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Block 9 Week 5 > Renal pathology-Fung > Flashcards

Renal pathology-Fung Flashcards

1
Q

What are the three major things that the kidney does?

A

Metabolism
Endocrine Functions
BP regulation

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2
Q

How does the kidney help with metabolism?

A

Excretion of H2O, Na+, Ca2+, P
Maintain acid-base balance
Excretion of toxic metabolite wast products

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3
Q

How does the kidney help with endocrine function?

A

Secrete erythropoietin, prostaglandins

Regulate vitamin D metabolism (hydroxylation of vit D)

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4
Q

How does the kidney regulate BP?

A

Renin secretion

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5
Q

What all does the urinary system include?

A

the kidneys (in retroperitoneum), ureters, bladder, and the urethra

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6
Q

What is the functional unit of the kidney? Where is it located?
What do you find in the medulla?

A

nephron-> cortex

medulla-> collecting tubules which empty ito the renal papila and into the calayx sytem.

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7
Q

What does the hilum of the kidney contain?

A

renal sinus, renal vasculature, renal pelvis

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8
Q

How does the blood flow from the aorta into the various parts of the kidney?

A

Aorta-> renal artery-> branch into the segmental artery-> interlobar artery-> arcuate artery-> Vasa recta + interlobuar artery-> afferent arterioles-> glomerulus-> efferent arteriole-> vasa recta artery to vasa recta vein-> interlobular vein-> arcuate vein-> interlobar vein->renal vein

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9
Q

If you see glomeruli, what part of the kidney are you looking at?

A

cortex

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10
Q

What is another name for the visceral layer of the glomerulus?
What does this blend into ?

A

podocyte layer

Blends into a layer of cuboidal cells that make the parietal layer of bowmen’s capsule

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11
Q

What determines what molecules will be filtered?

What anatomically allows for filtration?

A

size, charge, and configuration

fenestrations of endothelial capilary membrane

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12
Q

Podocytes have primary and secondary processes. Explain this

A

Primary process wrap around capillary and secondary processes create filtrations slits (foot processes)

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13
Q

What is the endothelium like in the renal cortex? what does it lay adjacent to?

A

-fenestrated endothelial cells
(70-100 nm diameter)
-To the lamina rara interna of the GBM

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14
Q

The visceral epithlium (podocytes) is located adjacent to the (blank). What does the visceral epithelium have that helps with filtration of WATER?

A

lamina rare externa of the GBM

-foot processes that are separated by filtration slits (20-30 nm))

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15
Q

Filtration slits are more involved more in the filtration of (blank) and not so much proteins

A

water

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16
Q

What are the three layers of the glomerular basement membrane (GBM)?

A
  • lamina rara interna
  • lamina densa
  • lamina rara externa
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17
Q

What makes up the GBM?

A
  • type IV collagne
  • laminin
  • heparan sulfate
  • fibronectin
  • entactin
  • glycoproteins
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18
Q

What is super important about the fact that type IV collagen is involved in the GBM?

A

-in a lot of autoimmune diseases, they attack type IV collagen

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19
Q

What does the mesangium do?

A
  • it supports the glomerular tuft and lies b/w capillaries
  • contract and are phagocytic
  • secretes mediators and lays down a matrix similar in composition to the BM
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20
Q

Blood filters into the glomerulus and the product of the filter will go into the (blank) which empties into the (blank)

A

bowman’s space

tubular system

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21
Q

The bulk of the cortex is (blank).

The proximal convoluted tubules are going to have (blank). DCT will not have this, why?

A

tubules
microvilli (increases absorption surface area)
because most of the absorption occurs in the PCT

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22
Q

(blank) will sense how much blood the kidney is getting – it is what releases renin based on this

A

Juxtoglomerulus apparatus

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23
Q

Histologically where is the juxtoglomerulus apparatus located?

A

separates the DCT from the Bowman’s capsule

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24
Q

What are the causes of renal disease?

A
  • primary
  • secondary
  • infectious
  • obstructive
  • neoplastic
  • glomerular
  • tubular
  • interstitial
  • vascular
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25
Q

What are secondary causes of renal disease?

A

DM, HTN, Lupus

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26
Q

When glomeruli are injured, there are 4 basic patterns of reactions, what are they?

A
  • hypercellularity
  • basement membrane thickening
  • hyalinosis
  • sclerosis
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27
Q

What can cause deposition of plasma protein in a glomerulus?

A

hyalinosis (due to eosinophilic processes)

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28
Q

What is sclerosis of the glomerulus due to?

A

laying down of collagen

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29
Q

What is diffuse glomerular injury?

A

involving all glomeruli

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30
Q

What is focal glomerular injury?

A

involving only a proportion of the glomeruli

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31
Q

What is global glomerular injury?

A

involving the entire glomerulus

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32
Q

What is segmental glomerular injury?

A

affecting a part of the glomerulus

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33
Q

Most glomerular injury is due to (blank) causes

A

immunologic

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34
Q

What are the three ways that glomerular injury can be caused by immunologic causes?

A
  • interaxns w/ intrinisic glomerular antigens or antigens implanted in the glomerulus
  • circulating antibody deposits w/in the glomerulus
  • cytotoxic antibody directed against glomerulus due to complement pathway
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35
Q

What is azotemia?

A

elevation of blood urea nitrogen (BUN) or creatinine (Cr)

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36
Q

What are the three types of azotemia?

A

prerenal
renal (intrinsic)
postrenal

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37
Q

What is the cause of prerenal azotemia?

A

volume status issues (hypovolemic), sepsis etc.

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38
Q

What is the cause of intrinsic azotemia?

A

tubular disease

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39
Q

What is the cause of postrenal azotemia?

A

obstruction

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40
Q

What is acute renal failure?

A

rapid (hours to days) decline in glomerular filtration rate (GFR)

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41
Q

What is acute renal failure characterized by?

A 
azotemia
fluid and electrolyte imbalance
-hyponatremia
-hyperkalemia
-hyperphosphatemia and hypocalcemia
-metabolic acidosis
oliguria or anuria
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42
Q

What are the causes of acute renal failure?

A
  • glomerular injury
  • interstitial injury
  • vascuar injury
  • tubular injur
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43
Q

What are the symptoms of acute renal failure?

A
  • decreased or absent urine output
  • lethargy
  • fatigue
  • nausea
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44
Q

A FENa+ of less than 1% indicates (blank) while greater than 1% indicates (blank)/

A

prerenal failure

renal failure

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45
Q

What does a BUN/Cr ratio of less than 20:1 indicate?

What does a BUN/Cr ratio greater than 20:1 indicate?

A

renal failure

prerenal failure

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46
Q

What does a urine Na+ of less than 20mEq/L indicate?

What does a urine Na+ of more than 20mEq/L indicate?

A

prerenal failure

renal failure

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47
Q

What does a urine osmolality of less than 400 mOsm/kg indicate?

What does a urine osmolality of more than 500 mOsm/kg indicate?

A

Renal failure

Prerenal failure

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48
Q

What does a specific gravity of less than 1.020 indicate?

What does a specific gravity of more than 1.020 indicate?

A

renal failure

prerenal failure

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49
Q

What does a diminished GFR (less than 60 mL) for at least 3 months indicate?

A

chronic renal failure

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50
Q

What is chronic renal failure characterized by?

A

azotemia
fluid and electrolyte imbalance
uremia

51
Q

What is uremia?

A

syndrome associated with fluid, electrolyte, and hormonal imbalances and metabolic abnormalities

52
Q

What are the symptoms of uremia?

A
  • nausea, vomiting, fatigue, anorexia, weight loss, muscle cramps, pruiritis
  • menta status change, visual disturbances, increased thirst
53
Q

What are the causes of chronic renal failure?

A
  • diabetes
  • hypertension
  • renal parenchymal disease
54
Q

What is this:
GFR=50% of normal
BUN/Cr=normal
asymptomatic symptoms

A

Diminished renal reserve

55
Q

What is this:
GFR=20-50%
BUN/Cr=azotemia
Symptoms=anemia, HTN, polyuria

A

Renal insufficiency

56
Q

What is this:
GFR= less than 20-25%
BUN/Cr=azotemia
Symptoms=uremia

A

Chronic renal failure

57
Q

What is this:
GFR=less than 5%
BUN/Cr=azotemia
Symptoms=uremia

A

End stage renal disease

58
Q

In nephritic syndrome, what do patients present with?

What is it characterized by?

A
  • hematuria (red cell casts)
  • azotemia
  • oliguria
  • slight proteinuria

inflammation of the glomeruli

59
Q

Nephritic syndrome presents with (blank) in the urine while nephrotic syndrome present with (blank) in the urine

A

blood

protein

60
Q

What is this:
A 6 year old male presents to his pediatrician with his mom with complaints of dark discolored urine for 1 day duration. The boy has no significant past medical history but mom states that 3 weeks prior he missed 2 days of school due to a sore throat, cold and fever.

A

Acute proliferative glomerulonephritis (Post-infectious glomerulonephritis-strep pyogenes)

61
Q

What are the symptoms of acute proliferative glomerulonephritis (Post-infectious glomerulonephritis strep pyogenes)?

A
  • URI or skin infection 1-6 weeks prior (like impetigo)
  • Gross hematuria (cola-colored urine)
  • Periorbital edema
  • Oliguria
  • RBC casts
  • Peripheral edema
  • HTN
  • Azotemia
  • Mild proteinuria
62
Q

Acute proliferative glomerulonephritis is more commonly associated with strep infections of the skin like (blank)

A

impetigo

63
Q

What is the pathogenesis of acute proliferative glomerulonephritis (Post-infectious glomerulonephritis strep pyogenes)?

A

Strep pyogenes (group A strep) produces a M type protein that causes immune complex deposition in glomerulus in the subepithelium

64
Q

What will acute proliferative glomerulonephritis (post-infectious glomerulonephritis) present like on H and E? What will it look like on EM? What will it look like on IF?

A
  • hypercellularity from inflammation
  • subepithelial humps
  • immune complex deposition (granular pattern)
65
Q

Who typically gets acute proliferative glomerulonephritis (post-streptococcal glomerulonephritis)?
What is the treatment an prognosis like?

A

usually seen in children, but may occur in adults.

  • tx is supportive
  • 95% of children recover totally w/ therapy aimed at maintaining Na and water balance (1% progress to renal failure)
  • In adults only 60% recover (25% develop rapidly progressive clomerulonephritis (RPGN)
66
Q

(blank) is a syndrome associated with glomerular injury. What is it characterized by?

A

Rapidly progressive glomerulonephritis

  • rapid and progressive loss of renal function
  • oliguria
  • nephritic syndrome symptoms (limited proteinuria less than 3.5g/day, oliguria and azotemia, salt retention w/ periorbital edema, htn, RBC casts, and dysmorphic RBCs in urine)
67
Q

What is rapidly progressive glomerulonephritis characterized by in an H and E stain?

A

Characterized by cresecents in Bowman space (of glomeruli).

68
Q

What are the crescents made up of in rapidly progressive glomerulonephritis?

A

fibrin and macrophages

69
Q

What are the three types of rapidly progressive glomerulonephritis?

A 
Type I (anti- GBM antibody)
Type II (immune complex)
Type III (Pauci-immune)
70
Q

What is the immunofluorescence pattern like in type I Rapidly Progressive Glomerulonephritis (anti-GBM antibody)?

A

linear pattern caused by deposits of IgG/C3

immune complex is formed against the glomerular BM

71
Q

What disease will you see a type 1 rapidly progressive glomerulonephritis (anti basement membre)?

A

Goodpasture syndrome

72
Q

What is the treatment for Anti-GBM antibody (type I rapidly progressive glomerulonephritis)?

A

Plasmapheresis

Immunosuppression

73
Q

What is the immunofluorescence patter of type II Rapidly Progressive Glomerulonephritis?

What are the diseases associated with this?

A

Immune complex deposition-> Granular

  • PSGN (most common)
  • Lupus nephritis (due to diffuse proliferative glomerulonephritis)
  • IgA nephropathy
74
Q

What is the treatment of rapidly progressive glomerulonephritis type II?

A

treat the underlying disease

No plasmpheresis

75
Q

Diffuse proliferative glomerulonephritis is due to diffuse antigen-antibody complex deposition, usually located (blanK); most common type of renal disease in (blank)

A

sub-endothelial

SLE

76
Q

What is the IF pattern of Pauci-immune (type III) Rapidly Progressive Glomerulonephritis?

A

It doesnt show anything

77
Q

What are the diseases that cause Pauci-immune (type III) rapidly progressive glomerulonephritis?

What is the most common cause of Pauci-immune (type III) rapidly progressive glomerulonephritis?

A 
Wegener granulomatosis (C-ANCA)
Microscopic polyangiitis (p-ANCA)
Churg-Strauss syndrome (p-ANCA)

Most common cause is idiopathic

78
Q

How do you treat pauci-immune (type III) rapidly progressive glomerulonephritis?

A

therapy includes steroids and cytotoxic agents

79
Q

What are the characteristics of nephrotic syndrome?

Why?

A
  • massive proteinuria (>3.5 gm)
  • Hypoalbunemia (<3 gm/dL)
  • Generalized edema
  • Hyperlipidemia/hyperlipiduria

-glomerular injury allows for loss of proteins including albumin which results in loss of oncotic pressure and thus edema

80
Q

In nephrotic syndrome, proteinuria can be selective. What proteins are highly selective?
What proteins are poorly selective?

A

low molecular weight albumin
and transferrin

Higher molecular weight globulins and albumin

81
Q

What are the primary glomerular diseases that cause nephrotic syndrome?

A
  • membranous glomerulopathy
  • minimal change disease
  • focal segmental glomerulosclerosis
  • membranoproliferative glomerulonephritis
  • IgA nephropathy
82
Q

What are the systemic diseases that cause nephrotic syndrome?

A
  • Diabetes
  • Amyloidosis
  • Lupus
  • Drugs (NSAIDs, Penicillamine)
  • Infections (malaria, syphillis, Hep B/C, HIV)
  • Carcinoma/lymphoma
83
Q

What is the most common cause of nephrotic syndrome in children?

A

minimal change disease

84
Q

What will MCD (minimal change disease) look like on H&E?
What is it characterized by EM?
How do you treat it and why does this work?

A

normal (normal on light microscopy too)

  • diffuse effacement of podocyte foot processes
  • steroids, because disease is due to cytokines
85
Q

What causes minimal change disease?

A

-immune dysfunction leads to an elaboration of cytokines that damage visceral epithelial cells and cause proteinuria

86
Q

What is MCD associated with?

A
  • Respiratory illness
  • post immunization
  • increased incidence with Hodgkin lymphoma
  • atopic disorders
  • Presence of HLA haplotypes
87
Q

What are the clinical features of MCD?

Whats the treatment?

A
  • highly selective proteinuria (albumin)
  • No htn or hematuria

Corticosteroids

88
Q

What is the most common case of nephrotic syndrome in caucasian adults and is immune complex mediated?

A

-Membranous nephropathy

89
Q

What are the ways that you can get secondary immune complex mediated membranous nephropathy?

A

-SLE, Infections, Drugs, malignant tumors, Hep B, Hep C

90
Q

What is membranous nephropathy characterized by?

What will it look like on EM?

A
  • diffuse thickening of the glomerular capillary wall by Ig deposition along the subepithelial side of the BM
  • Spike and Dome appearance
91
Q

Where does IgE deposit in membrnous nephropathy?

A

subepithelial deposis

92
Q

What are the clinical features of membranous nephropathy?

A
  • insidious onset of nephrotic syndrome (nonselective proteinuria)
  • mild HTN and hematuria posible
93
Q

What will progression of membranous nephropathy result in?

How do you treat it?

A

sclerosis of glomeruli

  • tx of the underlying condition (secondary)
  • does not respond to steroids
94
Q

What is this:

characterized by focal and segmental sclerosis of the capillary tuft.

A

Focal segmental glomerulosclerosis

95
Q

What are the causes of focal segmental glomerulosclerosis?

A

Idiopathic
Secondary (HIV, heroin, sickle-cell, obesity)
Complication of focal glomerulonephritis
Adaptive response to loss of renal tissue

96
Q

What is the most common cause of nephrotic syndrome in hispanics and african americans? What will you see on EM? on IF?

A

Focal segmental glomerulosclerosis
EM: effacement of foot processes
IF: normal, no immune complex deposits

97
Q

Focal segmental glomerulosclerosis is thought to possibly be a phase in the evolution of (blank). Whats this due to?

A

minimal change disease

  • An accentuation of diffuse epithelial cell change of MCD
  • cytokine mediated or defects of slit diaphragm proteins
98
Q

Focal segmental glomerlosclerosis presents with (blank and blank) due to entrapment of plasma proteins

A

Hyalinosis

Sclerosis

99
Q

Focal segmental glomerulosclerosis is usually idiopathic, but may be associated with (blank x 3)

A

HIV
Heroin use
sickle cell disease

100
Q

What are the clinical features of focal segmental glomerulosclerosis?

A

little tendency for spontaneous remission in idiopathic form, response to steroids is variable

101
Q

In membranoproliferative glomerulonephritis, patients present with (blank) symptoms

A

nephritic/nephrotic or asymptomatic

102
Q

What is membranoproiferative glomerulonephritis characterized by?

A
  • Alterations of the GBM
  • Tram-track appearance on H and E
  • Proliferation of glomerular cells
  • Immune complex deposition
  • leukocyte proliferation
103
Q

Membranoproliferative glomerulonephritis can be caused primarily, or secondarily by (blank, blank, blank)

A

chronic immune disorders
malignant disease
alpha-1 antitrypsin deficiency

104
Q

What is type I Primary membranoproliferative glomerulonephritis?

A

immune complex deposition of C3 in the SUBENDOTHELIUM w activation of classical and alternative complement pathways

105
Q

What can type I primary membranoproliferative glomerulonephritis be due to?

A

Planted exogenous antigens (Hep B/C)

Circulating immune complexes

106
Q

What is type II primary membranoproliferative glomerulonephritis due to?

A

AKA DENSE DEPOSIT DISEASE

  • dysregulation of alternative complement pathway
  • autoantibody to C3 convertase leading to persistent C3 activation and hypocomplementemia (low levels of C3)
107
Q

Where do the immune complexes deposit in Type II membranoprliferative glomerulonephritis?

A

intramembranous (Basement membrane)

108
Q

What are the clinical features of membraneoproliferative glomerulonephritis? How do you treat it?

A

few spontaneous remissions with a slowly progressive and unremitting course

-not one, steroids or immunosuppressives are not effective INSTEAD patients go into chronic renal failure

109
Q

What is the most common type of glomerulonephritis worldwide?

What do patients present with?

A

IgA nephropathy

-recurrent gross or microscopic hematuria with RBC casts, usually following mucosal infections (gastroenteritis)

110
Q

What is the systemic form of IgA nephropathy?

A

Henoch-schonlein purpura

111
Q

IgA nephropathy is characterized by IgA deposits in the (blank) region of the glomerulus and increased levels of polymeric forms of (blanK)

A

mesangial region

IgA1

112
Q

IgA nephropathy is believed to be due to a genetic or acquired abnormality of immune regulation upon exposure to environmental agents in the (blank and blank). What are 2 examples of this?

A

Lungs and GI tract

Gluten enteropathy, Liver disease

113
Q

What is the pathogenesis of IgA nephropathy?

A

IgA and IgA immune complexes are trapped in the mesangium and then activate the coplement pathway leading to glomerular injury
(IgA production is increased during infection)

114
Q

What will you see on H&E and IF with IgA nephropathy?

A

thickening of the mesangium

115
Q

What are the clinical features of IgA nephropathy?

A
  • presents with gross hematuria after a respiratory or GI infection
  • may present with microscopic hematuria with or w/out proteinuria or acute nephritic syndrome
  • may retain renal function for decades
116
Q

What is one of the leading causes of kidney failure and what three glomerular syndromes are associated with it?

A

diabetic nephropathy

  • non-nephrotic proteinuria
  • nephrotic syndrome
  • chronic renal failure
117
Q

Diabetic nephropathy also affects other portions of the kidney such as….?

A

Hyalinizing arteriolar sclerosis
Pyelonephritis
Tubular lesions

118
Q

What causes the nephrotic changes in diabetic nephropathy?

A

high serum glucose and hemodynamic factors leads to nonenzymatic glycosylation of vascular BM resulting in hyaline sclerosis

119
Q

In diabetic nephropathy, what part of the glomerulus is affected?

A

The efferent arteriole is more affects lead to high glomerular filtration pressure.

120
Q

In diabetic nephropathy you will have high GFR which will result in what?
What can this eventually progress to?

A

hyperfiltration injury leading to microalbuminuria

Nephrotic syndrome

121
Q

What is diabetic nephropathy characterized by?

How can you treat this?

A

sclerosis of mesangium w/ formation of Kimmelstiel-Wilson nodules, thickening of glomerular BM and BM thickening of tubules

-ACE inhibitors slow progression of hyperfiltration-induced damage

122
Q

What is Alport syndrome?

A

X-linked syndrome of defective collagen Type IV (thinning and splitting of the glomerular BM)

123
Q

What is Alport syndrome characterized by?

A

Hematuria w/ progression to renal failure
Nerve deafness
Ocular disorders

124
Q

What is thin basement membrane disease? What is its presentation?

A

Benign familial hematuria due to defects in a collagen Type IV.

  • Normal renal function and excellent prognosis.
  • asymptomatic hematuria
  • mild proteinuria
  • thin GBM

Block 9 Week 5 (5 decks)

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