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SAMS > Glomerulotubular Disorder > Flashcards

Glomerulotubular Disorder Flashcards

1
Q

Glomerular disease

A

Breakdown in the normal function of the glomerulus and resultant abnormal leakage of large quantities of protein into the urine (esp. albumin)
- associated with a protein losing nephropathy

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2
Q

_____ of plasma entering becomes tubule filtrate

A

20%

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3
Q

Glomerulus is not permeable to _____

A

Proteins

- passage of substances based on size and charge

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4
Q

Albumin

A

Large quantities only get thru if there is a breakdown in the glomerular membrane

  • 69,000 daltons
  • negative charge
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5
Q

2 causes of glomerular disease

A
  • glomerulonephritis

- amyloidosis

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6
Q

Glomerulonephritis

A

Secondary, deposition of preformed Ag-Ab complexes within the glomeruli

  • deposition of Ag in capillary wall with resultant Ab binding and formation of Ag-Ab complexes
  • stimulate production of proinflammatory cytokines, vasoactive substances, proteases
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7
Q

How the glomerulus responds to glomerulonephritis

A

Glomerular cell proliferation, basement membrane thickening, eventual fibrosis
- RAAS is activated –> vasoconstriction of efferent glomerular arteriole and intraglomerular hypertension (contributes to protein loss)

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8
Q

Amyloidosis

A

Deposition of excessive amounts of amyloid A protein

  • serum amyloid A produced by liver (acute phase protein), result of tissue injury and inflammation
  • reactive amyloidosis
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9
Q

Amyloidosis - breed disposition

A
  • Shar-pei

- Abyssinian

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10
Q

Causes of glomerular disease

A
  • idiopathic

- secondary: infectious, inflammatory, neoplastic

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11
Q

Once glomerulus is irreversibly damaged, _______

A

Entire nephron becomes non-functional

  • total GRF decreases –> hypertension
  • remaining nephrons increase individual GFR to compensate
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12
Q

Hyperfiltration can result in _______

A

Progressive loss of remaining nephrons and renal failure

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13
Q

Hypoalbuminemia

A

Oncotic pressure is lost and fluid lost from vascular space

  • edema
  • ascites
  • pleural effusion
  • hypovolemia
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14
Q

Clinical signs of hypoalbuminemia begins at ______

A

1.4 - 1.6 g/dl

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15
Q

Nephrotic syndrome

A
  • hypoalbuminemia
  • proteinuria
  • hypercholesterolemia
  • edema and/or ascites
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16
Q

Protein losing nephropathy

A

Proteinuria!

  • excessive amounts of any protein in the urine (albumin is main urine protein
  • must be in the absence of active sediment or hemorrhage!
17
Q

Evaluating the magnitude of protein in the urine

A
  • dipstick evaluation
  • sulfosalicylic acid test
  • urine protein creatinine ratio
18
Q

Dipstick Evaluation

A

Most common screening test

  • concentration of urine can affect protein levels
  • can give false negative results! –> low concentration of albumin, dilute urine
19
Q

What causes a false positive for proteinuria via dipstick?

A

Alkaline urine

20
Q

Other reasons to have proteinuria via dipstick evaluation

A
  • increased SG
  • hematuria
  • pyuria
  • semen
21
Q

Slufosalicylic acid test

A

SSA reagent added to small volume of urine supernatant

- acidification causes precipitation of protein in the sample (increasing turbidity), subjectively graded as trace

22
Q

SSA reaction will detect _______

A

Albumin and globulins (more sensitive to albumin)

- considered confirmatory for positive proteinuria rxn on urine dipstick

23
Q

Urine protein: creatinine ratio

A

Gives better quantitative evaluation of protein loss in the urine

  • creatinine is filtered and excreted at a constant rate
  • serves as correction factor
24
Q

UPC ratio values

A

Normal: less than 0.2

  • borderline: 0.2-0.5 (dogs), 0.2-0.4 (cats)
  • increased: >0.5 (dogs), >0.4 (cats)
25
Q

Diagnosis

A
  • history/PE
  • blood work/UA/urine culture
  • bp measurement
  • aspirate lumps and bumps
  • serology for suspect infectious dz
  • imaging
26
Q

Nonspecific management of glomerular dz

A
  • treatment of underlying cause
  • reduce the proteinuria
  • management of complications
27
Q

Reduction of proteinuria

A

Inhibition of RAAS system reduces glomerular capillary bed hydrostatic pressure, thrus reducing proteinuria

28
Q

Reduction of proteinuria

A

ACE inhibitors help w/ decreasing glomerular capillary hydrostatic pressure - decreased efferent arteriolar resistance

  • decrease hydrostatic pressure across glomerulus
  • less protein is forced out into the urine
29
Q

Treatment significantly reduces _________

A

Proteinuria and delays onset/progression of azotemia

- standard of care w/ glomerular dz in dogs!!

30
Q

Diet changes

A

Feed high-quality, reduced quantity protein diet

- omega 3 polyunsaturated FAs supplementation

31
Q

Beta pleated sheet conformation resistant to proteolysis

A

Amyloidosis

  • colchicine: impair release of serum amyloid A from hepatocytes
  • DMSO: decrease in interstitial fibrosis and inflammation (may improve renal function)
32
Q

Management of complications

A
  • treatment of renal failure
  • ascites and edema
  • systemic hypertension
  • hypercoagulability and thromboembolism
33
Q

Proteinuria leads to

A

Abuminuria –> hypoalbuminemia

- albumin between 1.6-1.4 = begin transudation of fluid into interstitial spaces

34
Q

Therapy depends on _____

A

Severity

  • mild: cage rest, no salty treats
  • moderate/severe: consider plasma, synthetic colloids, diuretics
35
Q

Systemic hypertension

A

Present in 80% of dogs

  • eyes, heart, kidneys, CNS most susceptible to damage
  • treat w/ ACE inhibitors, amlodipine
36
Q

Hypercoagulability and thromboemolism

A

Loss of antithrombin 3, increased platelet activation
- antiplatelet therapy used to reduce glomerular inflammation and decrease platelet aggregation, decreasing incidence of thromboembolism

37
Q

Prognosis

A

Depends on:

  • underlying disorder
  • severity and extent of renal insult
  • response to treatment
  • glomerulonephritis (variable)
  • amyloidosis (severe, irreversible)

SAMS (13 decks)

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