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Pathology Flashcards

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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
Immune Complex Deposition of rapidly progressive glomerulonephritis
Post-infectious, LN, IgA nephropathy, HSP Granular pattern of staining Treat underlying disease Granular immune deposits
26
Pauci-immune type
Lack of anti-GBM antibodies or immune complexes by IF and EM Circulating antineutrophil cytoplasmic antibodies (ANCAs) Little or no deposition of immune reactants
27
Gross exam of rapidly progressive glomerulonephritis
kidneys are enlarged and pale | petechial hemorrhages on cortical surfaces
28
rapidly progressive glomerulonephritis on EM
Deposits (immune complex cases) | Distinct ruptures in the GBM
29
Rapidly Progressive Glomerulonephritis | Clinical Course
Hematuria with red blood cell casts in the urine Moderate proteinuria--can reach nephrotic range Variable hypertension and edema as it progresses - severe oliguria
30
Rapidly Progressive Glomerulonephritis | Serum Analysis
Anti-GBM antibodies Antinuclear antibodies Antineutrophil cytoplasmic antibodies
31
Membranous Nephropathy
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
32
Membranous Glomerulopathy on light microscopy
Glomeruli Normal in the early stages of the disease Exhibit uniform, diffuse thickening of the glomerular capillary wall
33
Membranous Glomerulopathy on EM and immunofluorescence
EM - Irregular dense deposits of immune complexes Between the basement membrane and the overlying epithelial cells IF - granular deposits of both Ig and complement
34
Membranous Glomerulopathy Clinical
slow onset of nephrotic syndrome, hematuria, mild HTN in 15-35% poor prognosis is concurrent sclerosis of glomeruli spontaneous remission more in women
35
most common cause of nephrotic syndrome in children
minimal change disease
36
Minimal Change Disease peak incidence and tx
Peak 2-6years follos respiratory tract infections of after immunization Responds to corticosteroids
37
Minimal Change disease on light microscopy and EM
LM - normal glomeruli | EM - diffuse effacement of foot processes of visceral epithelial cells in glomeruli
38
In adults, what is associated with minimal change disease?
hodgkin lymphoma
39
Clinical Feature of Minimal Change Disease
massive proteinuria, good renal function, no HTN or hematuria
40
Focal Segmental Glomerulosclerosis
sclerosis in some of glomeruli showing capillary tufts nephrotic syndrome or heavy preoteinuria has different types primary disease is idiopathic
41
possible diseases associated with focal segmental glomerulosclerosis
HIV, heroin addicition, sickle cell disease and massive obesity
42
secondary event of Focal Segmental Glomerulosclerosis
IgA nephropathy
43
Adaptive response of Focal Segmental Glomerulosclerosis
reflux nephropathy, hypertensive nephropathy, unilateral renal agenesis
44
Focal Segmental Glomerulosclerosis - light microscopy
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)
45
immunofluorescence microscopy - what deposits and where
IgM and C3 | sclerotic areas and.or mesangium
46
Membranoproliferative Glomerulonephritis (MPGN)
2 types alters glomerular BM, proliferation of glomerular cells, leukocyte infiltration combo of nephrotic and nephritic
47
Primary MPGN
idiopathic type I and type II Type II is dense depositi disease
48
Secondary MPGN
systemic disorders/known etiologic agents
49
Key words Membranoproliferative Glomerulonephritis
proliferative cells in mesangium endocapillary proliferation involving capillary endothelium and infiltrating leukocytes crescents "lobular appearance: "double-contour" or "tram-track" appearance
50
Type I MPGN
majority of cases discrete subendothelial electron-dense deposits mesangial and subepithelial deposits C3, IgG, C1q and C4 in granular pattern
51
Type II MPGN
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
mesangial rings
Type II Membranoproliferative Glomerulonephritis
53
Berger Disease
IgA Nephropathy IgA in mesangial regions frequent hematuria most common glomerulonephritis worldwide
54
Berger Disease - Glomeruli Appearance
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
Henoch-Schönlein Purpura | Clinical
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
Henoch-Schönlein Purpura | Morphology
``` focal mesangial proliferation diffuse mesangial proliferation crescentic glomerulonephritis IgA deposition (sometimes IgG, C3) Subepidermal hemorrhages necrotizing vasculitis of small vessels in dermis ```
57
Alport Syndrome
``` heterohenous familial renal disease glomerular injury hematuria => chronic renal failure red cell casts nerve deafness eye disorders X-linked and autosomal recessive/dominant ```
58
Renal disease associated with various eye disorders
Alport Syndrome | lens dislocation, posterior cataracts, and corneal dystrophy
59
X-linked Alport's
85% of cases males express full syndrome females are carriers and present with hematuria
60
Autosomal recessive/dominant Alport Syndrome
males and females are equally susceptible to full syndrome
61
Disease where glomeruli BM have alternative thickening and thinning
Alport Syndrome
62
Disease with interstitial foam cells filled with neutral fats and mucopolysaccharides
Alport Syndrome
63
Disease Progression of Alport
focal segmental and global glomerulosclerosis
64
Disease with pronouced splitting and laminatino of lamina densa *basket-weave"
Alport Syndrome
65
Ages associated with Alport
symptoms 5-20years | onset of overt renal failure: 20-50years
66
Diseases associated with Chronic Glomerulonephritis
End-stage glomerular disease Poststreptococcal glomerulonephritis (adults) Crescentic glomerulonephritis Membranous nephropathy, MPGN, IgA nephropathy, and FSGS
67
Chronic Glomerulonephritis | morphology
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
Causes of acute tubular necrosis or acute kidney injury (AKI)
ischemia, direct toxic injury to tubules - drugs, radiocontrast, myoglobin, Hb, radiation acute tubulointerstitial nephritis (HS rxn to drugs) urinary obstruction
69
Acute Kidney Injury Morphology
``` focal tubular necrosis tubulorrhexis eosinophilic hyaline casts Tamm-Horsfall protein accum leukocytes in vasa recta ```
70
Toxins associated with Toxic AKI
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
Acute Tubulointerstitial Nephritis
rapid onset, leukocytes, interstitial edema, focal tubular necrosis
72
Chronic Tubulointerstitial Nephritis
mononuclear leukocytes, interstitial fibrosis, tubular atrophy
73
Acute Pyelonephritis
suppurative inflammation of kidney | bacterial and viral (polymavirus)
74
Hallmarks of Acute Pyelonephritis
Patchy interstitial suppurative inflammation Intratubular aggregates of neutrophils Tubular necrosis
75
3 Complications of Acute Pyelonephritis
papillary necrosis Pyonephrosis perinephric abscess
76
Causes of papillary necrosis
``` SODA sickle cell obstructive pyelonephritis diabetes analgesics ```
77
Pyonephrosis
suppurative destruction of renal parenchyma or loss of kidney function fever, chills, flank pain assoc with acute pyelonephritis
78
perinephric abscess
collection of suppurative material in perinephric space | assoc with acute pyelonephritis
79
Pyelonephritic scar
inflammation, fibrosis, deformation, of underlying calyx and pelvis assoc with acute pyelonephritis
80
Chronic Pyelonephritis
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
Hallmarks of Chronic Pyelonephritis
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
Analgesic Nephropathy
type of chronic renal disease cause: excessive analgesics Chronic tubulointerstitial nephritis and renal papillary necrosis
83
Morphology of Analgesic Nephropathy
``` 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
Clinical Analgesic Nephropathy
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
Acute Uric Acid Nephropathy
precip of urate crystals in tubules (collcting ducts) obstructs nephrons leukemias and lymphomas undergoing chemo
86
Chronic Urate Nephropathy (gouty nephropathy)
Deposition of monosodium urate crystals in distal tubules, collecting ducts, interstitium birefringent needle-like crystals in the tubular lumens or interstitium Tophus
87
tophus
foreign-body giant cells, other mononuclear cells and a fibrotic reaction
88
nephrolithiasis
uric acid stone in 22% with gout | 42% with secondary hyperuricemia
89
Urolithiasis (Gender and Age)
Men > women 20-30y/o herediatry predisposition
90
types of caliculi
Calcium Stone (70%) Triple Stone of Strucite Stones (15%) Uric Acid Stones (5-10%) Cystine (1-2%)
91
calcium stone
Calcium oxalate or calcium oxalate mixed with calcium phosphate
92
triple stones or struvite stones
Magnesium ammonium phosphate Largest stones; staghorn calculi Infections by bacteria (Proteus and some staphylococci)
93
uric acid stone
Hyperuricemia (gout) | Radiolucent
94
Sporadic abnormal metanephric differentiation Persistence in the kidney of abnormal structures - Cartilage, undifferentiated mesenchyme, and immature collecting ductules
Multicystic Renal Dysplasia
95
Multicystic Renal Dysplasia Morphology
enlarged, multicystic kidney lined by flattened epithelium islands of undifferentiated mesenchyme with cartilage and immature collecting ducts
96
Autosomal-Dominant Polycystic Kidney Disease
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
Autosomal-Recessive Polycystic Kidney Disease | who it affects, what gene?
CHILD Perinatal, neonatal, infantile, and juvenile subcategories Time of presentation and presence of associated hepatic lesions Mutations of the PKHD1 gene
98
Autosomal-Recessive Polycystic Kidney Disease | Morphology
``` 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
Medullary Sponge Kidney
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
Diseases associated with Medullary Sponge Kidney
Marfan's Caroli's Ehlers-Danlos
101
Medullary Sponge Kidney - Microscopic findings
Medullary cysts lined by cuboidal epithelium or urothelium Severe inflammation and scarring in interstitium Tubular atrophy near papillary tips
102
Renal Papillary Adenoma
``` Benign Tumor small, discrete from renal tubular epithelium complex, branching, papillomatous structures size of tumor of 3cm will metastasize ```
103
Angiomyolipoma
Benign Tumor vessels, smooth muscle and fat 25-50% patients with tuberous sclerosis susceptible to spontaneous hemorrhage
104
Oncocytoma
``` 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
Renal Cell Carcinoma
``` 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
Clear Cell Carcinoma
70-80% renal cancers derive - prox tubule orange/yellow (lipid), upper pole, hemorrhage, necrosis and calcification freq involve renal vein and renal sinus
107
bilateral clear cell carcinoma
in 1% von Hippel Lindau tuberous sclerosis
108
Clear cell carcinoma - microscopic
Compact, tubulocystic, alveolar patterns Clear/granular cytoplasm (glycogen/lipid) Cell size is 2x normal epithelial tubule cell
109
Clear Cell Carcinoma Genetics
deletion of short arm chromosome 3 (-3p)
110
Papillary Carcinoma | %, origin, size
10-15% renal cancers AKA chromophil renal carcinoma origin: prox or distal convoluted tubules size >5mm
111
Papillary Carcinoma - Microscopic
Well-circumscribed, often with distinct fibrous capsule Papillary growth pattern Foamy macrophages and intracellular hemosiderin
112
Forms of Papillary Carcinoma
Sporadic: Trisomies 7, 16, 17 and loss of Y in men Familial: trisomy 7
113
Chromophobe Renal Carcinoma | %, origin, gross
5% renal cancers origin: intercalated cells of collecting ducts well-circumscribed, tan brown, geographic necrosis ~8cm Excellent prognosis
114
Chromophobe Renal Carcinoma - Microscopic
nests or broad alveoli/trabeculae Prominent cell membranes and pale eosinophilic cytoplasm Halo around the nucleus Positive for Hale’s colloidal iron stain
115
Chromophobe Renal Carcinoma - genetics
multiple chromosome losses and extreme hypodiploidy
116
``` Collecting Duct (Bellini Duct) Carcinoma - %, Origin, Gross Prognosis ```
<1% renal carcinomas origin: collecting duct cells in medulla Gross: infiltrative, firm, gray-white, ~5cm, may have intrarenal metastases Death in weeks-months
117
Collecting Duct (Bellini Duct) Carcinoma - microscopic
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
Hyperacute Renal Rejection
within minutes to hours after transplantation result from: pre-sensitization, imcompatible blood/HLA groups, complement activation vasc thrombosis and ischemic necrosis
119
Acute Renal Rejection
first 5-7days post-transplant CMI injury delayed HS and cytotoxicity mechanisms immune injury against HLA expressed by tubular epithelium and vascular endothelium
120
Banff Schema
acute renal rejection with tubulitis and intimal arteritis | intimal arteritis - infiltration of arterial intima

Renal (3 decks)

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