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CRRAB II > Renal Pathology (Warren) - W3 > Flashcards

Renal Pathology (Warren) - W3 Flashcards

1
Q

What are the three parts of the glomerular basement membrane?

What makes up the backbone of the GBM?

What gives the GBM its negative charge?

A
  • 3 parts
    • lamina rara interna
    • lamina dense
    • lamina rara externa - by podocytes
  • Type IV collagen
  • heparin sulfate gives negative charge
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2
Q

What proteins make up the slit diaphragm?

What do you see in the podocytes with nephrotic syndrome?

A
  • nephrin and podocin
  • podocyte fusion (flattened and merged) is characteristic of nephrotic syndrome
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3
Q

What part of the kidney tubule system is most sensitive to ischemia & toxins?

A
  • Proximal tubules
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4
Q

How many people does chronic renal disease affect?

A

11% in US

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5
Q

What is the definition of azotemia?

A
  • biochemical abnormality
    • increased BUN and creatinine
  • can be…
    • pre-renal: hypoperfusion (hemorrhage, shock, dehydration, CHF)
    • renal disease
    • post-renal
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6
Q

What is the definition of uremia?

A
  • azotemia and clinical symptoms
    • gastroenteritis, anemia, peripheral neuropathy, pruritis (horrible itching), pericarditis
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7
Q

Symptoms of nephritic syndrome

A
  • Hematuria - red cells in urine
  • mild to moderate proteinuria
  • hypertension
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8
Q

What are the clinical symptoms of nephrotic syndrome?

A
  • >3.5gm/day proteinuria
  • hypoalbuminemia
  • edema
  • hyperlipidemia
  • lipiduria
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9
Q

What do you see with acute renal failure?

A
  • rapid decline in GFR - rapid onset azotemia
    • increased BUN/Cr
  • oliguria or anuria
  • caused by glomerular, tubulointerstitial or vascular disease
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10
Q

What do you see with chronic renal failure?

A
  • GFR less than 60 ml/min for at least 3 months
  • persistent albuminuria
  • end result of all renal disease
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11
Q

What are the four stages of renal disease?

A
  1. Diminished renal reserve
    1. GFR 50% of normal
    2. see in elderly
    3. normal range BUN/Cr
  2. Renal insufficiency
    1. GFR = 20-50% of normal, azotemia, anemia, hypertension
  3. Renal failure
    1. GFR 20-25%, edema, metabolic acidosis, uremia
  4. End stage renal disease
    1. GFR <5% of normal
    2. need dialysis or transplant
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12
Q

What is clearance test and equation?

A
  • clearance = approximation of glomerular filtration rate (GFR)
  • clearance = UV/P
    • urine concentration x urine volume
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13
Q

What are the issues w/creatinine as measurement?

How does it compare to the true GFR?

A
  • overestimation of true GFR
  • secreted by proximal tubule
  • related to muscle mass and meat in diet
  • may have extrarenal elimation
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14
Q

What is the risk if a GFR is below 60?

When should you see a nephrologist?

A
  • below 60 = high risk for CV disease
  • below 30 = see nephrologist
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15
Q

In what situations do we use some clearance measures?

A
  • Unusual body habitus
    • severe muscle wasting
  • Rapidly changing kidney function
  • Patients with GFR of 60 or greater
    • kidney donor eval
    • research protocols
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16
Q

What is the BUN?

What is normal?

A
  • major end product of protein nitrogen metabolism - liver will make urea from ammonia
  • normal = 10-20 mg/dl
  • can combine w/serum creatinine to determine cause of azotemia
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17
Q

What can cause a pre-renal increase in BUN?

A
  • Catabolism (burns, fever, stress)
  • high protein diet
  • GI bleed
  • Hemolysis
  • Malignancy
  • decreased renal perfusion
    • hypotension/shock
    • CHF
    • dehydration
    • renal vein thrombosis
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18
Q

What is BUN sensitive to?

A
  • decreased renal perfusion
  • low flow activates renin-angiotensin system that increases water and Na reabsorption
  • urea is passivley reabsorbed along with it
  • serum BUN increases out of proportion to any change in the GFR
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19
Q

What are 3 diseases cause a renal increase in BUN?

A
  • Glomerular disease
  • ATN
  • interstitial disease
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20
Q

What factors cause a post-renal increase in BUN?

A
  • Urinary Tract Obstruction
    • benign prostatic hypertrophy
    • prostatic carcinoma
    • tumor of bladder or ureter
    • retroperitoneal mass
    • urinary calculi
  • basically anything that affects OUTFLOW
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21
Q

What can cause a decrease in BUN?

A
  • decreased synthesis - low protein intake, liver disease
  • hemodilution - overhydration, psychogenic polydipsia, diabetes insipidus, pregnancy
  • generally not diagnostically useful
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22
Q

How is creatinine formed and what is the normal excretion?

A
  • waste product formed by the spontaneous dehydration of body creatinine
  • Normal = 0.7-1.2mg/dL
  • BETTER THAN BUN
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23
Q

What can cause a pre-renal increase in creatinine

A
  • Increased synthesis
    • ​muscle hypertrophy
    • muscle necrosis
    • anabolic steroid use
    • high meat diet
    • intense exercise
  • Decreased reanl perfusion
    • ​CHF, hypotension/shock
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24
Q

What can cause a post-renal increase in creatinine

A
  • urinary tract obstruction
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25
Q

What is a normal BUN: Creatinine ratio?

When is the ratio ELEVATED?

A
  • NORMAL IS 15:1
  • elevated in pre-renal conditions
    • BUN is excessively elevated compared to creatinine
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26
Q

What is fraction of excreted sodium used for?

FeNa calcuation?

What do the % mean?

A
  • differential diagnosis of pre-renal vs. renal disease
  • FeNa = urineNa xplasmaCr x 100 / urineCrx plasmaNa
  • FeNa < 1.0% = pre-renal
  • FeNa > 2.0% = ATN
    • tubules fail so urine sodium is high (>40mEq/L)
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27
Q

What is the urine dipstick used for?

What is it sensitive to?

When can it give a false +?

A
  • sensitive to albumin
  • used to detect protein in urine
  • False +
    • alkaline urine
    • gross hematuria
    • dilute urine
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28
Q

What is the quantitative protein to creatinine ratio used for?

A
  • estimates if there is significant increase in 24 hour urine protein excretion
  • used after + dipstick
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29
Q

What can cause proteinuria without renal disease?

A
  • postural orthostatic (young adults)
  • transient
  • functional
    • heavy exercise, cold exposure, fever
    • won’t be a lot - <0.5gm/24hours
    • hyaline/granular casts
  • CHF - <0.5gm/24hours
  • massive obesity
  • constrictive pericarditis
  • renal vein thrombosis
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30
Q

what is seen with selective proteinuria?

What is seen with nonselective proteinuria?

A
  • albumin and small globulins = nonselective
    • post infectious GN
  • albumin = selective
    • nephrotic syndrome and minimal change disease
  • show glomerular pattern
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31
Q

What is seen with renal disease and shows a tubular pattern

A

beta-2 microglobulin

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32
Q

What is hypoplasia?

What do you see with it?

A
  • failure of development of kidneys to normal size
  • no scarring - see decreased number of renal lobes
    • 6 or less required for true hypoplasia
  • most cases are acquired
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33
Q

What is the most common congential kidney disorder?

A

Horseshoe kidney

10% upper pole fusion

90% lower pole fusion

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34
Q

What is the kidney trapped behind with horseshoe kidney?

A

behind the root of the inferior mesenteric artery in the pelvis

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35
Q

What is seen with cystic renal dysplasia?

How do people get it?

A
  • enlarged, mulitcystic gross features
  • MICRO: tissue that doesn’t bleong
    • ​cartilage & undifferentiated mesenchyme
  • may have other lower tract anomlaies
  • sporadic disorder - not inherited
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36
Q

How is adult polycystic kidney disease inherited?

Is it unilateral or bilateral?

when do we see renal failure?

A
  • autosomal dominant
  • bilateral - initially only involes part of kidney
  • by age 75, 75% have renal failure
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37
Q

What causes adult PCKD?

What are the defects seen with each type?

A
  • multiple expanding cysts destroy renal parenchyma
  • PKD1 - gene on chromo 16p13.3
    • POLYCYSTIN 1
  • PKD2 - gene on 4q21
    • polycystin 2
    • less caes and less severe
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38
Q

What are the gross features of PCKD?

What are the symptoms?

A
  • bilaterally enlarged kidneys (HUGE) - look like bag of cysts
  • may be asymptomatic, have pain, or hematuria
39
Q

What are extra-renal anomalies seen in PKCD?

A
  • Liver cysts
  • Intracranial berry aneurysms
  • Mitral valve prolapse
40
Q

How is childhood polycystic kidney disease inherited?

what is seen on gross features?

bilateral or unilateral?

what else can you see?

A
  • autosomal RECESSIVE
  • 4 categories
  • enlarged, smooth kidneys externally
    • cut section shows small cysts in cortex and medulla
  • BILATERAL
  • liver cyts and duct proliferation
41
Q

What is potter sequence?

why does it occur?

Features?

A
  • abnormalities in fetal kidneys
  • occurs with low amniotic fluid leading to olighydramnios
  • findings
    • low set ears
    • parrot beak nose/flat mid fase
    • lung hypoplasia
42
Q

4 cystic diseases of the medullla

A
  1. Medullary sponge kidney
    1. normal kidney function w/ cysts
  2. Nephronophthisis
    1. polyuria or polydipsia
  3. Acquired cystic disease
    1. long term dialysis
  4. simple cysts
    1. not vascular
43
Q

What do you see with medullary sponge kidney?

A
  • cystic dilutions of collectin gducts
  • disease of ADULTS
  • hematuria, infection or stones
    • NORMAL KIDNEY FUNCTION
44
Q

Nephronophthisis - Uremic Medullary Cystic Disease Complex

Presenation?

Onset?

A
  • presents in childhood
  • progressive
  • see cortical tubular atrophy and interstitial fibrosis - will eventually have small kidneys
  • polyuria and polydipsia
45
Q

What is the major cause of aquired cystic disease?

A

long term dialysis - up to 50%

46
Q

What are the features of a simple cyst?

A
  • `1-5 cm
  • clear fluid inside
  • not vascular
47
Q

what is normally the main cause of glomerulonephritis?

A

immune mediated disease

48
Q

what 3 histological patterns of injury are common with glomerulonephritis?

A
  1. hypercellularity
  2. basement membrane thickening
  3. hyalinization and sclerosis
49
Q

Define:

Diffuse

Focal

Global

Segmental

A
  • diffuse = all glomeruli involved
  • focal = proportion of all glomeruli invovled
  • global = entire single glomeruli invovled
  • segmental = part of single glomeruli invovled
50
Q

Immune mechanisms of injury for glomerulus

A
  1. Antibody mediated
    1. insitu immune complex deposition
    2. circulating immune complex deposition
  2. cell mediated immune injury
  3. activation of alternative complement path
51
Q

What are 3 in situ immune complex depositions?

A
  • Anti-GBM glomerulonephritis
  • heymann nephritis
  • planted antigens
52
Q

What is Anti-GBM glomerulonephritis?

A
  • in situ immune complex depositition - antibodies directed against normal GBM components
  • homogenous, diffuse, linear pattern
  • can cause hemoptysis in lungs - goodpasture syndrome
  • antigen component of alpha 3 chain of type IV collagen
  • <5% of human GN
53
Q

Heymann Nephritis

type

antigen

see on EM

A
  • in situ complex deposition
  • M type phospholipase A2 receptor (PLA2R)
  • granular and interrupted pattern
  • deposits on subepithelial aspect of GBM
54
Q

What are planted antigens?

A
  • non glomerular in origin
  • localize to kidneys
  • antibodies form against them
  • can be DNA, bacterial products, aggregated immunoglobulins
55
Q

What is this?

A

Anti - GBM

diffuse.

56
Q

What occurs with circulating immune complex nephritis?

A
  • glomerular injury caused by trapping circulating complexes within glomerulis - not sepcific for glomerulus
  • type III hypersensitivity
  • antigens endogenous or exogenous
  • can have may types of deposits
57
Q

At what GFR will you progress to end stage renal disease no matter the enciting event w/glomerulonephritis?

A

30-50%

58
Q

What is an adaptive change that occurs with glomerulonephritis?

What is the issue?

how do we treat?

A

FSGS

  • occurs w/loss of functioning nephron
  • known as compensatory hypertrophy
  • see increased flow, filtration and pressure
  • leads to segmental scerlosis - cell injury, protein accumulation
  • treat with ACE
59
Q

What develops with glomerulonephritis over tiem?

What happens to downstream tubules?

A
  • Tubulointersitital fibrosis
  • occurs due to proteinuria that is directly toxic to downstream tubular cells - see ischemic tubules downstream from sclerotic glomeruli
  • increased acute & chronic inflammation
60
Q

What do you see with nephritic syndrome?

A
  • Hematuria and red cell casts
  • variable proteinuria
  • azotemia
  • hypertension - signficant
61
Q

What do you see with nephrotic syndrome?

A
  • proteinuria > 3.5g
  • hypoalbuminemia
  • edema
  • hyperlipidemia
  • oval fat bodies
  • fusion of podocytes
62
Q

What can cause acute poststreptococcal glomerulonephritis?

What are some tests for it?

A
  • caused by group A streptococci - 12, 4 and 1
  • nephritic syndrome
  • serum complement - low
  • antistreptolysin O and antiDNAse B
63
Q

What is seen on IF and EM w/poststreptococcal GN?

Histology?

A
  • large, hypercellular gloomeruli
  • infiltration of neutrophils and monocytes
  • IF
    • granular IgG, IgM, C3 deposits along GBM and mesangium
  • EM
    • subepithelial humps “camel”
64
Q

Prognosis and clinical presentation of acute post-streptococcal GN

A
  • nephritic presentation
    • malaise, oliguria, hematuria “smoky urine”
    • red cell casts
    • periorbital edema
  • 95% of children recover
  • 60% of adults recover
65
Q

Syndrome that causes SEVERE injury to the glomerulus

A

Rapidly progressive (Crescentic) GN

66
Q

What makes up a crescent w/rapidly progressive GN

A

proliferations of parietal epithelial cells of Bowman’s capusle mixed w/inflammatory cells

67
Q

What are the 3 types of crescentic gN

A
  1. Type 1: anti-GBM glomerulonephritis
    1. IgG, C3 in GM
  2. type 2: immune complex mediated
    1. lumpy bumpy granular pattern
    2. SLE, IgA nephropathy
  3. Type 3: Pauci-immune type
    1. lack of IF staining
    2. P or c anca
68
Q

What is the clinical course of crescentric GN?

What is the treatment?

A
  • progressive over weeks w/severe oliguria
  • treated w/plasma exchange, steroids and chemo
69
Q

Describe the pathophysioloy of nephrotic syndrome

A
  • increased permeability to plasma proteins - massive proteinuria - low albumin - reduces colloid osmotic pressure leading to edema
  • increased synthesis of lipoproteins
  • infections due to Ig and complement loss
  • hypercoaguable state due to ATIII loss
70
Q

Who is membranous GN common in?

What are the assciations?

A
  • adults - caucasian population
  • assocations
    • drugs; peenicillamine, captopril, gold, NSAIDs
    • lung, colon cancer, melanoma
    • SLE
    • HBV, HCV, syphillis, shcistosomiasis malaria
    • DM, thyroiditis
71
Q

What is the pathogenesis of membranous GN?

A
  • chronic antigen-antibody medaited disease - phospholipase A2 is autoantigen in many adult cases
  • damage to GBM is complement mediated
72
Q

What is seen on pathology of membranous GN?

Silver stain?

EM?

IF?

A
  • DIFFUSE process
    • thickening of capillary wall - looks like cheeros
  • silver stain - spikes - GBM laid down between deposits
  • Subepithelial deposits - may also see effacement of podocytes
  • IF: lumpy, bumpy pattern
73
Q

What is the clinical course of membranous GN?

A
  • chronic proteinuria and slow deteriation
    • 40% develop renal insufficiency
    • 10% die
  • HIGHLY VARIABLE
74
Q

What is the most common nephrotic disease in children

What are the associations?

A
  • minimal change disease (lipoid nephrosis)
  • associations
    • atopy
    • respiratory infection, immunization
    • Hodgkin lymphoma
75
Q

What is the pathogenesis of minimal change disease?

A
  • possible T cell dysfunction and release of cytokines that damages visceral epithelial cells - may lose charge barrier
  • slit diaphragm loses architecture
76
Q

what is seen clinically with minimal change disease?

What is the treatment?

A
  • massive proteinuria
    • highly selective - mostly albumin
  • no renal failure or hypertension
  • corticosteroids - reverse the damage.
77
Q

What is the pathology of minimal change disease?

M:

IF:

EM

A
  • normal under light micrscope
  • IF shows no staining
  • EM - effacement of foot processes - no deposits
78
Q

What population is focal segmenal glomerulosclerosis (FSGS) common in?

Associations?

A
  • most common cause of nephrotic syndrome in adults
  • Associations
    • HIV
    • heroin addiction
    • sickle cell disease
    • OBESITY - making it more common
79
Q

What is seen with pathology of FSGS?

A
  • M: see focal necrosis - need a good biospy
    • may see collapse of GBM, hyalinization, increased matrix
  • EM: effacement of foot processes
  • IF: not helpful

look for damage to visceral epithelial cells

80
Q

What is shown in the image?

A

Membranous gN

81
Q

what is shown in the picture

A

Focal segmental glomerulosclerosis (FSGS)

82
Q

What is the clinical course of FSGS?

A
  • nephrotic syndrome w/hypertension
  • poor response ot steroids
  • 50% have ESRD in 10 years
83
Q

What is associated w/FSGS and has a worse prognosis?

A

HIV Nephropathy

  • most common renal complication is FSGS
  • common in african americans
  • see tubuloreticular inclusions in ENDOTHELIAL CELLS
84
Q

What can be a mixed nephrotic and nephritic syndrome and is common in YOUNG ADULTS or children

A

membranoproliferative GN

85
Q

What is shown in the picture?

A

membranoproliferative GN

86
Q

What is seen on pathology of membranoproliferative GN?

Associations?

A
  • see proliferation of glomerular cells, leukocyte infiltration and changes in the GBM
  • Assoc.
    • SLE
    • Hep B
    • Hep C
    • endocarditis
    • infected ventricle shunts
    • partial lipodystrophy
    • alpha 1 antitrypsin def.
    • malignancy (CLL, lymphoma, melanoma)
87
Q

What is seen under the microscope for membranoproliferative GN

A
  • thickened GBM
  • silver stain: shows tram-track or dobule contour due to mesangial cell interposition into the GBM
88
Q

What is seen with type I membranoproliferative GN

A
  • 2/3 of cases
  • granular C3, IgG, C1q, C4
  • subendothelial deposits
  • immune complex disease + complement activation
89
Q

What is seen with type II membranoproliferative GN

A
  • granular C3 only
  • dense deposit disease
  • lamina dense of GBM is ribbon-like and extremely dense due to deposits of unknown material
  • excess activation of alternative complement
    • may have C3 nephritic autoantibody
90
Q

What is the course of membranoproliferative GN

A
  • 50% have renal failure in 10 years
  • steroids NOT helpful
  • very common post transplant
    • esp. type II
91
Q

What is the most common nephropathy worldwide and causes recurrent hematuria with or without proteinuria

A

Berger Disease (IgA nephropathY)

92
Q

What is Berger Disease (IgA nephropathY) associated with?

A
  • Henoch-Schnolein purpura
  • Celiac sprue patients
  • liver disease
93
Q

How does Berger Disease (IgA nephropathY) occur?

What is seen on IF?

A
  • plasma polymeric IgA is increased - may be glycosylated.
  • IF: shows mesangial deposition of IgA
  • microscope: mesangial widening
  • EM: mesangial deposits
94
Q

What presents with hematuria following respiratory, GI or urinary tract infection?

A

IgA Nephropathy

CRRAB II (26 decks)

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