Bod: Renal: Glomerular Diseases 2, Nephrotic Diseases

Front 1

Definition of the nephrotic disease

Back 1

Spilling more than 3.5 g of protein in the urine per day.

Front 2

Primary Focal and Segmental Glomerulosclerosis: light microscopy

Back 2

See scarring of glomeruli

Front 3

Primary Focal and Segmental Glomerulosclerosis: Electron microscopy

Back 3

See effacement of podocytes in every glomerulus.

Front 4

What is the pathological consequence of FSGS and glomerular sclerosis in general?

Back 4

Hyperfiltration

Front 5

Minimal change disease: light microscopy

Back 5

Looks normal, nothing by immunofluorescence

Front 6

Minimal change disease: electron microscopy

Back 6

Effacement of podocytes

Front 7

If a nephron becomes sclerotic, what happens to the other nephons

Back 7

They become stressed and eventually become sclerotic themselves

Front 8

Minimal change disease: immune complexes?

Back 8

No

Front 9

FSGS: immune complexes?

Back 9

No

Front 10

What is the main difference between primary FSGS and secondary FSGS?

Back 10

In secondary FSGS you see some preservation of foot processes on EM

Front 11

Membranous Nephrophathy: cause?

Back 11

Immune complexes on the subEPITHELIAL side of the basement membrane.

Front 12

Membranous nephropathy: is there inflammation?

Back 12

No, immune cells can't get to immune complexes.

Front 13

What tries to reestablish the BM in membranous nephropathy?

Back 13

The podocyte

Front 14

In membranous nephrophathy, what are the structures that the podocyte creates as it tries to repair the BM?

Back 14

Puts down collagen --> forms spikes

Front 15

Membanous nephropathy is like what type of HSR?

Back 15

Type II

Front 16

What is the difference between membranous nephropathy and membranoproliferative glomerulonephritis?

Back 16

Location of immune complexes and immune reaction. No inflammation in membranous nephropathy.

Front 17

What is another thing that "spikes" in membranous nephropathy can look like on light microscope?

Back 17

"craters"

Front 18

What does membranous nephropathy look like on immunofluoresence microscopy?

Back 18

Granular deposits

Front 19

Hematuria and inflammation = what type of general renal disease?

Back 19

Nephritic disease

Front 20

Would a pt with minimal change disease have hematuria?

Back 20

No.

Front 21

One of the most important parts of the glomerular filtration apparatus?

Back 21

The slit pore.

Front 22

Normal protein filtration/excretion

Back 22

400 mg/day, < 200 mg/day in urine

Front 23

Amount of protein secretion in nephrotic disease.

Back 23

400,000 mg/day, 20,000 mg/day excreted

Front 24

Hypoalbuminemia reults when what happens?

Back 24

When albumin loss exceeds the capacity of the kidney to recycle filtered albumin and the liver to increase production.

Front 25

What is underfill

Back 25

Oncotic pressure down --> plasma volume down --> renin/ang up, symp nervous system --> renal sodium retention up --> edema

Front 26

EdemA

Back 26

Starling force + constant force to retain sodium

Front 27

Overfill edema

Back 27

Expanded volume.

Proteinuria --> renal sodium ret --> plasma volume up --> pressure in capillaris up --> edema

Front 28

Pathogenesis of hyperlipidemia in the nephrotic syndrome

Back 28

Albumin is synthesized by the liver.

Protein lost in urine --> liver synthesizes more albumin --> at the same time the liver ALSO synthesizes more LIPIDS and CLOTTING FACTORS --> (leads to a hypercoagulable state because of ANTI-coagulants lost in the urine)

Front 29

Morphology of lipid in urine

Back 29

Fatty casts. See a Maltese cross shape.

Front 30

In secondary nephrotic syndrome, what is the treatment?

Back 30

Treat the underlying disorder.

Supportive measures
Diuretics
Lipid lowering agents (ex FSGS pt that has cholesterol of 1440!)
Anticoagulation
prevention of progression to renal failure (antihypertension, etc)

Front 31

As we lose nephrons we lose ____?

Back 31

GFR

Front 32

ACE inhibtors do what to the efferent arteriole

Back 32

Dilate the efferent arteriole. If do this, the pts GFR might go down, but DECREASES stress on nephrons.

Front 33

What are the major symptoms of the nephrotic syndrome?

Back 33

Bland urine sediment
Proteinuria (>3.5 g/day)
Hypoalbuminemia
Hyperlipidemia
Hypercoagulability
Edema

Front 34

Pathogenesis of a procoagulant state in the nephrotic syndrome.

Back 34

Clotting factors are synthesized by the liver.

Protein lost in urine --> liver synthesizes more albumin --> at the same time the liver ALSO synthesizes more LIPIDS and CLOTTING FACTORS --> (leads to a hypercoagulable state because of ANTI-coagulants (antithrombin III) lost in the urine)

Hypercoagulable especially when the albumin is below 2.0 mg/dL

Front 35

The three most common causes of the nephrotic syndrome all share one morphologic feature on EM, what is it?

Back 35

See diffuse effacement of podocytes.

Front 36

What accounts for hyperfiltration in the nephrotic kidney?

Back 36

Effacement of podocytes --> podcytes smush down against the BM --> this creates thickened areas, but it also creates some large pores --> the slit pores are the "size filters" of the GBM, so now large molecules like albumin can escape (but RBCs cannot escape because the BM is still intact.)

Front 37

What is the etiology of minimal change disease?

Back 37

Hereditary form has been linked to mutations in nephrin and podocin, proteins that make up the slit pore.

Non-hereditary form: immune-mediated damage to the podocyte (explains why minimal change disease can happen after immunization or after transplantation or with B-cell lymphoma)