#26 Virmani - Glomerular Disease Flashcards

(37 cards)

1
Q

Identify

A

Maltese CrOss

NephrOtic Syndrome

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2
Q

Identify

A

Oval Fat bodies

NephrOtic Proteinuria

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3
Q

Identify

A

Minimal Change Glomerulopathy

Thickening of basement membrane

Tx: prednisone

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4
Q

Identify

A

Focal Segmental Glomeruloscelerosis

podocyte alteration

Rapid deterioration to ESRD with collapsing variant

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5
Q

Identify

A

Collapsing FSGS

Commonly seen with HIV infection or bisphosphonates

Jones Silver stain:

The significant proliferation of podocytes to a point where it forms a pseudo crescent that obliterates the urinary space

Severe wrinkling and retraction of the GBM

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6
Q

Identify

A

Membranous GN

Nephrotic syndrome

development of immune complexes in SubEPIthelial

M-type phospholipase A2 recepter

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7
Q

Identify

A

Diabetic Nephropathy

(Nodular Glomerulosclerosis)

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8
Q

Identify

A

Membranoproliferative Glomerulonephritis (MPGN) SubENDOthelial deposits

Hematuria and proteinueria almost always present

‘tram track’

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9
Q

Identify and list lab results that might be seen.

A

Poststreptococcal GN

Group A, beta-hemolytic streptococcal

Cola-colored urine - RBCs and RBC casts

elevated ASO titer

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10
Q

Identify

A

Normal

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11
Q

What is the major component of the slit diaphragm in the podocyte?

A

Nephrin

Podocyte - highly differentiated epithlial cell

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12
Q

What type of collagen makes up the GBM?

A

Type IV

Structural support of capillary loop

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13
Q

What is the function of fenestrated endothelial cells?

A

Negatively charged and limit the passage of albumin/large molecules

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14
Q

When trying to distinguish the mechanism of glomerular disease which cause will target the podocytes?

Non-immune or Immune

A

Non-immune

Podocytopathy - fusion of the epithelial cells

Minimal change disease and FSGS

filtration barrier is compromised

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15
Q

What underlies most forms of primary GN and many secondary forms?

A

Immune mechanisms:

Antibody-mediated injury

Immune complex formation

Cytotoxic antibodies

Cell-mediatied Immune Injury

Alternative Complement Pathway

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16
Q

What are the general clinical manifestations of glomerular disease?

A

Hypertension

Malaise

Edema

Proteinuria

Hematuria

17
Q

What are the five major features of nephrotic syndrome?

A

Proteinuria >3.5 g/day

Hypoalbuminemia

Edema

Hyperlipiduria

Hyperlipidemia

18
Q

What makes urine “bland”?

Which nephrotic diseases have bland urine?

A

Bland - No casts

1* - Minimal change nephropathy

Focal GN

Membranous Nephropathy

2* - Diabetic nephropathy

Amyloidosis

19
Q

A boy comes in with a rapid onset of nephrotic syndrome. Lab findings indicate normal renal function and normal complement levels. On EM foot process are fused. Diagnosis?

A

Minimal Change nephropathy

(Nil lesion, Lipoid nephrosis)

Secondary Causes: Hodgkin’s lymphoma

NSAIDS

Atopy/Eczema

20
Q

How would you treat minimal change disease?

A

Predisone

Relapse - adjunctive therapy with alkylating agents (cyclosporine, cyclophosphamide, chlorambucil)

21
Q

Define focal vs diffuse.

A

Focal - the disease is “focused” on only one part of the glomeruli (less than 50% of the glomeruli is affected)

Diffuse - the disease has diffused across the entire glomeruli (more than 50% of the glomeruli is affected)

22
Q

Define segmental vs global.

A

Segmental - only a segment of the glomerulus is affected

Global - the glomerulus is a globe; the entire glomerulus is affected.

23
Q

What is a distinctive basement membrane feature in membranous GN?

A

spike formation with granular deposits of IgG

24
Q

FSGS is not a diagnosis but a pattern of disease. What could be the cause?

A

Perihilar lesion (hyperfiltration in setting of HTN)

Collapsing Variant (HIV, IV drug abuse)

Glomerular tip lesion (no HTN, *sensitive to steroids, other side of vascular pole)

25
Identify
Perihilar FSGS IgM
26
20% of cases of membranous GN are non-idiopathic. What can it be associated with?
Malignancy (lung, stomach, breast cancer) Infections (hep B, syphilis) Autoimmune disease (SLE, mixed connective tissue disease) Drugs (gold, D-penicillamine, captopril)
27
Membranous GN is characterized by deposits in what area of the glomerulus?
SubEPIthelial space | (subpodocyte)
28
How would you treat Membranous GN?
Tx: ACEi or ARB Severe: prednisone and chlorambucil/cyclophosphamide
29
What would you find on 20% of diabetic nephropathy renal biopsies?
Kimmelstield-Wilson nodular glomerulosclerosis
30
Immune complexes (IgG + C3) are depositing in the subENDOthelial lining. What is the pattern of injury called?
Membranoproliferative GN (MPGN) young people HEP C Pathology: Tram trak (MPs going to get on the tram trak)
31
How would you treat MPGN?
treat underlying condition (Type 1 - treat HepC) Steroids - poor results
32
A patient comes in with ANA (anti-neutrophilic antibody) + dsDNA with multi-organ involvement. What is the cause and how would you treat it?
Systemic Lupus Erythematosus GN Tx: steroids + cytotoxic drugs
33
Where can isolated hematuria (with or without proteinuria) be found?
IgA nephropathy Hereditary (Alports, thin basement membrane) Benign recurrent hematuria
34
On histology, mesangial hypercellularity, tubular atrophy and segmental sclerosis are found. There are also mesangial deposits of an Ig. Diagnosis?
IgA nephropathy
35
Patient comes in with oliguria, azotemia, salt and water retention with edema. BP is also high. Syndrome?
Acute nephritic syndrome
36
Laboratory findings indicate low serum complement, azotemia, and elevated ASO titer. Diagnosis?
Poststreptococcal Glomerulonephritis (PSGN)
37
RPGN can be classified in three ways which will affect treatment. What are they and what are the treatments?
AntiGBM (Goodpasture's) - [IgG] prednisone and plasma exchange Immune complex (MPGN, IgA, Lupus, PostGN)- treat underlying condition Non-immune-mediated (Wegeners, microPAN) - cyclophospamide and steroids