Proteinuria Flashcards
quantification of proteinuria
dip stick sulphosalicyic acid test 24h protein loss protein creatinine ratio protein electrophoresis
dip stick
qualitative
cheap, convenient
false -ves + +ves occur
protein creatinine ratio
practical for routine use
widely available
site of origin
pre-glomerular
glomerular
tubular
post-globerular
mechanisms of renal proteinurea
loss of filter size barrier - large proteins get into filtrate
proximal tubular dysfunction - lack of resorption of protein
pre-glomerular proteinuria - functional
fever
exercise
pre-glomerular proteinuria - overload
small proteins
immunoglobulin light chains
haemoglobin
myoglobin
post-glomerular proteinuria - lower urinary tract - causes
haemorrhage
infl/infection
neoplasia
effect of UTI
variable + hard to predict
UTI should be ruled out before investigating glomerular cause
gross proteinuria - effects
marker of glomerular disease
may lead to nephrotic syndrome
causes protein loosing nephropathy (PLN)
needs treatment
micro-proteinuria
marker of glomerular hypertension
not direct clinical signs
needs investigation
when to suspect PLN
hypoalbuminemia
renal failure
clinical signs
glomerular disease
gross proteinuria is hallmark
glomerulonephritis
amyloidosis
familial glomerulonephropathies
nephrotic syndrome - effects
hypoalbuminemia proteinuria hyperlipidaemia oedema azotaemia
nephrotic syndrome - clinical signs
muscle wasting
renal failure
hypertension
thromboembolism
nephrotic syndrome - diagnostic plan
CBC/chemistry imaging serology CSF/joint taps Felf/FIV specialised tests
diagnostic plan in all proteinuric patients
urea/creatinine/usg albumin/cholesterol urine culture blood pressure fundic exam clotting function
renal biopsy - pro’s
characterise the disease
prognostic
renal biopsy - con’s
haemorrhage
renal injury
expense
complications in 13% dogs + 18% cats
renal biopsy
u/s guided or surgical wedge biopsy
cortical tissue
glomerulonephritis (GN)
immune mediated disorder
deposited pre-formed antigen-antibody complexes
infiltration of infl cells, complement activation, cytokine release etc.
GN - remove inciting cause
eliminate antigenic source
often no cause can be identified
removal may not be possible
immunosuppression
glucocorticoids?? - use only if is to treat underlying disease/if biopsy confirms immune-mediated disease
amyloidosis
extra-cellular deposition of insoluble fibrillar proteins in tissues
compromise organ function
pathophysiology - reactive systemic amyloidosis
infl/tissue injury
serum amyloid A protein (SAA) - usually converted to other protein which can be broken down but instead converted to insoluble AA amyloid
amyloidosis - dogs
mid-old age
females more
deposition may be non-glomerular
amyloidosis - cats
mid-old age
breed linked
specific therapy - amyloidosis
no therapy to dissolve AA amyloid
colchicine - not helpful if in RF, may worsen clinical signs, give if animal at high risk of amyloidosis
familial glomerulopathies
young dogs
no specific treatments
hereditary nephritis
non-specic treatment glomerular disease
diet - protein high quality + restricted
ACE inhibition - dogs with idiopathic GN
anti-thrombotic therapy
aspirin
anti-hypertensive therapy
ACE inhibition
can give amlodipine if BP high
oedema/ascites - treatment
sodium restriction thoracocentesis abdominocentesis plasma transfusion diuretics - avoid if possible
prognosis
variable often progressive remission + recovery occasionally seen worse if azotaemic poor if have nephrotic syndrome
