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Pathology Block C > Disease of Kidneys I - Nephritic > Flashcards

Disease of Kidneys I - Nephritic Flashcards

1
Q

What is generally seen in nephrotic syndrome?

A

proteinuria (>3.5 mg/day; foamy/frothy urine); hypoalbuminemia (dec oncotic pressure-> edema); severe edema; hyperlipidemia; lipiduria

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2
Q

Define azotemia.

A

acute renal failure resulting in an increase in nitrogenous wastes in blood (BUN, creatinine) - exists WITHOUT clinical symptoms but can progress to chronic renal failure

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3
Q

What are some causes of azotemia?

A

prerenal (decreased blood flow), post renal (ureter obstruction), intrarenal (tubular necrosis or interstitial nephritis)

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4
Q

What is uremia?

A

chronic renal failure : azotemia + clinical manifestations

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5
Q

What are the 3 general cell types in glomerulus?

A

podocytes (renal epithelial cells), vascular endothelial cells, mesangial cells

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6
Q

Where are neoplastic changes usually found?

A

tubular epithelial cells (since there’s regenerative capacity)

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7
Q

Endothelial cells line _____.

A

vascular spaces

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8
Q

Podocytes line _____.

A

urinary space

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9
Q

What is seen histological in normal glomerulus?

A

one mesangial cell nucleus, mesangial matrix, endothelial and epithelial cells

BM thin and delicate with uniform thickness

Capillary lumens open

Tubule epithelial cells back-to-back -> interstituim is not thickened

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10
Q

What is significant about the width of podocyte foot processes at EM?

A

same width as BM

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11
Q

Why is fluorescent microscopy essential for diagnoses?

A

usu H&E not enough to determine pathology

essential to detect immune complexes

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12
Q

Name and describe 2 patterns of pathology seen on fluorescent microscopy.

A
  1. homogenous staining: thin, delicate BM -> uniform ribbon staining reflective of autoimmune anti-BM disease
  2. granular aspect: lots of deposits; representative of thousands of immune complexes (“dense, strings of pearls look”
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13
Q

What is seen generally in acute nephritic syndrome?

A

hematuria (“red urine); glomerular hypercelluarity; RBC casts in urine; diminished GFR; mild to moderate proteinuria; HTN; azotemie; oliguria

associated with acute onset

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14
Q

What is another name for acute nepritic syndrome?

A

acute glomerulonephritis

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15
Q

How do RBC casts form?

A

as the RBC cross the BM, the rate of flow in the tubules slow down -> RBCs start sticking together and forming a cast

Tubules produce protein matrix on the cell membrane surfaces -> causes stickiness within tubules

when flow restored -> washed out in urinalysis!

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16
Q

What are RBC casts indicative of?

A

urinary tract damage in kidneys - nephritic

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17
Q

What do WBC casts indicate?

A

tubular inflammatory/infectious diseases of kidneys

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18
Q

What’s another name for acute proliferative glomerulonephritis?

A

Post-infection, Post-streptococcal

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19
Q

Is acute proliferative glomerulonephritis nephritic or nephrotic?

A

nephritic

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20
Q

What age group is targeted for acute proliferative glomerulonephritis?

A

pediatrics (but can occur at any age)

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21
Q

What is clinically seen in acute proliferative glomerulonephritis?

A
  1. usually comes about 1-4 weeks after acute infection (usu pharnygeal or skin)
  2. non-infectious; immunologically mediated (at this point, infection as resolved so we won’t see organism in urine)
  3. sub-epithelial immune complexes (anti-strep Abs -> Ag-Ab complex forms -> deposit in glomeruli -> triggers 2O immune-mediated response)
  4. low complement
22
Q

What is seen in H&E stains of acute proliferative glomerulonephritis?

A
  1. neutrophils plugging up glomerular lumens
  2. cells have multi-lobed nuclei
  3. cannot distinguish epithelial from mesangial from endothelial etc.
  4. marked hypercellularity (many black dots)
  5. structural loss
23
Q

What is expected in FM of acute proliferative glomerulonephritis?

A

huge chunks of varying sizes

24
Q

What is expected in EM of acute proliferative glomerulonephritis?

A

large, irregular clumps on sub-epithelial side of BMl - don’t distort BM!

25
Q

What’s the plan of treatment for acute proliferative glomerulonephritis?

A

supportive

26
Q

What’s the prognosis for acute proliferative glomerulonephritis?

A

pediatrics: good
adults: variable - after clearance, lots of urination

27
Q

What is the general description of rapidly progressive GN?

A

nephritic syndrome

rapid deterioration (within hours)

crescent glomerulonephiritis

28
Q

What creates crescent glomerulonephritis?

A

hypercellularity due to proliferation of the epithelial cells (podocytes) in Bowman’s (urinary) space

29
Q

What is seen in Type I RPGN?

A

idiopathic, anti-GMB (Goodpasture’s Syndrome)

  1. AI anti-BM antibodies (attacks BM and LUNGS) - hematuria and hemoptysis
  2. no discrete deposits - ribbon-like immunofluorescence
  3. most common
30
Q

What is seen in Type II RPGN?

A

idiopathic, postinfectious, SLE, Henock Schonlein Purpura

  1. immune complex-mediated - GRANULAR immunofluorescence
31
Q

What is seen in Type III RPGN?

A

Pauci-immune, anti-neutrophil cytoplasmic antibodies (ANCA)

  1. NEGATIVE immunofluorescence
32
Q

What is seen in H&E of RPGN?

A

crescents (pink bc containg fibrin and macrophages)

circles = collapsed glomeruli

tubules are not back-to-back bc interstitial edema

33
Q

What is seen in FM for RPGN?

A

Type I RPGN = homogenous ribbon like

Type II and III RPGN = chunky bumpy

this is enough for dx - EM no longer needed

34
Q

What’s the plan of treatment for RPGN?

A

supportive, plasmapheresis, steroids

35
Q

What’s the prognosis for RPGN?

A

long-term poor; chronic dialysis; transplant often needed

36
Q

IgA glomerular disease is also called ____?

A

Berger’s disease

37
Q

Berger’s Disease is nephritic or nephortic?

A

nephritic

38
Q

What is seen in Berger’s disease?

A
  1. IgA mesangial deposits - usu following mucosal infections
  2. mesangial hypercelluarity - no neutrophil infiltration
  3. excerbations and remissions of hematuria (disease can be subtle and common - some patients won’t even know)
  4. azotemia: elevated BUN, creatinine
39
Q

What must be considered for differentials of IgA GN (Berger’s disease?

A
  1. IgA deposits are also seen in SLE and Henoch-Schonlein-Purpura
  2. distinguished from other renal problems (no recent strep, not rapidly deteriorating)
  3. need to be biopsied
40
Q

What is seen in IgA/Berger’s H&E?

A
  1. tubules are back-to-back (no interstitial edema), interstitial and vasculature looks normal
  2. dark clumps within glomeruli - mesangial deposits
  3. mesangium is thickened: 4-8 nuclei btwn capillaries
41
Q

What’s seen in IgA/Berger’s FM?

A

“dead tree in winter” - immune complexes restricted to mesangial cells

uniquely IgA-associated immne complex

42
Q

What’s seen in Berger’s EM?

A

BM not affected

deposits in mesangial matrix

43
Q

What’s the treatment plan for IgA?

A

supportive

44
Q

What’s the prognosis for IgA?

A

poor (progressive; recurs even with transplant)

death within few years (bc not acute)

long term prognosis will end up on dialysis

45
Q

Describe Benign Recurrnt Hematuria.

A

diagnosis of exclusion

no histo abnormalities, no renal insufficiency (no azotemia)

what do we see? leaky infiltration; recurrent hematuria

need to biopsy

46
Q

What’s the prognosis for Benign Recurrent Hematuria?

A

long term prognosis is generally better than the other acute glomerulonephritic disease

47
Q

Hereditary Glomerular Disease is ____.

A

heterogenous group including Alport Syndrome and Benign familial hematuria

48
Q

What’s seen clinically in Alport Syndrome?

A

eye disorders (lenticular changes), deafness, male predominance, nephrotic syndrome may develop

49
Q

What mutation brings about Alport syndrome?

A

Type IV collagen genes

50
Q

How do we diagnose for Alport Syndrome?

A

EM : strange looking GBM

-> basketweave appearance: irregular thickening and lamination of GBM

51
Q

What’s seen in benign familial hematuria?

A

structural problem/anatomic defect: Thin GBM disease, good prognosis -> kidney is functionally fine

differentiate from benign recurrent -> here, the BM are very attenuated and thinned out (as opposed to the normal BM in recurrent

52
Q

How do we diagnose bening familial hematuria?

A

EM for structural abnormality

light microscope fine and FM negative

Pathology Block C (7 decks)

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