyloid-like intermediates to soluble peptides except in chronic inflammation and familial dz where conversion of SAA protein to AA amyloid-like intermediates is inhibited
44
Q

Tx - amyloidosis

A
  • no tx which solubilises amyloid fibrils once formed
  • COLCHICINE: used to tx nephrotic syndrome in humans but not beneficial once renal failure has developed. Late diagnosis in dogs andhigh occurence of side effects (V, D, neutropaenia) has limited its use. consider in animals at high risk of devloping amyloidosis (shar pei’s with recurrent hock swelling as v likely to develop renal failure), unproven benefit, may cause GI upset, not advised once patient azotaemic
45
Q

How to monitor tx

A
  • sequential UPC evaluation
  • in combination with serum [creatinine]
  • as # functioning nephrons declines UPC may actually fall
46
Q

Px - PLN

A
  • variable
  • often progressive
  • remission and recovery occasionally reported
  • worse if azotaemic
  • poor if have nephrotic syndrome
47
Q

Why are azotaemia and proteinuria not related?

A
  • AZOTAEMIA = reduced # of functioning nephrons

- PROTEINURIA = damaged filtration barrier

48
Q

Describe the source of protein normally present in urine

A
  1. Low molecular wt (freely filtered, not reabsorbed)
  2. some larger proteins up to size of albumin, this is 25-70% urinary protein
  3. small amounts of protein secreted by renal tubular cells
  4. small amounts of protein from LUT or genital tract (enzymes, mucoproteins, immunoglobulins)
49
Q

How must urine protein concentration be considered?

A
  • in relation to urine concentration

- in general, trace or 1+ proteinuria, in a urine sample that is highly concentrated, is normal

50
Q

Which LUT dz can cause proteinuria and should be ruld out before proceeding with further urinary protein quantification?

A
  • infection
  • inflammation
  • neoplasia
  • haemorrhage
51
Q

Why is urinary protein loss usually quantified in practice?

A
  1. abnormal amounts of urine protein are detected on a dipstick
  2. isolated hypoalbuminaemai (because globulin is a much larger protein, it is rarely lost into the urine so PLN would not be expected to cause panhypoproteinaemia)
  3. a high suspicion of familial renal disease typically resulting in proteinuria
  4. paraproteinuria or Bence-Jones proteinuria is suspected (usually because animal is hyperglobulinaemic)
52
Q

Describe the UPC test

A

the protein measurement is divided by the creatinine concentration in the urine, which corrects for the volume of urine that is being produced. IF an animal produces lots of very dilute urine, the protein concentration will be relatively low but so will the creatinine concentration.

53
Q

Does the severity of proteinuria tend to be worse in dogs/cats with CKD or primary glomerular disease?

A

tends to be worse in primary glomerular dz (may have UPCs of 5, 10 or even 20)

54
Q

At what level of proteinuria does systemic hypoalbuminaemia occur?

A

with proteinuria of UPC 5, 10 or 20. (even then the systemic hypoalbuminaemia is inconsistent in its severity)

55
Q

Define paraprotein

A

a monoclonal immunoglobulin or light chain present in blood or urine, produced by a clonal population of mature BC, commonly plasma cells

56
Q

Name the 4 categories of causes of proteinuria

A
  1. pre-glomerular
  2. glomerular
  3. tubular
  4. post-glomerular
57
Q

Describe pre-glomerulr proteinuria

A
  • low MWt proteins pass through glomerulus, reabsorbed in renal tubule. If their conc is v high, reabsorption ability will be overcome and protein excreted in urine
  • example: excretion of bence-jones proteins (Ig light chains) in patients with multiple myeloma
58
Q

Describe glomerular proteinuria

A
  • if renal dz or hypertension, may have mild glomerular proteinuria d/t increased glomerular capillary pressure which results in more protein being forced through glomerular capillary barrier.
  • associated with shorter MST
59
Q

Define moderate-to-severe proteinuria in terms of UPC

A

UPC > 2

  • usually glomerular
  • d/t GN, amyloidosis or familiar glomerulopathies
60
Q

Pathogenesis - glomerulopathies

A

presence of intra-glomerular immune complexes (from circulating antigen-antibody complexes being trapped in glomerulus or formed in situ). –> inflammatory response (cellular proliferation, thicking of glomerular BM, evenutally hualinisation and sclerosis). –> ultimately nephron destruction and renal failure

61
Q

Breeds - familial amyloidosis

A
  • shar-pein dog

- abyssinian cat

62
Q

Outline familial glomerulopathies

A
  • various dog breeds
    = inherited defect in structure of glomerular barrier
  • although defect present from birth, proteinuria doesn’t manifest until young adulthood and this preceds development of azotaemia by months/years
63
Q

Describe tubular proteinuria

A
  • only mild
  • when tubules don’t resorb protein filtered by glomeruli
  • e.g. CKD d/t reduced functional nephrons or specific tubular defect (e.g. Fanconi syndrome)
64
Q

Describe post-glomerular (post-renal) proteinuria

A

= inflammation of LUT or repro. tract depending on how the urine was collected
- commonly: UTIs and urolithiasis

65
Q

How does haemorrhage (e.g. from cystocentesis) affect proteinuria?

A
  • don’t over-interpret mild blood contamination from cystocentesis
  • blood contamination must be really severe (>3+ on dipstick, visibly discoloured urine) before UPC is significantly altered
66
Q

T/F: all dogs with PLN have signs of nephrotic syndrome

A

False - some dogs and cats with PLN havve signs of nephrotic syndrome. Many dogs have only v non-specific signs.

67
Q

T/F: dogs with significant proteinuria, even those with nephrotic syndrome, will not necessarily be azotaemic at presentation

A

True

68
Q

Other presenting signs in dogs with PLN

A
  • TE (usually HL lame or acute dyspnoea)
  • hypertension (blind, hymphema, cardiac changes)
  • signs referable to underlying dz
  • oxxacionally shar-peis and orientl or siamese cats with amyloidosis will present with signs of acute intra-abdominal haemorrhage d/t hepatic rupture
69
Q

What is the tetrad of nephrotic syndrome?

A
  • significant proteinuria
  • hypoalbuminaemia
  • hypercholesterolaemia
  • oedema and/or fluid accumulation into body cavities (ascities or pleural effusion)
70
Q

Work up of proteinuric patients

A
  • signalment, hx and PE
  • renal function and plasma albumin, globulin and cholesterol
  • haematology
  • complete biochem
  • thoracic and abdominal radiographs/ultrasound
  • various serologic tests
  • BP
  • fundic exam
71
Q

Indications - renal bipsy

A

when signficant and persistent proteinuria of renal origin is identified

72
Q

Method - renal biopsy

A
  • ultrasound-guided if expert
  • less experiend: sx obtain wedge or ‘tru-cut’ biopsy of renal cortex
  • assess haemostatic paraemeters prior to biopsy
  • FNA provides inadequate structural information except renal lymphoma which may cause PLN in cats
  • send to specialist nephropathology centre (light microscope, immunofluorescence, EM)
  • unable to tell if dz is I-M without EM
73
Q

Outline tx plan of PLN

A
  • ID and tx underlying dz
  • dietary modification
  • immunosuppressive drugs
  • tx amyloidosis
  • ACEI
  • anti-thrombotic drugs
  • anti-hypertensive drugs

Renal (30 decks)

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