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Systemic Pathology I > Renal Pathology - Glomerular Disease > Flashcards

Renal Pathology - Glomerular Disease Flashcards

1
Q

What 3 structures make up the urine filtration barrier? What else is present in the glomerulus?

A
  1. endothelial cells of the glomerular capillaries
  2. basement membrane of the glomerular capillaries
  3. visceral epithelium (podocytes)
    (filters blood and forms primary urine)

mesangial cells, mesangial matrix, parietal cells, Bowman’s capsule

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2
Q

What affects glomerular filtration? What is the primary function of the glomeruli?

A

size and electrical charge - water, particles <3.5 nm, potassium, sodium, glucose

maintains ionic and osmotic homeostasis in the blood
(glomerular damage = problems with filtration)

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3
Q

What 2 molecules are typically not filtered and remain in the blood?

A
  1. albumin
  2. antithrombin III

(may be leaked in the urine with glomerular disease)

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4
Q

What are 3 indications of glomerular injury?

A
  1. proteinuria - presence of abnormal quantities of protein in urine
  2. albuminuria —> edema
  3. loss of antithrombin III —> thrombi formation
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5
Q

Tubular injury can also result in proteinuria. How does this compare to glomerular disease?

A

only small molecules will be leaked into urine - aminoaciduria, glucosuria

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6
Q

What are the major results of albuminuria due to glomerular disease?

A
  1. ascites
  2. hydrothorax/hydropericardium
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7
Q

What is the result of antithrombin III loss in urine due to glomerular disease?

A

hypercoagulable state —> thrombi formation common in the lungs and pulmonary artery

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8
Q

What are the 3 hallmarks of glomerular disease?

A
  1. proteinuria
  2. hypercoagulable state due to the loss of antithrombin III
  3. nephrotic syndrome - severe proteinuria + severe hypoalbuminemia + generalized edema + hypercoagulable state + hyperlipidemia
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9
Q

What causes hyperlipidemia in nephrotic syndrome?

A

liver tries to compensate and produce more albumin, which causes it to also produce cholesterol

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10
Q

What is the difference between glomerulitis and glomerulonephritis?

A

GLOMERLITIS: inflammation restricted to glomerulus caused by acute septicemia (glomerulus is the first to receive blood!)

*GLOMERULONEPHRITIS: usually of immune origin including glomerular disease and secondary tubulointerstitial and vascular changes

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11
Q

What is the difference between proliferative and membranous glomerulonephritis?

A

PROLIFERATIVE: proliferation of endotheliuml/podocytes/mesangial cells along with inflammatory cells

MEMBRANOUS: thickening of the basement membrane/mesangial membrane

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12
Q

What is a common cause of glomerulitis in foals? How does this cause disease?

A

Actinobacillus equuli —> suppurative glomerulitis

bacteria enter the kidney via vasculature and lodge in the capillaries of glomeruli, where they replicate and induce necrosis and inflammation (AKA embolic glomerulitis)

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13
Q

What is the cause of glomerulonephritis? What are specific causes in dogs and cats?

A

immune-mediated —> Ag-Ab complex deposition and complement activation often associated with persistent infections or diseases that have prolonged antigenemia

DOGS: pyometra, pyoderma, chronic parasitism (Dirofilaria), autoimmune disease (SLE), neoplasia
CATS: FeLV, FIV, FIP

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14
Q

What are the 2 mechanisms of immune-mediated glomerulonephritis?

A
  1. preformed circulating Ag-Ab compexes associated with persistent infections/disease —> prolonged antigenemia —> formation of soluble immune complexes
  2. antigen is trapped in glomerular capillary wall and circulating antibodies form complexes with them
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15
Q

What are the 4 main locations of immune complexes causing glomerulonephritis?

A
  1. mesangial - within the mesangial matrix
  2. intramembranous - in the BM of the glomerular basement membrane
  3. subepithelial - between feet of podocytes
  4. subendothelial - below endothelium of glomerular capillaries
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16
Q

What is the mechanism of injury to the glomerular structures in glomerulonephritis?

A
  • deposition of the immune complex
  • complement activation
  • chemotaxis of neutrophils
  • damage to BM through neutrophil release of enzymes and ROS
17
Q

What are the 4 outcomes of injury due to glomerulonephritis?

A
  1. proliferation of mesangial cells and podocytes
  2. influx of inflammatory cells
  3. thickeing of mesangial matrix and basement membrane
  4. loss of function of glomerular filtrate barrier
18
Q

What are the 3 histological patterns of glomerulonephritis? Which are most common in dogs and cats?

A
  1. MEMBRANOUS: thickened glomerular basement membrane/mesangial matrix (CATS)
  2. PROLIFERATIVE: hypercellularity of mesangial cells, podocytes, and WBCs
  3. MEMBRANOPROLIFERATIVE: combination of thickend GBM/matrix and proliferation of mesangial cells and podocytes (DOGS)
19
Q

Glomerulonephritis, histology:

A
20
Q

How does glomerulonephritis look grossly?

A

subtle granular cortex where the glomeruli are observable to the naked eye —> gray pinpoint lesions of inflammation

21
Q

What is the prevalence of glomerulonephritis in dogs, cats, horses, and pigs? What is the etiology of each?

A

DOGS: membranoproliferative; Borrelia, Dirofilaria, pyometra, lupus
CATS: membranous; FeLV, FIP, FIV
HORSES: membranoproliferative; Streptococcus equi, equine infectious anemia
PIGS: membranoproliferative; PCV-2

22
Q

What is amyloid? What are the 3 types of glomerular amyloidosis?

A

extracellular, eosinophilic, homogenous, insoluble fibrilar protein resistant to normal degradation

  1. PRIMARY: AL amyloidosis - plasma cell tumors caused by immunoglobulin light chain protein
  2. SECONDARY: AA amyloidosis - reactive, associated with chronic inflammatory diseases, caused by serum amyloid-a SAA —> DOMESTIC ANIMALS
  3. FAMILIAL: deposition in medullary interstitium common in Shar-Peis, Abyssinians, or Siamese cats
23
Q

What are the 2 common locations of amyloid deposition in kidneys? What 3 things does this lead to?

A
  1. GLOMERULI - primary site in the mesangium and subendothelial zones of glomerular capillaries
  2. MEDULLA - familial amyloidosis (Shar-Peis, Abyssinians, Siamese)
  • progressive renal insufficiency
  • proteinuria
  • progressive disease with poor prognosis
24
Q

What does glomerular amyloidosis look like grossly?

A

pale kidney with a granular cortex, similar to GN

25
Q

How can glomeruli be stained grossly to observe amyloidosis? What is the purpose of this procedure?

A

iodine solution (Lugol’s iodine) causes the glomeruli to stain red-brown

differentiated from GN

26
Q

How is glomerular amyloidosis confirmed?

A

microscopically with Congo red stain that has an apple gree birefringence with polarized light

27
Q

What are 3 possible downstream changes of glomerulonephritis?

A
  1. glomerulosclerosis
  2. interstitial fibrosis - tubular ischemia leads to tubular atrophy and replacement by fibrous connective tissue
  3. tubular injury - sclerotic glomeruli cause downstream tubular ischemia when connective tissue compresses the capillaries
28
Q

What is a major indication of glomerular disease on histology?

A

hyaline casts —> tubules are dilated and filled with eosinophilic amorphous material (protein)

29
Q

What are 3 sequelae of chronic glomerular disease?

A
  1. chronic renal failure
  2. nephrotic syndrome
  3. hypercoagulable state

Systemic Pathology I (25 decks)

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