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Renal > Pathology > Flashcards

Pathology Flashcards

1
Q

4 basic morphologic components of Renal Disease

A
  1. glomeruli
  2. tubules
  3. interstitium
  4. blood vessels
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2
Q

Azotemia

A

elevation of BUN and creatinine level seen in both acute and chronic kidney injury

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3
Q

Prerenal azotemia

A

hypoperfusion of the kidneys

hemorrhage, shock, volume depletion and CHF that impairs renal function in the absence of parenchymal damage

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4
Q

postrenal azotemia

A

urine flow is obstructed beyond the level of the kidney

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5
Q

uremia

A

azotemia associated with a constellation of clinical signs, symptoms, and biochem abnormalities
failure of renal excretory function
metabolic and endocrine abnormalities secondary to renal damage

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6
Q

4 Stages of Renal Failure

A
  1. Diminished renal reserve
  2. renal insufficiency
  3. chronic renal failure
  4. end-stage renal disease
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7
Q

Explain what diminished renal reserve is

A

GFR is ~50% of normal
serum BUN and creatinine values are normal
patients are asymptomatic
This is stage 1 of renal failure

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8
Q

Explain what renal insufficiency is

A

This is stage 2 of renal failure
GFR is 20-50% of normal
Azotemia appears associated with anemia and HTN
polyuria and nocturia secondary to decreased concentrating ability

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9
Q

Explain what chronic renal failure is

A

This is stage 3 of renal failure

GFR is t regulate volume and solute composition causing edema, metabolic acidosis and hyperkalemia

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10
Q

Explain what end-stage renal disease is

A

This is stage 4 of renal failure
GFR <5% of normal
terminal stage of uremia

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11
Q

Nephritic

A 
hematuria (RBC casts)
HTN
Azotemia
Oliguria
Proteinuria (<3.5g/day)
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12
Q

Nephrotic

A

severe proteinuria (>3.5g/day)
hypoalbuminemia (<3g.dL)
generalized edema, hyperlipidemia, lipiduria

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13
Q

Hypercellularity

A

inflammatory diseases
cellular proliferation - mesangial or endothelial cells
leukocytic infiltration
formation of crescents -accum of cells of proliferating parietal epithelial cells and infiltrating leukocytes

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14
Q

What does Basement membrane thickening look like?

A

thickening of capillary arteries
on EM - deposition of amorphous electron-dense material like immune complexes
- on endothelial or epithelial side on BM
thickening from increased synthesis of protein components (glomerulosclerosis)

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15
Q

Hyalinosis

A

accumulation of homogenous eosinophilic material
composed of plasma proteins insudated from circulation into glomerular structures
can obliterate capillary lumens of glomerular tuft
commonly in segmental glomerulosclerosis

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16
Q

sclerosis in kidneys

A

accumulations of extracellular collagenous matrix
- confined to masangium or capillary loops or both
form fibrous adhesions

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17
Q 
Acute Proliferative (Poststreptococcal, Postinfectious) Glomerulonephritis 
Cause and Age group
A

Diffuse proliferation of glomerular cells, influx of leukocytes
caused by immune complexes
1-4 weeks after strep
children 6-10 (rarely adults)

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18
Q 
Acute Proliferative (Poststreptococcal, Postinfectious) Glomerulonephritis 
on light microscopy
A 
Enlarged, hypercellular glomeruli 
Infiltration by leukocytes
Proliferation of endothelial and mesangial cells
Crescent formation—severe
Interstitial edema and inflammation
Tubules often contain red cell casts
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19
Q 
Acute Proliferative (poststreptococcal postinfectious) glomerulonephritis
Granular deposits
A

depositis IgG, IgM, and C3 in the mesangium and along the GBM

on EM will be on epithelial side of membrane looks like “humps”

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20
Q 
Acute Proliferative (poststreptococcal postinfectious) glomerulonephritis
Clinical Course
A

young child
abrupt malaise, fever, nausea, oliguria and hematuria
usually 1-2weeks after sore throat
Red cell casts in the urine
Mild proteinuria (usually less than 1 gm/day)
Periorbital edema
Mild to moderate hypertension

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21
Q 
Acute Proliferative (poststreptococcal postinfectious) glomerulonephritis
Lab Findings
A

elevations of antistreptococcal Ab titers

decline in serum concentration of C3

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22
Q

Rapidly Progressive Glomerulonephritis

A

AKA crescentic glomerulonephritis
Rapid and progressive loss of renal function
Severe oliguria and signs of nephritic syndrome
Crescents - Proliferation of parietal epithelial cells lining Bowman capsule
Infiltration of monocytes and macrophages
can have fibrin strands between cellular layers of the crescents

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23
Q

3 Groups of Rapidly Progressive Glomerulonephritis

A
  1. Anti-GBM Ab-induced disease (Goodpasture)
  2. Immune complex deposition
  3. Pauci-immune type
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24
Q

Goodpasture Syndrome

Anti-GBM Ab-induced dx

A

Linear deposits of IgG and C3 (most cases) in the GBM
Plasmapheresis
Serum has anti-GBM antibodies

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25
Q

Immune Complex Deposition of rapidly progressive glomerulonephritis

A

Post-infectious, LN, IgA nephropathy, HSP
Granular pattern of staining
Treat underlying disease
Granular immune deposits

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26
Q

Pauci-immune type

A

Lack of anti-GBM antibodies or immune complexes by IF and EM
Circulating antineutrophil cytoplasmic antibodies (ANCAs)
Little or no deposition of immune reactants

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27
Q

Gross exam of rapidly progressive glomerulonephritis

A

kidneys are enlarged and pale

petechial hemorrhages on cortical surfaces

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28
Q

rapidly progressive glomerulonephritis on EM

A

Deposits (immune complex cases)

Distinct ruptures in the GBM

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29
Q

Rapidly Progressive Glomerulonephritis

Clinical Course

A

Hematuria with red blood cell casts in the urine
Moderate proteinuria–can reach nephrotic range
Variable hypertension and edema

as it progresses - severe oliguria

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30
Q

Rapidly Progressive Glomerulonephritis

Serum Analysis

A

Anti-GBM antibodies
Antinuclear antibodies
Antineutrophil cytoplasmic antibodies

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31
Q

Membranous Nephropathy

A

Common cause of the nephrotic syndrome in adults
Diffuse thickening of the glomerular capillary wall
Accumulation of electron-dense, Ig-containing deposits along the subepithelial side of the basement membrane
Must have either - underlying malignant tumor, SLE, infection like hepB or C, syphilis, schistosomiasis, malaria, or other autoimmune disorders like thyroiditis

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32
Q

Membranous Glomerulopathy on light microscopy

A

Glomeruli
Normal in the early stages of the disease
Exhibit uniform, diffuse thickening of the glomerular capillary wall

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33
Q

Membranous Glomerulopathy on EM and immunofluorescence

A

EM - Irregular dense deposits of immune complexes
Between the basement membrane and the overlying epithelial cells
IF - granular deposits of both Ig and complement

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34
Q

Membranous Glomerulopathy Clinical

A

slow onset of nephrotic syndrome, hematuria, mild HTN in 15-35%
poor prognosis is concurrent sclerosis of glomeruli
spontaneous remission more in women

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35
Q

most common cause of nephrotic syndrome in children

A

minimal change disease

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36
Q

Minimal Change Disease peak incidence and tx

A

Peak 2-6years
follos respiratory tract infections of after immunization
Responds to corticosteroids

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37
Q

Minimal Change disease on light microscopy and EM

A

LM - normal glomeruli

EM - diffuse effacement of foot processes of visceral epithelial cells in glomeruli

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38
Q

In adults, what is associated with minimal change disease?

A

hodgkin lymphoma

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39
Q

Clinical Feature of Minimal Change Disease

A

massive proteinuria, good renal function, no HTN or hematuria

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40
Q

Focal Segmental Glomerulosclerosis

A

sclerosis in some of glomeruli showing capillary tufts
nephrotic syndrome or heavy preoteinuria
has different types
primary disease is idiopathic

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41
Q

possible diseases associated with focal segmental glomerulosclerosis

A

HIV, heroin addicition, sickle cell disease and massive obesity

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42
Q

secondary event of Focal Segmental Glomerulosclerosis

A

IgA nephropathy

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43
Q

Adaptive response of Focal Segmental Glomerulosclerosis

A

reflux nephropathy, hypertensive nephropathy, unilateral renal agenesis

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44
Q

Focal Segmental Glomerulosclerosis - light microscopy

A

focal, segmental lesions in some glomeruli
lipid droplets, foam cells
hyalinosis and thickened afferent arterioles
Vairant is collapsing glomerulopathy - retraction or collapse of glomerular tuft (characteristic of HIV assoc nephropathy)

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45
Q

immunofluorescence microscopy - what deposits and where

A

IgM and C3

sclerotic areas and.or mesangium

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46
Q

Membranoproliferative Glomerulonephritis (MPGN)

A

2 types
alters glomerular BM, proliferation of glomerular cells, leukocyte infiltration
combo of nephrotic and nephritic

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47
Q

Primary MPGN

A

idiopathic
type I and type II
Type II is dense depositi disease

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48
Q

Secondary MPGN

A

systemic disorders/known etiologic agents

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49
Q

Key words Membranoproliferative Glomerulonephritis

A

proliferative cells in mesangium
endocapillary proliferation involving capillary endothelium and infiltrating leukocytes
crescents
“lobular appearance:
“double-contour” or “tram-track” appearance

50
Q

Type I MPGN

A

majority of cases
discrete subendothelial electron-dense deposits
mesangial and subepithelial deposits
C3, IgG, C1q and C4 in granular pattern

51
Q

Type II MPGN

A

dense deposit disease
lamina densa of GBM is ribbon-like, extremely electron dense
C3 in mesangium in circles
C3 irreg or linear foci in BM on either side

52
Q

mesangial rings

A

Type II Membranoproliferative Glomerulonephritis

53
Q

Berger Disease

A

IgA Nephropathy
IgA in mesangial regions
frequent hematuria
most common glomerulonephritis worldwide

54
Q

Berger Disease - Glomeruli Appearance

A

May be normal or show mesangial widening and endocapillary proliferation
- leukocyte in glomerular capillaries
depositis in mesangium (IgA)
also seen: C3, properdin IgG or IgM

55
Q

Henoch-Schönlein Purpura

Clinical

A

purpuric lesions on extensor surfaces of arms, legs and booty
pain, vomit, intestinal bleeding
hematuria, nephrotic and nephritic syndrome
3-8years (sometimes adults)
follows URT infection

56
Q

Henoch-Schönlein Purpura

Morphology

A 
focal mesangial proliferation
diffuse mesangial proliferation
crescentic glomerulonephritis
IgA deposition (sometimes IgG, C3) 
Subepidermal hemorrhages
necrotizing vasculitis of small vessels in dermis
57
Q

Alport Syndrome

A 
heterohenous familial renal disease
glomerular injury
hematuria => chronic renal failure
red cell casts
nerve deafness
eye disorders
X-linked and autosomal recessive/dominant
58
Q

Renal disease associated with various eye disorders

A

Alport Syndrome

lens dislocation, posterior cataracts, and corneal dystrophy

59
Q

X-linked Alport’s

A

85% of cases
males express full syndrome
females are carriers and present with hematuria

60
Q

Autosomal recessive/dominant Alport Syndrome

A

males and females are equally susceptible to full syndrome

61
Q

Disease where glomeruli BM have alternative thickening and thinning

A

Alport Syndrome

62
Q

Disease with interstitial foam cells filled with neutral fats and mucopolysaccharides

A

Alport Syndrome

63
Q

Disease Progression of Alport

A

focal segmental and global glomerulosclerosis

64
Q

Disease with pronouced splitting and laminatino of lamina densa *basket-weave”

A

Alport Syndrome

65
Q

Ages associated with Alport

A

symptoms 5-20years

onset of overt renal failure: 20-50years

66
Q

Diseases associated with Chronic Glomerulonephritis

A

End-stage glomerular disease
Poststreptococcal glomerulonephritis (adults)
Crescentic glomerulonephritis
Membranous nephropathy, MPGN, IgA nephropathy, and FSGS

67
Q

Chronic Glomerulonephritis

morphology

A

symmetrical contraction of kidneys with diffusely granular cortical surfaces
cortex thinned with increase peripelvic fat
obliterated glomeruli due to acellular eosinophilic masses
arterial and arteriolar sclerosis
atrophy
irregular interstitial fibrosis
mononuclear leukocytic infiltration of interstitium

68
Q

Causes of acute tubular necrosis or acute kidney injury (AKI)

A

ischemia, direct toxic injury to tubules - drugs, radiocontrast, myoglobin, Hb, radiation
acute tubulointerstitial nephritis (HS rxn to drugs)
urinary obstruction

69
Q

Acute Kidney Injury Morphology

A 
focal tubular necrosis
tubulorrhexis
eosinophilic hyaline casts
Tamm-Horsfall protein
accum leukocytes in vasa recta
70
Q

Toxins associated with Toxic AKI

A

primarily affect proximal convoluted tubule
Mercuric chloride - acidophilic
carbon tetrachloride - neutral lipids
ethylene glycol - marked ballooning and hydropic or vacuolar degeneration of prox tubule and calcium oxalate crystals

71
Q

Acute Tubulointerstitial Nephritis

A

rapid onset, leukocytes, interstitial edema, focal tubular necrosis

72
Q

Chronic Tubulointerstitial Nephritis

A

mononuclear leukocytes, interstitial fibrosis, tubular atrophy

73
Q

Acute Pyelonephritis

A

suppurative inflammation of kidney

bacterial and viral (polymavirus)

74
Q

Hallmarks of Acute Pyelonephritis

A

Patchy interstitial suppurative inflammation
Intratubular aggregates of neutrophils
Tubular necrosis

75
Q

3 Complications of Acute Pyelonephritis

A

papillary necrosis
Pyonephrosis
perinephric abscess

76
Q

Causes of papillary necrosis

A 
SODA
sickle cell
obstructive pyelonephritis
diabetes
analgesics
77
Q

Pyonephrosis

A

suppurative destruction of renal parenchyma or loss of kidney function
fever, chills, flank pain
assoc with acute pyelonephritis

78
Q

perinephric abscess

A

collection of suppurative material in perinephric space

assoc with acute pyelonephritis

79
Q

Pyelonephritic scar

A

inflammation, fibrosis, deformation, of underlying calyx and pelvis
assoc with acute pyelonephritis

80
Q

Chronic Pyelonephritis

A

Chronic tubulointerstitial inflammation and renal scarring
involves calyces and pelvis
important cause of kidney destructino in children with severe urinary tract abnormalities
- chronic reflux
- chronic obstructive

81
Q

Hallmarks of Chronic Pyelonephritis

A

kidneys irregulrly scarred
coarse, discrete, corticomedullar scars overlying dilated, blunted, or deformed calyces, flattening papillae
thyroidization - Dilated tubules with flattened epithelium filled with colloid casts
periglomerular fibrosis

82
Q

Analgesic Nephropathy

A

type of chronic renal disease
cause: excessive analgesics
Chronic tubulointerstitial nephritis and renal papillary necrosis

83
Q

Morphology of Analgesic Nephropathy

A 
normal or smaller kidney
cortical atrophy over necrotic papillar
cortical loss, atrophy of tubules
papillar with necrosis, calcification, fragmentation and sloughing
interstitial fibrosis and inflammation
84
Q

Clinical Analgesic Nephropathy

A

women > men
recurrent headaches and muscle pain, GI upset, HTN
psychoneurotic, factory workerstips of necrotis papillar are excreted causing hematuria or renal colic
withdrawal of drug = renal fx stabilizes or improves

85
Q

Acute Uric Acid Nephropathy

A

precip of urate crystals in tubules (collcting ducts)
obstructs nephrons
leukemias and lymphomas undergoing chemo

86
Q

Chronic Urate Nephropathy (gouty nephropathy)

A

Deposition of monosodium urate crystals in distal tubules, collecting ducts, interstitium
birefringent needle-like crystals in the tubular lumens or interstitium
Tophus

87
Q

tophus

A

foreign-body giant cells, other mononuclear cells and a fibrotic reaction

88
Q

nephrolithiasis

A

uric acid stone in 22% with gout

42% with secondary hyperuricemia

89
Q

Urolithiasis (Gender and Age)

A

Men > women
20-30y/o
herediatry predisposition

90
Q

types of caliculi

A

Calcium Stone (70%)
Triple Stone of Strucite Stones (15%)
Uric Acid Stones (5-10%)
Cystine (1-2%)

91
Q

calcium stone

A

Calcium oxalate or calcium oxalate mixed with calcium phosphate

92
Q

triple stones or struvite stones

A

Magnesium ammonium phosphate
Largest stones; staghorn calculi
Infections by bacteria (Proteus and some staphylococci)

93
Q

uric acid stone

A

Hyperuricemia (gout)

Radiolucent

94
Q

Sporadic
abnormal metanephric differentiation
Persistence in the kidney of abnormal structures -
Cartilage, undifferentiated mesenchyme, and immature collecting ductules

A

Multicystic Renal Dysplasia

95
Q

Multicystic Renal Dysplasia Morphology

A

enlarged, multicystic kidney
lined by flattened epithelium
islands of undifferentiated mesenchyme with cartilage and immature collecting ducts

96
Q

Autosomal-Dominant Polycystic Kidney Disease

A

Multiple expanding cysts of both kidneys (4kg/kidney)
Destroy the renal parenchyma and cause renal failure
high penetrance
cysts are 3-4cm filled with clear, serous fluid or turbid red/brown fluid that come from tubules
ADULT

97
Q

Autosomal-Recessive Polycystic Kidney Disease

who it affects, what gene?

A

CHILD
Perinatal, neonatal, infantile, and juvenile subcategories
Time of presentation and presence of associated hepatic lesions
Mutations of the PKHD1 gene

98
Q

Autosomal-Recessive Polycystic Kidney Disease

Morphology

A 
enlarged kidneys with smooth external appearance
Numerous small cysts in the cortex and medulla
Spongelike appearance
Cysts
Uniform lining of cuboidal cells
Origin from the collecting ducts
Liver has cysts
Associated portal fibrosis
Proliferation of portal bile ducts
99
Q

Medullary Sponge Kidney

A

sporadic
BL cystic dilations of medullary collecting ducts
Normal cortex
presents in adulthood
asymptomatic with normal renal fx
Dx with IV pyelography
Normal sized kidneys, mult small cysts in medullary pyramids and papillae

100
Q

Diseases associated with Medullary Sponge Kidney

A

Marfan’s
Caroli’s
Ehlers-Danlos

101
Q

Medullary Sponge Kidney - Microscopic findings

A

Medullary cysts lined by cuboidal epithelium or urothelium
Severe inflammation and scarring in interstitium
Tubular atrophy near papillary tips

102
Q

Renal Papillary Adenoma

A 
Benign Tumor
small, discrete
from renal tubular epithelium
complex, branching, papillomatous structures
size of tumor of 3cm will metastasize
103
Q

Angiomyolipoma

A

Benign Tumor
vessels, smooth muscle and fat
25-50% patients with tuberous sclerosis
susceptible to spontaneous hemorrhage

104
Q

Oncocytoma

A 
Benign Tumor
composed of large eosinophilic cells
small, round nuclei with large nucleoli
from intercalated calls of collecting ducts
Tan/ Mahongany Brown and encapsulated
NUMBEROUS MITOCHONDRIA
105
Q

Renal Cell Carcinoma

A 
6th-7th decade
2:1 male
risk factor: tobacco
from tubular epithelium
yellow in color
Includes: Collecting duct (Bellini duct) carcinoma, chromophobe, papillary and clear cell carcinoma
106
Q

Clear Cell Carcinoma

A

70-80% renal cancers
derive - prox tubule
orange/yellow (lipid), upper pole, hemorrhage, necrosis and calcification
freq involve renal vein and renal sinus

107
Q

bilateral clear cell carcinoma

A

in 1%
von Hippel Lindau
tuberous sclerosis

108
Q

Clear cell carcinoma - microscopic

A

Compact, tubulocystic, alveolar patterns
Clear/granular cytoplasm (glycogen/lipid)
Cell size is 2x normal epithelial tubule cell

109
Q

Clear Cell Carcinoma Genetics

A

deletion of short arm chromosome 3 (-3p)

110
Q

Papillary Carcinoma

%, origin, size

A

10-15% renal cancers
AKA chromophil renal carcinoma
origin: prox or distal convoluted tubules
size >5mm

111
Q

Papillary Carcinoma - Microscopic

A

Well-circumscribed, often with distinct fibrous capsule
Papillary growth pattern
Foamy macrophages and intracellular hemosiderin

112
Q

Forms of Papillary Carcinoma

A

Sporadic: Trisomies 7, 16, 17 and loss of Y in men
Familial: trisomy 7

113
Q

Chromophobe Renal Carcinoma

%, origin, gross

A

5% renal cancers
origin: intercalated cells of collecting ducts
well-circumscribed, tan brown, geographic necrosis
~8cm
Excellent prognosis

114
Q

Chromophobe Renal Carcinoma - Microscopic

A

nests or broad alveoli/trabeculae
Prominent cell membranes and pale eosinophilic cytoplasm
Halo around the nucleus
Positive for Hale’s colloidal iron stain

115
Q

Chromophobe Renal Carcinoma - genetics

A

multiple chromosome losses and extreme hypodiploidy

116
Q 
Collecting Duct (Bellini Duct) Carcinoma - %, Origin, Gross
Prognosis
A

<1% renal carcinomas
origin: collecting duct cells in medulla
Gross: infiltrative, firm, gray-white, ~5cm, may have intrarenal metastases
Death in weeks-months

117
Q

Collecting Duct (Bellini Duct) Carcinoma - microscopic

A

Poorly circumscribed tubulopapillary tumor, infiltrative borders
Nests of malignant cells in fibrotic stroma
Medullary location
Irregular channels lined by high grade hobnail cells
Marked desmoplastic response
Brisk neutrophilic infiltrate
Mucin production

118
Q

Hyperacute Renal Rejection

A

within minutes to hours after transplantation
result from: pre-sensitization, imcompatible blood/HLA groups, complement activation
vasc thrombosis and ischemic necrosis

119
Q

Acute Renal Rejection

A

first 5-7days post-transplant
CMI injury
delayed HS and cytotoxicity mechanisms
immune injury against HLA expressed by tubular epithelium and vascular endothelium

120
Q

Banff Schema

A

acute renal rejection with tubulitis and intimal arteritis

intimal arteritis - infiltration of arterial intima

Renal (3 decks)

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