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My Board study cards > Nephropathies > Flashcards

Nephropathies Flashcards

1
Q

Amyloidosis is nephrotic or nephritic? what is it associated with?

A

Nephrotic. Associated with chronic conditions ex. multiple myeloma, TB, RA.

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1
Q

Cause of DPGN

A

Due to SLE or MPGN. Most common cause of death in SLE. SLE and MPGN can present as nephrotic syndrome and nephritic syndrome concurrently.

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2
Q

Minimal change disease is a nephrotic or nephritic syndrome?

A

nephrotic syndrome

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2
Q
A

Diabetic glomerulonephropathy

  • Nonenzymatic glycosylation ( EG) of GBM leads to increased permeability, thickening.
  • NEG of efferent arterioles causes increased GFR leading to mesangial expansion.
  • LM-mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesion).
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3
Q

Bergers disease is a nephritic or nephrotic syndrome?

A

Nephritic syndrome

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4
Q

This gets filtrated and is found in urine in minimal change disease

A

Selective loss of albumin, not globulins, caused by GBM polyanion loss.

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5
Q

Most frequent patient population to see post-strept glomerulonephritis and presentation?

A

Most frequently seen in children. Peripheral and periorbital edema, dark urine, and hypertension. Resolves spontaneously.

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5
Q

Is Acute poststreptococcal glomerulonephritis a nephrotic or nephritic syndrome?

A

Nephritic syndrome.

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5
Q
A

Rapidly progressive (crescentic) glomerulonephritis (RPGN)

  • LM and IF-crescent-moon shape.
  • Crescents consist of fibrin and plasma proteins (e.g., C3b) with glomerular parietal cells, monocytes, and macrophages.
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6
Q

What is MPGN Type I associated with?

A

Is associated with HBV, HCV

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7
Q

Is Diabetic glomerulo-nephropathy a nephrotic or nephritic syndrome?

A

Nephrotic syndrome

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7
Q

Nephritic syndrome presentation and associated with?

A

An inflammatory process. When it involves glomeruli, it leads to hematuria and RBC casts in urine. Associated with azotemia, oliguria, hypertension (due to salt retention), and proteinuria (

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8
Q

Pathological process causing damage in glomerulo-nephropathy

A

*Nonenzymatic glycosylation (NEG) of GBM –>increased permeability, thickening *NEG of efferent arterioles –>increases GFR –>mesangial expansion

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8
Q

Nephrotic syndrome presentation and associated with?

A

*Presents with massive proteinuria (>3.5g/day, frothy urine), hyperlipidemia, fatty casts, edema. *Associated with thromboembolism (hypercoagulable state due to AT III loss in urine) and increased risk of infection (loss of immunoglobulins)

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8
Q

Berger’s disease (IgA nephropathy) is related to what clinical disorder?

A

Related to Henoch-Schonlein purpura

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8
Q

What is the pathological process of Alport syndrome

A

Mutation in type IV collagen –> split basement membrane. X-linked.

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9
Q

Berger’s disease (IgA nephropathy) often presents/flares with?

A

Often presents/flares with a URI or acute gastroenteritis.

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10
Q

Whats the prognosis on RPGN

A

Poor prognosis. Rapidly deteriorating renal function (days to weeks)

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11
Q

LM, EM, IM findings in Diffuse proliferative glomerulonephritis (DPGN)

A

**LM-“wire looping” of capillaries *EM-subendothelial and sometimes intramembranous IgG-based IC’s often with C3 deposition. *IF-granular

12
Q

Is RPGN a nephrotic or nephritic syndrome?

A

Nephritic syndrome

14
Q

Membrano proliferative glomerulonephritis (MPGN) type I findings

A

Subendothelial IC depositis with granular IF; “tram-track” appearance due to GBM splitting caused by mesangial ingrowth.

15
Q

Rapidly progressive (crescentic) glomerulonephritis (RPGN) LM and IF findings

A

LM and IF-crescent-moon shape. Crescents consist of fibrin and plasma proteins (ex. C3b) with glomerular parietal cells, monocytes, and macrophages.

16
Q

LM findings of Amyloidosis

A

LM-congo red stain shows apple green bifringence under polarized light

17
Q

LM and EM findings in Minimal change disease (lipoid nephrosis)

A

LM-normal glomeruli EM-foot process effacement

18
Q

What are some disease processes that can result in RPGN

A

*Good pastures syndrome-type II hypersensitivity; antibodies to GBM and aveolar basement membrane –>linear IF. Present with Hematuria/hemoptysis. *Granulomatosis with polyangiitis (c-ANCA) *Microscopic polyangiitis (p-ANCA)

20
Q

Cause of Minimal change disease (lipoid nephrosis)

A

May be triggered by a recent infection or an immune stimulus.

22
Q

Most common patient found with minimal change disease and what is the Treatment?

A

Is most common in children and it responds to corticosteroid Tx.

24
Q

LM and EM findings in Focal segmental glomerulosclerosis

A

LM-segmental sclerosis and hyalinosis. EM-effacement of foot process similar to minimal change disease.

25
Q

LM findings in Diabetic glomerulo-nephropathy

A

LM-mesangial expansion, GBM thickening, eosiniphilic nodular glomerulosclerosis, (Kimmelstiel-Wilson lesion)

27
Q

Cause of Membranous nephropathy

A

Can be idiopathic or caused by drugs, infections, SLE, solid tumors.

28
Q

Focal segmental glomerulosclerosis associations

A

Associated with HIV infection, heroin abuse, massive obesity, interferon treatment, and chronic kidney disease due to congenital absence or surgical removal.

29
Q

Alport Syndrome presents with what?

A

Glomerulonephritis, deafness, and less commonly, eye problems

31
Q

MPGN is nephrotic or nephritic?

A

It is nephrotic, but it can also present as nephritic syndrome.

32
Q
A
  • Minimal change disease (lipoid nephrosis)
    • LM-normal glomeruli.
    • EM-foot process effacement
33
Q

Berger’s disease (IgA nephropathy) LM, EM, and IF findings

A

LM-mesangial proliferation EM-mesangial IC depositis IF-IgA-based IC depositis in mesangium

34
Q

Acute poststreptococcal glomerulonephritis LM, EM, and IM findings

A

*LM-glomeruli enlarged and hypercellular, neutrophils, “lumpy-bumpy” appearance. *EM-subepithelial immune complex (IC) humps. *IF-granular appearance due to IgG, IgM, and C3 deposition along GBM and mesangium.

35
Q
A
  • Membranous nephropathy
    • LM-diffuse capillary and GBM thickening.
    • EM-“spike and dome” appearance with subepithelial deposits.
    • IF -granular. SLE’s nephrotic presentation.
36
Q

Focal segmental glomerulosclerosis is nephrotic or nephritic?

A

nephrotic

37
Q

What is MPGN type II associated with?

A

Is associated with C3 nephritic factor

38
Q

LM, EM, and IF findings in Membranous nephropathy

A

LM-diffuse capillary and GBM thickening EM-“spike and dome” appearance with subepithelial deposits IF-granular. SLE’s nephrotic presentation

39
Q

2nd most common cause of primary nephrotic syndrome in adults?

A

Membranous nephropathy

41
Q

Most common cause of nephrotic syndrome in adults

A

Focal segmental glomerulosclerosis

43
Q

Membrano proliferative glomerulonephritis (MPGN) type II findings

A

Intramembranous IC depositis; “dense depositis.”

44
Q
A
  • Focal segmental glomerulosclerosis
    • LM-segmental sclerosis and hyalinosis.
    • EM-effacement of foot process similar to minimal change disease.
    • Most common cause of nephrotic syndrome in adults.
45
Q
A

Membranaproliferative glomerulonephritis

  • Type 1-subendothelial IC deposits with granular IF; “tram-track” appearance clue to GBM splitting caused by mesangial ingrowth (in picture)
    • Type I is associated with HBV, HCV.
  • Type II-intramembranous IC deposits; “dense deposits.”
  • Can also present as nephritic syndrome.
  • Type II is associated with C3 nephritic factor.

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