Bod: Renal: Nephritic Diseases

Front 1

What are immune complexes made out of?

Back 1

Antibody and antigen.

Front 2

What do you think when you see RBC (erythrocyte) casts in the urine?

Back 2

Think glomerular disease. Almost always signify a break in the glomerular membrane.

Front 3

Glomerular basement membrane breaks are usually a result of what?

Back 3

Local inflammation.

Front 4

c/c Type II hypersensitivity with type III hypersensitivity

Back 4

Type II: antigen is in one spot.

Type III: immune complexes form in circulation and become trapped in the basement membrane due to size and charge of the immune complex.

Front 5

Where do immune complexes form in acute glomerulonephritis?

Back 5

They are subendothelial (between the endothelial cells of the capillaries and the basement membrane).

Front 6

What are the four general steps involved in developing acute glomerular nephritis?

Back 6

1. Antibody binds to the basement membrane.

2. Circulating complement binds to the bound antibodies.

3. Fc and complement receptor immune cells (neutrophils and monocytes) are recruited. (BECAUSE THEY CAN ACCESS THE IMMUNE COMPLEXES)

4. Digestion of the filtration barrier.

Front 7

What do you see in a glomerulus with acute glomerulonephritis?

Back 7

Inflammatory cells (neutrophils) in the capillary lumens.

Front 8

What type of hypersensitivity reaction do you usually see with acute glomerulonephritis?

Back 8

Type III (circulating) - can deposit in a subendothelial OR mesangial location.

Front 9

What are the steps necessary to create a "crescent" pattern of injury in the context of a severe glomerulonephritis?

Back 9

1. Disruption of the BM leads to release of tissue factor, etc.

2. Fibrin cross-linking occurs on both sides of the glomerular capillary wall (because blood has escaped through the hole in the BM).

3. Proliferation of the parietal EPITHELIAL cells due to fibrin, etc. This is to basically seal the hole. These proliferating cells comprise the crescent.

Front 10

Name the cells that filtrate will pass through as it goes through the glomerulus.

Back 10

1. Fenestrations of the endothelium of the glomerular capillaries.

2. The basement membrane.

3. The slit pores of the podocytes of the epithelium of the visceral lining of Bowman's capsule.

Front 11

Often see what pathologic process concurrently with crescent formation?

Back 11

Fibrinoid necrosis.

Front 12

Goodpasture's disese is an example of what type of hypersensitivity?

Back 12

Type II

Front 13

In Goodpasture's disese, an autoantibody is directed against what antigen?

Back 13

Type IV collagen.

Front 14

Goodpasture's disese causes what type of kidney disease?

Back 14

Cresenteric glomerulonephritis.

Front 15

Where else can an autoantibody directed against type IV collagen bind besides the kidney?

Back 15

BM of the lung --> pulmonary hemorrhage.

Front 16

What type of collagen is "scar" collagen?

Back 16

Type I

Front 17

IgG granular immunofluorescence

Back 17

Type III hypersensitivity

Front 18

IgG linear immunofluorescence

Back 18

Type II hypersensitivity (Goodpasture disease - the ONLY one)

Front 19

IgG, no immunofluorescence

Back 19

Pauci-immune crescenteric glomerulonephritis.

Front 20

What is main player in pauci-immune crescenteric glomerulonephritis?

Back 20

ANCA (anti-neutrophil cytoplasmic antibodies)

Front 21

In what stage of crescenteric glomerulonephritis do you see fibrinoid necrosis?

Back 21

In the early stages.

Front 22

What sort of glomerulonephritic disease would you expect to see with chronic, subacute immune complex deposition?

Back 22

Membranoproliferative glomerulonephritis.

Front 23

Membranoproliferative glomerulonephritis: pathogenic mechanism.

Back 23

Waves of immune complex deposition --> immune cells can't clear all complexes --> so endothelial cells elaborate new basement membrane material over the the subendothelial deposits.

Mesangial deposits result in the expansion of mesangium and proliferation of mesangial cells.

Front 24

Membranoproliferative glomerulonephritis: EM

Back 24

See "tram tracks": new BM that entraps immune deposits and cell debris.

Front 25

What is a consequence of "tram tracks?"

Back 25

The distance between the capillary lumen and the urinary space has greatly increased. Filtration is not as efficient.

Front 26

Membranoproliferative glomerulonephritis: light microscope

Back 26

Can see "tram tracks"

Front 27

What is always present in the urine in nephritic disease?

Back 27

Hematuria. May also see some WBC casts, cellular casts.

Front 28

What is gross hematuria?

Back 28

Hematuria that is significant enough to cause discoloration of the urine.

Front 29

Smokey or "Coca-cola" colored urine.

Back 29

Acute poststreptococcal glomerulonephritis.

Results from the oxidation of blood pigments during the abnormally slow urinary transit time.)

Front 30

IgA nephropathy (Berger's disease): hematuria

Back 30

Pass bright red blood despite having normal kidney function.

Front 31

Acute poststreptococcal glomerulonephritis: hematuria

Back 31

Smokey or Coca-cola colored urine.

Results from the oxidation of blood pigments during the abnormally slow urinary transit time.)

Front 32

Fulminant, idiopathic crescenteric glomerulonephritis: hematuria

Back 32

Rarely presents with macroscopic hematuria.

Front 33

Most hematuria is due to what?

Back 33

Kidney stones, urologic tumors, UTIs, etc. NOT glomerulonephritis.

Front 34

What is azotemia?

Back 34

Abnormal levels of urea, creatinine, and other nitrogen containing compounds in the urine.

Front 35

Hematuria, hypertension, oliguria, fluid overload.

Back 35

The nephritic syndrome.

Front 36

What are some examples of diseases that cause primary glomerulonephritis?

Back 36

- IgA nephropathy (Berger's disease)
- Acute poststreptococcal glomerulonephritis
- Idiopathic crescenteric glomerulonephritis
- Membranoproliferative glomerulonephritis

Front 37

What are some examples of diseases that cause secondary glomerulonephritis?

Back 37

- Collagen vascular disease
- Systemic lupus erythrmatosis
- Vasculitis (P. nodosa, HSP, cryoglobulinemia, Wegener's granulomatosis)
- Goodpasture's syndrome
- Bacterial endocarditis
- Other chronic bacteremic states.

Front 38

Two major factors in nephritic edema.

Back 38

1. Hypoalbuminemia
2. Inability to excrete Na (but still have normal Na intake)

"The most acutely fluid-retentive type of disease there is!"

Front 39

Volume overload means that what is low?

Back 39

Renin

Front 40

Dysmorphic RBCs

Back 40

Evidence for abnormal basement membranes. RBCs may have been damaged while squeezing through.

Front 41

What is the paradox of renal failure and what is excreted into the urine?

Back 41

"Even though the filtration barrier to macromolecules may be damaged, resulting in proteinuria, the overall ability of the glomerulus to allow passage of smaller molecules like urea and creatinine is hampered."

Front 42

True or false: The basement membrane does not close off each capillary loop.

Back 42

True. The BM moves across the mesangium to the next capillary without closing off the loop.

Front 43

IgA nephropathy is common in which demographics?

Back 43

SE asian populations.

Front 44

What other disease looks similar to IgA nephropathy?

Back 44

Diabetic glomerulopathy.

Front 45

What do you think if you see bloody urine and hemoptysis?

Back 45

Goodpasture's syndrome