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Disease Mechanisms > Ch 20: The Kidney > Flashcards

Ch 20: The Kidney Flashcards

1
Q

what is the name of the portion of the collecting duct that is in the cortex

A

cortical

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2
Q

what is the name of the portion of the collecting duct throughout most of the medulla

A

medullary

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3
Q

what is the name of the portion of the collecting duct abutting the minor calyx

A

papillary

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4
Q

what is the flow of blood through the kidney

A

glomerulus
proximal tubule
nephron loop
distual tubule
collecting duct
papillae
minor calyx
major calyx
renal pelvis
ureter

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5
Q

what three things made up the renal medulla

A

renal pyramids
renal columns
renal papillae

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6
Q

what is the order of the renal hilum starting most superficial

A

renal vein
renal artery
renal nerve

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7
Q

what is the main purpose of the renal corpuscle

A

filtering blood

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8
Q

what are the two components of the renal corpuscle

A

glomerulus
glomerular capsule (Bowman’s capsule)

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9
Q

what is the glomerulus

A

group of looping fenestrated (holed) capillaries

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10
Q

what is the outer layer of the glomerular (Bowman’s) capsule made of

A

parietal layer that is made of squamous epithelium

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11
Q

what is the inner layer of the glomerular (Bowman’s) capsule made of

A

visceral layer made of podocytes

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12
Q

what is the layer between the visceral and parietal layers of the glomerular (bowman’s) capsule called

A

capsular space

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13
Q

what are podocytes and what do they do

A

cells that make up the visceral layer of the glomerular (bowman’s) capsule
have foot processes or pedicles
responsible for making components of the glomerular basement membrane

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14
Q

what do the foot processes or pedicles of podocytes do

A

surround glomerular capillaries forming filtration slits

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15
Q

what are the three portions of the filtration membrane

A

fenestrated glomerular capillary endothelial cells
glomerular basement membrane
podocytes

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16
Q

what are fenestrated glomerular capillary endothelial cells

A

make up the innermost layer of the filtration membrane - first to come into contact with blood

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17
Q

what is the glomerular basement membrane

A

middle portion of the filtration membrane

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18
Q

what three main things make up the glomerular basement membrane

A

glycoproteins
proteoglycans
collagen fibers (type 4)

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19
Q

what is the main type of proteoglycan found in the glomerular basement membrane

A

heparan sulfate

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20
Q

what are the three domain types of type 4 collagen found in the glomerular basement membrane

A

7S domain (left-most portion)
triple helix domain (middle portion)
chain selection NC1 domain (right-most portion)

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21
Q

what are the three types of triple helical domains in type 4 collagen

A

alpha 3, 4, and 5

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22
Q

explain the arrangment of podocytes in the outermost layer of the glomerular filtration membrane

A

foot processes are separated by filtration slits but still connected by a diaphragm

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23
Q

what is a major component of the diaphragm that connects podocytes

A

nephrin

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24
Q

what is the filtration membrane most permable to

A

small, positively (cationic) charged molecules like: water, small solutes, and proteins smaller than albumin

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25
Q

what is glomerular filtration rate (GFR)

A

amount of filtrate formed by both kidneys in one minute

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26
Q

what percentage of cardiac output enters the kidneys each minute

A

20-25% of cardiac output

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27
Q

how many mL/min is filtered at the glomerulus

A

125 mL/min (20% of renal plasma flow)

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28
Q

what is commonly used to estimate glomerular filtration rate to estimate renal function

A

creatinine

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29
Q

what are mesangial cells and what do they do

A

contractile, phagocytic cells that are found in the mesangial matrix between capillaries
can proliferate, lay down matrix/collagen, and secrete active mediators in response to damage

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30
Q

what is the juxtaglomerular apparatus (JGA) and what does it do

A

area found at transition point between ascending limb of nephron loop and distal tibule
regulates blood pressure and glomerular filtration rate

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31
Q

what three things make up the juxtaglomerular apparatus

A

macula dense (MD)
juxtaglomerular cells (JG)
nongranular cells (extraglomerular mesangial cells)

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32
Q

what are the macula densa (MD)

A

portion of the juxtaglomerular apparatus
tightly packed group of cells abutting the distal tubule

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33
Q

what type of cells are the juxtaglomerular (JG) cells

A

modified smooth muscle cells

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34
Q

if you see glomeruli on a histology slide, where in the kidney are you

A

cortex

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35
Q

changes to which four basic morphologic components of the kidney help to categorize urinary system diseases

A

glomeruli
tubules
interstitium
blood vessels

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36
Q

what two main things affect the tubules and interstitium of kidneys

A

toxins and infectious agents

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37
Q

what is the interstitium and what three things is it made of

A

space outside of vessels and tubules
made of cells like fibroblasts, ECM, and interstitial fluid

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38
Q

what is azotemia

A

a clinical manifestation of renal disease
characterized by an elevation of blood urea nitrogen (BUN) and creatinine levels due to decreased glomerular filtration rate

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39
Q

what are the two categories of extrarenal disorders that cause azotemia

A

prerenal
postrenal

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40
Q

what is prerenal azotemia

A

hypoperfusion (lack of bloodflow) of the kidneys leads to impaired renal function
eventually leads to elevation of blood urea nitrogen
ex. cardiac failure and dehydration

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41
Q

what is postrenal azotemia

A

obstruction distal (following) to kidney
ex. prostate cancer or kidney stone

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42
Q

what are the two broad cause categories of azotemia

A

renal disorders
extrarenal (outside of kidney) disorders

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43
Q

what is nephritic syndrome

A

a clinical manifestation of kidney disease
caused by inflammation in the glomeruli

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44
Q

which syndrome, nephrotic or nephritic, is characterised by acute onset

A

nephritic syndrome

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45
Q

what is the mechanism of nephritic syndrome

A

cell proliferation in glomeruli accompanied with WBC infiltration damages the capillary walls
damage leads to decreased glomerular filtration rate and causes RBC, WBC, and proteins to leak out and end up in the urine

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46
Q

what are the three main symptoms of nephritic syndrome

A

proteinuria
hematuria
hypertension

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47
Q

what are RBC casts and in which syndrome are they seen

A

RBCs and other proteins get stuck and end up in the urine
seen in nephritic syndrome

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48
Q

what can proteinuria lead to

A

edema

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49
Q

what are two examples of nephritic syndromes

A

acute poststreptococcal glomerulonephritis
rapidly progressive glomerulonephritis (RPGN)

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50
Q

what is nephrotic syndrome

A

a clinical manifestation of kidney disease caused by increased permeability of glomeruli

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51
Q

what is the mechanism of nephrotic syndrome

A

damage to filtration membrane leads to increased permeability of plasma proteins

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52
Q

what is the main difference between nephritic and nephrotic syndromes

A

nephritic: inflammation of glomeruli
nephrotic: increased permeability of glomeruli

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53
Q

what are the five main symptoms of nephrotic syndrome

A

heavy proteinuria
hypoalbuminemia
severe edema
hyperlipidemia
lipiduria

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54
Q

what is the mechanism of generalized severe edema in nephrotic syndrome

A

decreased albumin in vessels leads to decreased intravascular colloid osmotic pressure and therefore swelling

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55
Q

in which syndrome, nephritic or nephrotic, could you see blood clots

A

nephrotic due to loss of anticoagulant 3 which leads to blood clotting (DVT/PE)

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56
Q

what are three examples of nephrotic syndromes

A

membranous nephropathy
minimal change
membranoproliferative glomerulonephritis (MPGN)

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57
Q

what is chronic kidney disease (CKD)

A

clinical manifestation of kidney disease
characterized by irreversible loss of renal function over time
indicated by less than 60 mL/min of glomerular filtration rate

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58
Q

what are two most common causes of chronic kidney disease (CKD)

A

diabetes mellitus (type 2)
hypertension

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59
Q

what are the clinical presentations of someone with chronic kidney disease

A

start off asymptomatic
eventually have symptoms of uremia

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60
Q

what are the four stages of chronic kidney disease

A

diminshed renal reserve
renal insufficiency
renal failure
end-stage renal disease (ESRD)

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61
Q

explain the diminished renal reserve stage of chronic kidney disease

A

this is the first step
glomerular filtration rate is about 50% of the normal
patients are asymptomatic with normal blood urea and creatinine levels

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62
Q

explain the renal insufficiency stage of chronic kidney disease

A

this is the second step
glomerular filtration rate is 20-50% of normal
patients have azotemia

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63
Q

explain the renal failure stage of chronic kidney disease

A

this is the third step
glomerular filtration rate is less than 20% of normal
patients experience edema, hyperkalemia, and metabolic acidosis

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64
Q

explain the end-stage renal disease (ESRD) stage of chronic kidney disease

A

this is the last step
glomerular filtration rate is less than 5% of normal
patients experience multiple organ failure

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65
Q

what are three consequences of loss of nephron function

A

low erythropoietin
low glomerular filtration rate
low vitamin D

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66
Q

what are the three main categories of glomerular diseases

A

primary glomerulopathies
systemic diseases with glomerular involvement
hereditary disorders

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67
Q

what are the four pathologic responses of the glomerulus injury

A

hypercellularity
basement membrane thickneing
hyalinosis
sclerosis

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68
Q

what is hypercellularity in terms of glomerulus injury

A

when the glomeruli are injured, the mesanigial or endothelial cells begin proliferating
leukocytes come in
both lead to crescent formation

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69
Q

what does hypercellularity lead to

A

crescent formation

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70
Q

what is hyalinosis in terms of glomerulus injury

A

accumulation of hyaline

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71
Q

what is sclerosis in terms of glomerulus injury

A

deposition of extravellular collagenous matrix

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72
Q

what are the three mechanisms of glomerular injury

A

immunologic
non-immunologic
hereditary

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73
Q

what is the most common mechanism of glomerular injury

A

immunologic

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74
Q

what are the two types of immunologic mechanisms that cause glomerular injury

A

immune complex deposition
deposition of anti-GBM antibody

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75
Q

what are the two types of non-immunologic mechanisms that cause glomerular injury

A

defective regulation of compliment activation
podocytes injured by toxins

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76
Q

what is the hereditary mechanism that leads to glomerular injury

A

mutations in genes lead to abnormal permability

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77
Q

what is subepithelial IC deposition

A

IC deposition at the between the foot processes of the podocytes, attached to the underlying basement membrane

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78
Q

what is subendothelial IC deposition

A

IC deposition between the basement membrane and endothelial layer

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79
Q

what is mesangial IC deposition

A

IC deposits around mesangial cells

80
Q

what is the IF pattern when immune complexes deposit subendothelial, subepithelial, and mesangial

A

granular immunofluroescence - granular pattern

81
Q

what is the IF pattern when an antibody and anti-podocyte antigen complex binds to podocytes

A

granular immunofluorescence - granular pattern

82
Q

what is the IF pattern when an antibody and anti-basement membrane antigen complex binds to basement membrane

A

linear immunofluorescence - diffuse linear pattern

83
Q

what is acute proliferative glomerulonephritis

A

a type of primary glomerulopathy caused by glomerular deposition of immune complexes

84
Q

what is the mechanism of proliferative glomerulonephritis

A

immune complexes deposit in the glomerulus
leads to an influx of leukocytes and diffuse proliferation of endothelial and mesangial cells (glomerular hypercellularity)

85
Q

what is the clinical manifestation of acute proliferative glomerulonephritis

A

nephritic syndrome (inflammation of glomerulus)

86
Q

what is the immunofluorscence for acute proliferative glomerulonephritis

A

granular deposit of IgG and C3 in glomerular basement membrane and mesangium

87
Q

what’s an exogenous cause of acute proliferative glomerulonephritis

A

infection
ex. acute poststreptococcal glomerulonephritis

88
Q

what’s an endogenous cause of acute proliferative glomerulonephritis

A

post-infectious (most common)
ex. nephritis of SLE

89
Q

what is the mechanism of SLE nephritis

A

after having SLE, circulating immune complexes deposit on regions 1 (subepithelial), 3 (subendothelial), or 4 (mesangial)
deposition causes activation of complement and Fc receptor mediated inflammation which affects the glomerulus

90
Q

what is acute poststreptococcal glomerulonephritis

A

an exogenous, antigen-induced type of acute proliferative glomerulonephritis
most common in children 6-10
presents 1-4 weeks after streptococcal infection

91
Q

what is the mechanism of acute poststreptococcal glomerulonephritis

A

exotoxin B of streptococci causes increase of antibody titers and decreased complement levels
antigens are planted in the subendothelial region 3
causes in situ formation of immune complexes which leads to inflammatory response
immune complexes dissociate and migrate across glomerular basement membrane where they reform their immune complex on the subepithelial side of the glomerular basement membrane

92
Q

what is the clinical manifestation of acute poststreptococcal glomerulonephritis

A

nephritic syndrome

93
Q

what is crescentic (rapidly progressive) glomerulonephritis (RPGN)

A

a type of primary glomerulopathy which is characterized by formation of crescents in glomeruli

94
Q

what are the two clinical manifestations of crescentic (rapidly progressive) glomerulonephritis (RPGN)

A

nephritic syndrome
rapid renal failure

95
Q

what typically causes crescentic (rapidly progressive) glomerulonephritis (RPGN)

A

severe glomerular injury

96
Q

what is the mechanism of crescentic (rapidly progressive) glomerulonephritis (RPGN)

A

necrosis, breaks in the glomerular basement membrane, and proliferation of parietal epithelial cells leads to crescent formation

97
Q

what are the three types of crescentic (rapidly progressive) glomerulonephritis (RPGN)

A

anti-GBM AB 1
immune complex 2
pauci-immune 3

98
Q

what is the main type of type 1 RPGN (anti-GBM Ab)

A

goodpasture syndrome

99
Q

what are the three main types of type 2 RPGN (immune complex)

A

postinfectious glomerulonephritis
lupus nephritis
henoch-schonlein purpura

100
Q

what is the main type of type 3 RPGN (Pauci-immune)

A

granulomatosis with polyangiitis (Wegener granulomatosis)

101
Q

what is goodpasture syndrome

A

an example of type 1 crescentic (rapidly progressive) glomerulonephritis
systemic disease with glomerular involvement
anti-GBM Ab disease

102
Q

what is the mechanism of Goodpasture syndrome

A

anti-GBM autoantibodies deposit along GBM
specifically, they bind to NCI domain of a3 chain on type 4 collagen
this activates complement which leads to destructive inflammation

103
Q

what do the anti-GBM autoantibodies bind to in goodpasture syndrome

A

mostly binds to NC1 domain of a3 chain of collagen type 4
can less commonly bind to respiratory basement membrane leading to lung hemorrhages

104
Q

what are three different proposed causes of goodpasture syndrome

A

viral
hydrocarbon solvents
genetics

105
Q

mutation in which gene is thought to cause goodpasture syndrome

A

HLA-DRB1

106
Q

what is the clinical manifestation of goodpasture syndrome

A

nephritic syndrome

107
Q

what is the immunofluoresence of goodpasture syndrome

A

linear deposit of IgG and C3 in GBM

108
Q

what is membranous nephropathy

A

a type of primary glomerulopathy
autoimmune response directed against the PLA2R antigen on podocytes or planted antigens

109
Q

what is the mechanism of membranous nephropathy

A

primary: antibody binds to endogenous podocyte antigen
secondary: antibody binds to planted antigen
both are binding subepithelial
leads to compliment activation, injury of the glomerular capillary wall, and thickening of GBM

110
Q

what is the etiology of membranous nephropathy

A

etiology is unknown
75% of cases are primary
25% of cases secondary

111
Q

what are the 2 main secondary causes of membranous nephropathy

A

infections
therapeutic drugs

112
Q

which 3 types of infections can cause membranous nephropathy

A

malaria
syphilis
hepatatis

113
Q

which three types of therapeutic drugs can cause membranous nephropathy

A

penicillamine
NSAIDs
catopril

114
Q

what is the clinical manifestation of membranous nephropathy

A

nephrotic syndrome because of injury to capillary wall

115
Q

what is the IF of membranous nephropathy

A

granular deposits of IgG and C3 along GBM

116
Q

what are the electron microscope fetures of membranous nephropathy

A

subepithelial deposits with loss of foot processes

117
Q

what is the difference between a cortical and juxtamedullary nephron

A

cortical has much shorter loop of henle
juxtamedullary nephron’s loop of henle extends deep into the medulla

118
Q

what is minimal change disease

A

a type of primary glomerulopathy

119
Q

what are the three causes of minimal change disease

A

can follow respiratory infections, drugs, or vaccinations

120
Q

what is the most common cause of nephrotic syndrome in children (2-6yr olds)

A

minimal change disease

121
Q

explain the mechanism of primary minimal change disease

A

immune dysfunction leads to loss of foot processes of podocytes
this causes GBM to be leaky and leads to proteinuria

122
Q

what is the clinical manifestation of minimal change disease

A

nephrotic syndrome - leaky GBM

123
Q

what is the mechanism of primary membranoproliferative glomerulonephritis (MPGN)

A

subendothelial deposition of IC in mesangial matrix and capillary wall
this causes proliferation of cells and leukocytes to infiltrate
causes tram track appearence in GBM

124
Q

which disease is characterized by a tram-track appearence of the capillary wall

A

membranoproliferative glomerulonephritis (MPGN)

125
Q

secondary membranoproliferative glomerulonephritis (MPGN) is seen in which three conditions

A

SLE, viral hepatitis, and chronic infections

126
Q

what are the clinical manifestations of membranoproliferative glomerulonephritis (MPGN)

A

nephritic and nephrotic syndromes

127
Q

what is the IF of membranoproliferative glomerulonephritis (MPGN)

A

irregular granular deposits of IgG and C3

128
Q

what is dense deposit disease (DDD)

A

a type of primary glomerulopathy
technically type 2 MPGN that is characterized by dysregulation of the alternative complement pathway

129
Q

what is the mechanism of dense deposit disease (DDD)

A

intramembranous dense deposition in mesangial region and capillary wall
causes proliferation of glomerular cells and infiltration of leukocytes
both lead to GBM thickening

130
Q

who is most affected by dense deposit disease (DDD)

A

children and young adults
has a poor prognosis

131
Q

what are four clinical manifestations of dense deposit disease (DDD)

A

nephritic syndrome
nephrotic syndrome
hematuria
chronic renal failure

132
Q

what are the light microscopy features of dense deposit disease (DDD)

A

mesangial proliferation and GBM thickening

133
Q

what are the IF features of dense deposit disease (DDD)

A

C3 deposition with irregular granular pattern

134
Q

what is the electron micropscopy feature of dense deposit disease (DDD)

A

ribbon-like electron dense deposits in GBM

135
Q

which disease is characterized by ribbon-like electron dense deposits in GBM on electron microscopy

A

dense deposit disease

136
Q

what is IgA nephropathy (Berger Disease)

A

a type of primary glomerulopathy
deposition of IgA immune complexes in mesangial region

137
Q

what is the mechanism of IgA nephropathy (Berger Disease)

A

some sort of infection causes production of abnormal IgA
immune system releases IgG which binds to the abnormal IgA creating a complex
complexes deposit in the mesangial region
mesangial cells proliferate leading to inflammation and complement activation

138
Q

what is the most common type of glomerulonephritis in the world

A

IgA nephropathy (Berger Disease)

139
Q

who is most at risk for IgA nephropathy (Berger disease)

A

older children and young adults

140
Q

what is the main clinical manifestation of IgA nephropathy (Berger Disease)

A

recurrent hematuria

141
Q

what are the IF features of IgA nephropathy (Berger Disease)

A

IgA bound to either IgG or IgM
C3 deposition in mesangium

142
Q

what is Alport Syndrome

A

a type of hereditary glomerular disease
genetic disorder that leads to production of abnormal type 4 collagen in GBM

143
Q

what is the mechanism of Alport Syndrome

A

mutated genes in either alpha 3, 4, or 5 chain in type four collagen of GBM interferes with their folding

144
Q

Alport Syndrome is associated with which two issues

A

nerve deafness and eye disorders

145
Q

when do symptoms of Alport Syndrome first appear

A

ages 5-20

146
Q

85% of Alport Syndrome cases are what

A

X-linked domainant - males will express all symptoms

147
Q

what are the two main clinical manifestations of Alport syndrome

A

hematuria with RBC casts and proteinuria

148
Q

what are the IF features of Alport Syndrome

A

no deposits

149
Q

what are the electron microscopy features of Alport Syndrome

A

irregular thickening of GBM with basket-weave appearance

150
Q

which disease is characterized by basket-weave appearance

A

Alport Syndrome

151
Q

what is Henoch-Schonlein Purpura

A

a type of systemic glomerular disease
childhood syndrome characterized by skin lesions, abdomnial pain, and intestinal bleeding
in adults: renal abnormalities

152
Q

what is the mechanism of Henoch-Schonlein Purpura

A

immune complex deposition in vessels

153
Q

what are the clinical manifesations of Henoch-Schonlein Purpura

A

nephritic and nephrotic syndrome

154
Q

what are the four clinical feautres of diabetic nephropathy

A

end-stage kidney disease
glomerular lesions
vascular lesions
pyelonephritis

155
Q

what are the characteristics of glomerular lesions in diabetic nephropathy

A

GBM thickening
mesangial sclerosis
nodular glomerulosclerosis

156
Q

what does a PAS stain show for diabetic nephropathy

A

acellular nodules

157
Q

what is kimmelstiel-wilson disease

A

nodular glomerulosclerosis
ovoid or spheroid, laminated, hyaline masses found in periphery of glomerulus
a symptom of diabetic nephropathy

158
Q

what is lupus nephritis

A

a type of systemic glomerular disease
characteristic of SLE

159
Q

what is the mechanism of lupus nephritis

A

immune complex deposition in blood vessels, through kidneys, connective tissue, and skin
in kidney specifically: deposition in GBM, mesangium, and all throughout glomerulus

160
Q

what are the clinical manifestations of lupus nephritis

A

nephritic and nephrotic syndrome

161
Q

what are the two major processes that cause tubular and interstitial diseases

A

iscehmic or toxic tubular injury
inflammation of tubes and interstitium (tubulointerstitial nephritis)

162
Q

what is acute tubular injury (ATI)

A

damage to tubular epithelial cells and an acute decline in renal function

163
Q

what is the most common cause of acute kidney injury

A

acute tubular injury (ATI)

164
Q

what is a clinical sign of acute tubular injury (ATI)

A

muddy brown urine caused by shedding of granular casts and tubular cells in the urine

165
Q

what are the two main causes of acute tubular injury (ATI)

A

ischemia
direct toxic injury to the tubule

166
Q

what are the characteristics of acute tubular injury (ATI) caused by ischemia

A

large, skipped areas
rupture of BM
occlusion of lumen by casts

167
Q

what causes direct toxic injury to tubules, leading to acute tubular injury (ATI)

A

endogenous or exogenous substances

168
Q

where is direct toxic injury to the tubule most likely to be found

A

proximal tubule

169
Q

what is tubulointerstitial nephritis

A

group of diseases that involve inflammatory injuries of the tubes and intersititium

170
Q

what are the two main results of acute tubular injury

A

decreased urine output and decreased GFR

171
Q

what are the characteristics of acute tubulointerstitial nephritis

A

rapid onset with interstitial edema and leukocyte infiltration of the interstitium and tubules

172
Q

what are the characteristis of acute tubulointerstitial nephritis

A

leukocyte infiltration, interstitial fibrosis, and tubular atrophy

173
Q

what three types of disorders can secondarily cause tubulointerstitial nephritis

A

vascular
cystic
metabolic

174
Q

what is the clinical manifestation of tubulointerstitial nephritis

A

azotemia

175
Q

what are the two main hallmarks of tubulointerstitial nephritis

A

absence of nephritic or nephrotic syndromes
presence of defects in tubular function

176
Q

what are the 5 risks of developing a UTI

A

short urethra, obstruction, urine stasis, high pH, and vesicoureteral reflux due to congenital defect

177
Q

what are the two main pathways to renal infection

A

hematogenous infection
ascending infection

178
Q

what is the most common pathway of renal infection

A

ascending infection (bacteria climbs up the urethra)

179
Q

what are the two types of refluxes associated with kidney infections

A

vesicoureteral
intrarenal

180
Q

what is vesicoureteral reflux

A

the reflux of urine from the bladder back into the ureter
can be congenital (anatomic anomoly) or aquired (bacteria)

181
Q

what is intrarenal reflux

A

the reflux of urine back into the kidney from the papillae

182
Q

which two locations are most common for intrarenal reflux

A

upper and lower poles of kidney because their papillae have flattened or concave tips rather than convex tips

183
Q

what is cystitis

A

a bladder infection

184
Q

what is pyelonephritis

A

a kidney infection

185
Q

what is the most common UTI causing bacteria

A

gram negative bacilli from intestinal tract (E. coli)

186
Q

which fungus can cause UTIs

A

candida

187
Q

which parasite can cause UTIs

A

schistosomiasis

188
Q

which virus can cause an UTI

A

polyomavirus

189
Q

what is pyelonephritis

A

a serious complication of an UTI which is characterized by inflammation affecting the tubules, interstitium, and renal pelvis

190
Q

what is chronic pyelonephritis

A

changes in the kidney due to recurring or persistent infection
leads to pelvocalyceal damage, pyonephrosis (pus), and fibrosis of interstitium

191
Q

what is acute pyelonephritis

A

bacterial infection of the renal parenchyma and pelvis
can lead to abscess formation

192
Q

what is the mechanism of acute pyelonephritis

A

bacterial infection causes an inflammatory response
leads to arterial constriction and edema
eventually leads to abscess formation

193
Q

what are 5 risk factors for acute pyelonephritis

A

UTI
pregnancy
instrumentation
kidney transplant
diabetes mellitus

194
Q

which toxin can cause tubulointerstitial nephritis

A

analgesics

195
Q

which metabolic disease can cause tubulointerstitial nephritis

A

oxalate nephropathy

196
Q

which immunologic reaction can cause tubulointerstitial nephritis

A

sjogren syndrome

197
Q

what are the 7 categories of causes of tubulointerstitial nephritis

A

infections
toxins
metabolic diseases
physical factors
immunologic reactions
vascular diseases
miscellaneous

Disease Mechanisms (19 decks)

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