#26 Virmani - Glomerular Disease Flashcards

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
Q

Identify

A

Perihilar FSGS

IgM

26
Q

20% of cases of membranous GN are non-idiopathic. What can it be associated with?

A

Malignancy (lung, stomach, breast cancer)

Infections (hep B, syphilis)

Autoimmune disease (SLE, mixed connective tissue disease)

Drugs (gold, D-penicillamine, captopril)

27
Q

Membranous GN is characterized by deposits in what area of the glomerulus?

A

SubEPIthelial space

(subpodocyte)

28
Q

How would you treat Membranous GN?

A

Tx: ACEi or ARB

Severe: prednisone and chlorambucil/cyclophosphamide

29
Q

What would you find on 20% of diabetic nephropathy renal biopsies?

A

Kimmelstield-Wilson nodular glomerulosclerosis

30
Q

Immune complexes (IgG + C3) are depositing in the subENDOthelial lining. What is the pattern of injury called?

A

Membranoproliferative GN (MPGN)

young people

HEP C

Pathology: Tram trak

(MPs going to get on the tram trak)

31
Q

How would you treat MPGN?

A

treat underlying condition

(Type 1 - treat HepC)

Steroids - poor results

32
Q

A patient comes in with ANA (anti-neutrophilic antibody) + dsDNA with multi-organ involvement. What is the cause and how would you treat it?

A

Systemic Lupus Erythematosus GN

Tx: steroids + cytotoxic drugs

33
Q

Where can isolated hematuria (with or without proteinuria) be found?

A

IgA nephropathy

Hereditary (Alports, thin basement membrane)

Benign recurrent hematuria

34
Q

On histology, mesangial hypercellularity, tubular atrophy and segmental sclerosis are found. There are also mesangial deposits of an Ig. Diagnosis?

A

IgA nephropathy

35
Q

Patient comes in with oliguria, azotemia, salt and water retention with edema. BP is also high. Syndrome?

A

Acute nephritic syndrome

36
Q

Laboratory findings indicate low serum complement, azotemia, and elevated ASO titer. Diagnosis?

A

Poststreptococcal Glomerulonephritis (PSGN)

37
Q

RPGN can be classified in three ways which will affect treatment. What are they and what are the treatments?

A

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