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All the things > 12.3: Nephrotic Syndrome > Flashcards

12.3: Nephrotic Syndrome Flashcards

1
Q

What is the hallmark of nephrotic syndromes?

A

Proteinuria, with more than 3.5 g /day

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2
Q

What causes edema with nephrotic syndromes?

A

Hypoalbuminemia from urine losses leads to decreased oncotic pressure

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3
Q

What causes the hypercoagulable state with nephrotic syndrome?

A

Loss of antithrombin III

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4
Q

What causes the increased risk of infection with nephrotic syndrome?

A

Hypogammaglobulinemia

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5
Q

What role does antithrombin III play in coagulation?

A

Breaks down thrombin and other coagulation factors

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6
Q

Why is there hyperlipidemia and hypercholesterolemia with nephrotic syndrome?

A

Liver reacts to loss or protein by secreting more fat into the blood

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7
Q

What is the most common nephrotic disease in children?

A

Minimal change disease

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8
Q

What is the cause of minimal change disease?

A

Usually idiopathic, but can be seen with hodgkin lymphoma from cytokine production

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9
Q

What are the three filtration barriers in the glomerulus?

A
  • Fenestrated endothelium
  • BM
  • Podocytes
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10
Q

What is minimal change disease?

A

Loss/effacement of the podocytes from cytokines causes a loss of protein in the urine = Nephrotic syndrome

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11
Q

Why is minimal change disease seen with Hodgkin lymphoma?

A

Massive overproduction of cytokines leads to effacement of podocytes

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12
Q

What are the LM findings of MCD?

A

Normal glomeruli, with maybe lipid in proximal tubule

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13
Q

What are the EM findings of MCD?

A

Effacement of foot processes

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14
Q

Are there immune deposits with MCD? Are there any findings on IF?

A

No, and thus no IF findings

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15
Q

What proteins are lost with MCD? Why?

A

Loss of albumin but NOT immunoglobin d/t only loss of podocytes

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16
Q

What is the treatment and outcome of MCD? Why?

A

Steroids, with good response, since damage is mediated by cytokines from T cells

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17
Q

What is the only nephrotic syndrome that has an excellent response to steroids?

A

MCD

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18
Q

What are the cells that form the interstitium of the glomerulus? Function? What type of cells are these derived from

A
  • Mesangial cells
  • Phagocytic cells
  • Modified smooth muscle cells
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19
Q

What is the most common cause of nephrotic syndrome in Hispanics? African-americans?

A

FSGS for both

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20
Q

What is focal segmental glomerulosclerosis (FSGS)?

A

Idiopathic focal and segmental sclerosis

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21
Q

What are the viral, drug, and disease associations with FSGS?

A
  • HIV
  • Heroin
  • Sickle cell dz
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22
Q

HIV pt who develops renal disease has what specific renal disease?

A

FSGS

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23
Q

What are the histological findings of FSGS on LM? EM? IF?

A 
LM = focal and segmental sclerosis
EM = effacement of foot processes
IF = nothing (no immune complex deposition)
24
Q

What does segmental mean in terms of renal pathology?

A

Only a part of the glomerulus is affected

25
Q

What does focal mean in terms of renal pathology?

A

Involvement of only some of the glomeruli in the kidney

26
Q

What is the treatment and prognosis for FSGS?

A

Poor response to steroids, with eventual progression to chronic renal failure

27
Q

What is the most common cause of nephrotic syndrome in caucasian adults?

A

Membranous nephropathy

28
Q

What is the cause of membranous nephropathy? What are the associations (viruses, tumor, autoimmune dz etc)

A
  • Idiopathic
  • Hep B/C
  • Solid tumors
  • SLE
  • Drugs
29
Q

What is the most common cause of death in patients with SLE?

A

Renal failure 2/2 nephritic syndrome, but can also have membranous nephropathy

30
Q

SLE nephropathy = ?

A

Membranous nephropathy

31
Q

What are the LM, EM, and IF findings of membranous nephropathy?

A 
LM = Thick glomerular BM
EM = spikes and domes
IF = *Granular* Immune complex deposition
32
Q

What is the key pathophysiologic cause of membranous nephropathy?

A

Immune complex deposition

33
Q

Any renal disease that has membranous in the name is due to what underlying pathophysiology?

A

Immune complex deposition

34
Q

Why is there a “spike and dome” appearance to membranous nephropathy?

A

Immune complexes are deposited in the BM, but podocytes don’t like this. They synthesize more BM over the immune complexes. Thus the domes are the extra BM + immune complex, and the spikes are the spaces between podocytes

35
Q

Spike and dome appearance on EM = ?

A

Membranous nephropathy

36
Q

What is the underlying pathophysiology of membranoproliferative glomerulonephritis?

A

Immune complex deposition

37
Q

What is the appearance of membranoproliferative glomerulonephritis on LM, EM, and IF?

A 
LM = Tramtrack appearance
EM = Tramtrack appearance
IF = Granular
38
Q

What causes the tram-track appearance of membranoproliferative glomerulonephritis?

A

Mesangial cells proliferate into the granular immune deposition deposits, which separates the podocytes from the BM

39
Q

Tram track appearance on LM = ?

A

membranoproliferative glomerulonephritis

40
Q

What is type I membranoproliferative glomerulonephritis? What viruses is this type specifically associated with?

A

Subendothelial immune complex deposits

HBV and HCV associated

41
Q

Which is more often associated with the tram-track appearance on LM: type I or II membranoproliferative glomerulonephritis?

42
Q

What is type II membranoproliferative glomerulonephritis? What is the specific antibody that is found in the blood of these patients?

A

Immune complex deposition within the BM

C3 nephritic factor

43
Q

What is the role of C3 nephritic factor in type II membranoproliferative glomerulonephritis?

A

Stabilizes the C3 convertase, which increases the formation of C3a and C3b from C3, resulting in inflammatory damage to the BM

44
Q

What renal disease can produce either a nephrotic syndrome, or a nephritic syndrome?

A

Type II membranoproliferative glomerulonephritis

45
Q

Where are the immune complexes found in membranous glomerulonephropathy? Type I membranoproliferative glomerulonephritis? Type II membranoproliferative glomerulonephritis??

A

Membranous glomerulonephropathy = between podocytes and BM

Type I = Between BM and endothelial cells
Type II = Within BM

46
Q

What is the underlying pathophysiology of MCD, and FSGS?

A

Effacement of podocytes

47
Q

What is the underlying pathophysiology of membranous and membranoproliferative nephropathy?

A

Immune complex deposition

48
Q

How does DM cause renal disease?

A

Non-enzymatic glycosylation (NEG) of BM, resulting in hyaline arteriolosclerosis

49
Q

Which is more affected by NEG of DM: afferent or efferent arteriole? What is the consequence of this? How does this manifest?

A

Efferent, meaning there is a higher glomerular filtration pressure.

Initially manifests as microproteinuria, but eventual sclerosis of the glomerulus

50
Q

How do ACEIs slow the progression of glomerular sclerosis 2/2 DM?

A

ANG II would normally constrict the efferent arteriole to increase GFR, but this is already done by hyaline change.

ACEIs relieve the excess pressure

51
Q

What is the first change seen in the glomerulus with DM?

A

Non-enzymatic glycosylation of vascular BM

52
Q

What is the classic finding of glomerular sclerosis 2/2 NEG?

A

Kimmelstiel-Wilson nodules

53
Q

Kimmelstiel-Wilson nodules = ?

A

DM nephropathy (this is pathognomonic)

54
Q

What causes the nephropathy seen with systemic amyloidosis?

A

Amyloid deposition in the mesangium, resulting in nephrotic syndrome

55
Q

What is the classic histological appearance of systemic amyloidosis in the kidney?

A

Congo red stain reveals Apple-green birefringence under polarized light

56
Q

What are the two systemic diseases that cause nephrotic syndrome?

A

DM

Hyaline disease

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