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
what is glomerular filtration rate (GFR)
amount of filtrate formed by both kidneys in one minute
26
what percentage of cardiac output enters the kidneys each minute
20-25% of cardiac output
27
how many mL/min is filtered at the glomerulus
125 mL/min (20% of renal plasma flow)
28
what is commonly used to estimate glomerular filtration rate to estimate renal function
creatinine
29
what are mesangial cells and what do they do
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
30
what is the juxtaglomerular apparatus (JGA) and what does it do
area found at transition point between ascending limb of nephron loop and distal tibule regulates blood pressure and glomerular filtration rate
31
what three things make up the juxtaglomerular apparatus
macula dense (MD) juxtaglomerular cells (JG) nongranular cells (extraglomerular mesangial cells)
32
what are the macula densa (MD)
portion of the juxtaglomerular apparatus tightly packed group of cells abutting the distal tubule
33
what type of cells are the juxtaglomerular (JG) cells
modified smooth muscle cells
34
if you see glomeruli on a histology slide, where in the kidney are you
cortex
35
changes to which four basic morphologic components of the kidney help to categorize urinary system diseases
glomeruli tubules interstitium blood vessels
36
what two main things affect the tubules and interstitium of kidneys
toxins and infectious agents
37
what is the interstitium and what three things is it made of
space outside of vessels and tubules made of cells like fibroblasts, ECM, and interstitial fluid
38
what is azotemia
a clinical manifestation of renal disease characterized by an elevation of blood urea nitrogen (BUN) and creatinine levels due to decreased glomerular filtration rate
39
what are the two categories of extrarenal disorders that cause azotemia
prerenal postrenal
40
what is prerenal azotemia
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
41
what is postrenal azotemia
obstruction distal (following) to kidney ex. prostate cancer or kidney stone
42
what are the two broad cause categories of azotemia
renal disorders extrarenal (outside of kidney) disorders
43
what is nephritic syndrome
a clinical manifestation of kidney disease caused by inflammation in the glomeruli
44
which syndrome, nephrotic or nephritic, is characterised by acute onset
nephritic syndrome
45
what is the mechanism of nephritic syndrome
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
46
what are the three main symptoms of nephritic syndrome
proteinuria hematuria hypertension
47
what are RBC casts and in which syndrome are they seen
RBCs and other proteins get stuck and end up in the urine seen in nephritic syndrome
48
what can proteinuria lead to
edema
49
what are two examples of nephritic syndromes
acute poststreptococcal glomerulonephritis rapidly progressive glomerulonephritis (RPGN)
50
what is nephrotic syndrome
a clinical manifestation of kidney disease caused by increased permeability of glomeruli
51
what is the mechanism of nephrotic syndrome
damage to filtration membrane leads to increased permeability of plasma proteins
52
what is the main difference between nephritic and nephrotic syndromes
nephritic: inflammation of glomeruli nephrotic: increased permeability of glomeruli
53
what are the five main symptoms of nephrotic syndrome
heavy proteinuria hypoalbuminemia severe edema hyperlipidemia lipiduria
54
what is the mechanism of generalized severe edema in nephrotic syndrome
decreased albumin in vessels leads to decreased intravascular colloid osmotic pressure and therefore swelling
55
in which syndrome, nephritic or nephrotic, could you see blood clots
nephrotic due to loss of anticoagulant 3 which leads to blood clotting (DVT/PE)
56
what are three examples of nephrotic syndromes
membranous nephropathy minimal change membranoproliferative glomerulonephritis (MPGN)
57
what is chronic kidney disease (CKD)
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
58
what are two most common causes of chronic kidney disease (CKD)
diabetes mellitus (type 2) hypertension
59
what are the clinical presentations of someone with chronic kidney disease
start off asymptomatic eventually have symptoms of uremia
60
what are the four stages of chronic kidney disease
diminshed renal reserve renal insufficiency renal failure end-stage renal disease (ESRD)
61
explain the diminished renal reserve stage of chronic kidney disease
this is the first step glomerular filtration rate is about 50% of the normal patients are asymptomatic with normal blood urea and creatinine levels
62
explain the renal insufficiency stage of chronic kidney disease
this is the second step glomerular filtration rate is 20-50% of normal patients have azotemia
63
explain the renal failure stage of chronic kidney disease
this is the third step glomerular filtration rate is less than 20% of normal patients experience edema, hyperkalemia, and metabolic acidosis
64
explain the end-stage renal disease (ESRD) stage of chronic kidney disease
this is the last step glomerular filtration rate is less than 5% of normal patients experience multiple organ failure
65
what are three consequences of loss of nephron function
low erythropoietin low glomerular filtration rate low vitamin D
66
what are the three main categories of glomerular diseases
primary glomerulopathies systemic diseases with glomerular involvement hereditary disorders
67
what are the four pathologic responses of the glomerulus injury
hypercellularity basement membrane thickneing hyalinosis sclerosis
68
what is hypercellularity in terms of glomerulus injury
when the glomeruli are injured, the mesanigial or endothelial cells begin proliferating leukocytes come in both lead to crescent formation
69
what does hypercellularity lead to
crescent formation
70
what is hyalinosis in terms of glomerulus injury
accumulation of hyaline
71
what is sclerosis in terms of glomerulus injury
deposition of extravellular collagenous matrix
72
what are the three mechanisms of glomerular injury
immunologic non-immunologic hereditary
73
what is the most common mechanism of glomerular injury
immunologic
74
what are the two types of immunologic mechanisms that cause glomerular injury
immune complex deposition deposition of anti-GBM antibody
75
what are the two types of non-immunologic mechanisms that cause glomerular injury
defective regulation of compliment activation podocytes injured by toxins
76
what is the hereditary mechanism that leads to glomerular injury
mutations in genes lead to abnormal permability
77
what is subepithelial IC deposition
IC deposition at the between the foot processes of the podocytes, attached to the underlying basement membrane
78
what is subendothelial IC deposition
IC deposition between the basement membrane and endothelial layer
79
what is mesangial IC deposition
IC deposits around mesangial cells
80
what is the IF pattern when immune complexes deposit subendothelial, subepithelial, and mesangial
granular immunofluroescence - granular pattern
81
what is the IF pattern when an antibody and anti-podocyte antigen complex binds to podocytes
granular immunofluorescence - granular pattern
82
what is the IF pattern when an antibody and anti-basement membrane antigen complex binds to basement membrane
linear immunofluorescence - diffuse linear pattern
83
what is acute proliferative glomerulonephritis
a type of primary glomerulopathy caused by glomerular deposition of immune complexes
84
what is the mechanism of proliferative glomerulonephritis
immune complexes deposit in the glomerulus leads to an influx of leukocytes and diffuse proliferation of endothelial and mesangial cells (glomerular hypercellularity)
85
what is the clinical manifestation of acute proliferative glomerulonephritis
nephritic syndrome (inflammation of glomerulus)
86
what is the immunofluorscence for acute proliferative glomerulonephritis
granular deposit of IgG and C3 in glomerular basement membrane and mesangium
87
what's an exogenous cause of acute proliferative glomerulonephritis
infection ex. acute poststreptococcal glomerulonephritis
88
what's an endogenous cause of acute proliferative glomerulonephritis
post-infectious (most common) ex. nephritis of SLE
89
what is the mechanism of SLE nephritis
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
what is acute poststreptococcal glomerulonephritis
an exogenous, antigen-induced type of acute proliferative glomerulonephritis most common in children 6-10 presents 1-4 weeks after streptococcal infection
91
what is the mechanism of acute poststreptococcal glomerulonephritis
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
what is the clinical manifestation of acute poststreptococcal glomerulonephritis
nephritic syndrome
93
what is crescentic (rapidly progressive) glomerulonephritis (RPGN)
a type of primary glomerulopathy which is characterized by formation of crescents in glomeruli
94
what are the two clinical manifestations of crescentic (rapidly progressive) glomerulonephritis (RPGN)
nephritic syndrome rapid renal failure
95
what typically causes crescentic (rapidly progressive) glomerulonephritis (RPGN)
severe glomerular injury
96
what is the mechanism of crescentic (rapidly progressive) glomerulonephritis (RPGN)
necrosis, breaks in the glomerular basement membrane, and proliferation of parietal epithelial cells leads to crescent formation
97
what are the three types of crescentic (rapidly progressive) glomerulonephritis (RPGN)
anti-GBM AB 1 immune complex 2 pauci-immune 3
98
what is the main type of type 1 RPGN (anti-GBM Ab)
goodpasture syndrome
99
what are the three main types of type 2 RPGN (immune complex)
postinfectious glomerulonephritis lupus nephritis henoch-schonlein purpura
100
what is the main type of type 3 RPGN (Pauci-immune)
granulomatosis with polyangiitis (Wegener granulomatosis)
101
what is goodpasture syndrome
an example of type 1 crescentic (rapidly progressive) glomerulonephritis systemic disease with glomerular involvement anti-GBM Ab disease
102
what is the mechanism of Goodpasture syndrome
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
what do the anti-GBM autoantibodies bind to in goodpasture syndrome
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
what are three different proposed causes of goodpasture syndrome
viral hydrocarbon solvents genetics
105
mutation in which gene is thought to cause goodpasture syndrome
HLA-DRB1
106
what is the clinical manifestation of goodpasture syndrome
nephritic syndrome
107
what is the immunofluoresence of goodpasture syndrome
linear deposit of IgG and C3 in GBM
108
what is membranous nephropathy
a type of primary glomerulopathy autoimmune response directed against the PLA2R antigen on podocytes or planted antigens
109
what is the mechanism of membranous nephropathy
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
what is the etiology of membranous nephropathy
etiology is unknown 75% of cases are primary 25% of cases secondary
111
what are the 2 main secondary causes of membranous nephropathy
infections therapeutic drugs
112
which 3 types of infections can cause membranous nephropathy
malaria syphilis hepatatis
113
which three types of therapeutic drugs can cause membranous nephropathy
penicillamine NSAIDs catopril
114
what is the clinical manifestation of membranous nephropathy
nephrotic syndrome because of injury to capillary wall
115
what is the IF of membranous nephropathy
granular deposits of IgG and C3 along GBM
116
what are the electron microscope fetures of membranous nephropathy
subepithelial deposits with loss of foot processes
117
what is the difference between a cortical and juxtamedullary nephron
cortical has much shorter loop of henle juxtamedullary nephron's loop of henle extends deep into the medulla
118
what is minimal change disease
a type of primary glomerulopathy
119
what are the three causes of minimal change disease
can follow respiratory infections, drugs, or vaccinations
120
what is the most common cause of nephrotic syndrome in children (2-6yr olds)
minimal change disease
121
explain the mechanism of primary minimal change disease
immune dysfunction leads to loss of foot processes of podocytes this causes GBM to be leaky and leads to proteinuria
122
what is the clinical manifestation of minimal change disease
nephrotic syndrome - leaky GBM
123
what is the mechanism of primary membranoproliferative glomerulonephritis (MPGN)
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
which disease is characterized by a tram-track appearence of the capillary wall
membranoproliferative glomerulonephritis (MPGN)
125
secondary membranoproliferative glomerulonephritis (MPGN) is seen in which three conditions
SLE, viral hepatitis, and chronic infections
126
what are the clinical manifestations of membranoproliferative glomerulonephritis (MPGN)
nephritic and nephrotic syndromes
127
what is the IF of membranoproliferative glomerulonephritis (MPGN)
irregular granular deposits of IgG and C3
128
what is dense deposit disease (DDD)
a type of primary glomerulopathy technically type 2 MPGN that is characterized by dysregulation of the alternative complement pathway
129
what is the mechanism of dense deposit disease (DDD)
intramembranous dense deposition in mesangial region and capillary wall causes proliferation of glomerular cells and infiltration of leukocytes both lead to GBM thickening
130
who is most affected by dense deposit disease (DDD)
children and young adults has a poor prognosis
131
what are four clinical manifestations of dense deposit disease (DDD)
nephritic syndrome nephrotic syndrome hematuria chronic renal failure
132
what are the light microscopy features of dense deposit disease (DDD)
mesangial proliferation and GBM thickening
133
what are the IF features of dense deposit disease (DDD)
C3 deposition with irregular granular pattern
134
what is the electron micropscopy feature of dense deposit disease (DDD)
ribbon-like electron dense deposits in GBM
135
which disease is characterized by ribbon-like electron dense deposits in GBM on electron microscopy
dense deposit disease
136
what is IgA nephropathy (Berger Disease)
a type of primary glomerulopathy deposition of IgA immune complexes in mesangial region
137
what is the mechanism of IgA nephropathy (Berger Disease)
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
what is the most common type of glomerulonephritis in the world
IgA nephropathy (Berger Disease)
139
who is most at risk for IgA nephropathy (Berger disease)
older children and young adults
140
what is the main clinical manifestation of IgA nephropathy (Berger Disease)
recurrent hematuria
141
what are the IF features of IgA nephropathy (Berger Disease)
IgA bound to either IgG or IgM C3 deposition in mesangium
142
what is Alport Syndrome
a type of hereditary glomerular disease genetic disorder that leads to production of abnormal type 4 collagen in GBM
143
what is the mechanism of Alport Syndrome
mutated genes in either alpha 3, 4, or 5 chain in type four collagen of GBM interferes with their folding
144
Alport Syndrome is associated with which two issues
nerve deafness and eye disorders
145
when do symptoms of Alport Syndrome first appear
ages 5-20
146
85% of Alport Syndrome cases are what
X-linked domainant - males will express all symptoms
147
what are the two main clinical manifestations of Alport syndrome
hematuria with RBC casts and proteinuria
148
what are the IF features of Alport Syndrome
no deposits
149
what are the electron microscopy features of Alport Syndrome
irregular thickening of GBM with basket-weave appearance
150
which disease is characterized by basket-weave appearance
Alport Syndrome
151
what is Henoch-Schonlein Purpura
a type of systemic glomerular disease childhood syndrome characterized by skin lesions, abdomnial pain, and intestinal bleeding in adults: renal abnormalities
152
what is the mechanism of Henoch-Schonlein Purpura
immune complex deposition in vessels
153
what are the clinical manifesations of Henoch-Schonlein Purpura
nephritic and nephrotic syndrome
154
what are the four clinical feautres of diabetic nephropathy
end-stage kidney disease glomerular lesions vascular lesions pyelonephritis
155
what are the characteristics of glomerular lesions in diabetic nephropathy
GBM thickening mesangial sclerosis nodular glomerulosclerosis
156
what does a PAS stain show for diabetic nephropathy
acellular nodules
157
what is kimmelstiel-wilson disease
nodular glomerulosclerosis ovoid or spheroid, laminated, hyaline masses found in periphery of glomerulus a symptom of diabetic nephropathy
158
what is lupus nephritis
a type of systemic glomerular disease characteristic of SLE
159
what is the mechanism of lupus nephritis
immune complex deposition in blood vessels, through kidneys, connective tissue, and skin in kidney specifically: deposition in GBM, mesangium, and all throughout glomerulus
160
what are the clinical manifestations of lupus nephritis
nephritic and nephrotic syndrome
161
what are the two major processes that cause tubular and interstitial diseases
iscehmic or toxic tubular injury inflammation of tubes and interstitium (tubulointerstitial nephritis)
162
what is acute tubular injury (ATI)
damage to tubular epithelial cells and an acute decline in renal function
163
what is the most common cause of acute kidney injury
acute tubular injury (ATI)
164
what is a clinical sign of acute tubular injury (ATI)
muddy brown urine caused by shedding of granular casts and tubular cells in the urine
165
what are the two main causes of acute tubular injury (ATI)
ischemia direct toxic injury to the tubule
166
what are the characteristics of acute tubular injury (ATI) caused by ischemia
large, skipped areas rupture of BM occlusion of lumen by casts
167
what causes direct toxic injury to tubules, leading to acute tubular injury (ATI)
endogenous or exogenous substances
168
where is direct toxic injury to the tubule most likely to be found
proximal tubule
169
what is tubulointerstitial nephritis
group of diseases that involve inflammatory injuries of the tubes and intersititium
170
what are the two main results of acute tubular injury
decreased urine output and decreased GFR
171
what are the characteristics of acute tubulointerstitial nephritis
rapid onset with interstitial edema and leukocyte infiltration of the interstitium and tubules
172
what are the characteristis of acute tubulointerstitial nephritis
leukocyte infiltration, interstitial fibrosis, and tubular atrophy
173
what three types of disorders can secondarily cause tubulointerstitial nephritis
vascular cystic metabolic
174
what is the clinical manifestation of tubulointerstitial nephritis
azotemia
175
what are the two main hallmarks of tubulointerstitial nephritis
absence of nephritic or nephrotic syndromes presence of defects in tubular function
176
what are the 5 risks of developing a UTI
short urethra, obstruction, urine stasis, high pH, and vesicoureteral reflux due to congenital defect
177
what are the two main pathways to renal infection
hematogenous infection ascending infection
178
what is the most common pathway of renal infection
ascending infection (bacteria climbs up the urethra)
179
what are the two types of refluxes associated with kidney infections
vesicoureteral intrarenal
180
what is vesicoureteral reflux
the reflux of urine from the bladder back into the ureter can be congenital (anatomic anomoly) or aquired (bacteria)
181
what is intrarenal reflux
the reflux of urine back into the kidney from the papillae
182
which two locations are most common for intrarenal reflux
upper and lower poles of kidney because their papillae have flattened or concave tips rather than convex tips
183
what is cystitis
a bladder infection
184
what is pyelonephritis
a kidney infection
185
what is the most common UTI causing bacteria
gram negative bacilli from intestinal tract (E. coli)
186
which fungus can cause UTIs
candida
187
which parasite can cause UTIs
schistosomiasis
188
which virus can cause an UTI
polyomavirus
189
what is pyelonephritis
a serious complication of an UTI which is characterized by inflammation affecting the tubules, interstitium, and renal pelvis
190
what is chronic pyelonephritis
changes in the kidney due to recurring or persistent infection leads to pelvocalyceal damage, pyonephrosis (pus), and fibrosis of interstitium
191
what is acute pyelonephritis
bacterial infection of the renal parenchyma and pelvis can lead to abscess formation
192
what is the mechanism of acute pyelonephritis
bacterial infection causes an inflammatory response leads to arterial constriction and edema eventually leads to abscess formation
193
what are 5 risk factors for acute pyelonephritis
UTI pregnancy instrumentation kidney transplant diabetes mellitus
194
which toxin can cause tubulointerstitial nephritis
analgesics
195
which metabolic disease can cause tubulointerstitial nephritis
oxalate nephropathy
196
which immunologic reaction can cause tubulointerstitial nephritis
sjogren syndrome
197
what are the 7 categories of causes of tubulointerstitial nephritis
infections toxins metabolic diseases physical factors immunologic reactions vascular diseases miscellaneous