Renal Pathology - Dr. Dobson Part 1 Flashcards
(174 cards)
1
Q
most sensitive time in utero
A
week 3-9 peaking 4th and 5th
2
Q
cause most commonly for glomerular and tubular and interstitial renal disorders
A
Glomerular = immunological
Tubular + interstitial = toxic or infectious
3
Q
glomerular capillary filtration barrier 3 layers
A
- endothelium :
- BM :
- foot processes Podocytes:
4
Q
glomerular endothelium is made up of what
A
fenestrated and permeable to water, small solutes, small proteins (not cells, large proteins, plts)
= - charges (repel albumin
4
Q
glomerular endothelium is made up of what
A
fenestrated and permeable to water, small solutes, small proteins (not cells, large proteins, plts)
= - charges (repel albumin
5
Q
glomerular endothelium is made up of what
A
fenestrated and permeable to water, small solutes, small proteins (not cells, large proteins, plts)
= - charges (repel albumin
6
Q
the endothelial cells of Bowmans capsule release what chemical substances
A
- NO = vasodilator
- Endothelin-1 = vasoconstrictor
(control Renal plasma flow RPF)
7
Q
the basement membrane is composed of what
A
- charge matrix
= charge selective barrier
= also size barrier
8
Q
kidney role in endocrine ways
A
erythropoietin, renin, PGE, regulates Vit D metabolism
9
Q
6 warning signs of kidney disease
A
- Cr and BUN high
- GFR < 60
- blood, protein in urine
- high BP
- high urination, painful urination
- puffy eyes or hands or feet
10
Q
distal tubule role
A
secretes H+ and reabsorbs the HCO-3
11
Q
buffers for H+
A
HPO4 and NH3 = H2PO3 + NH4+
12
Q
Azotemia
A
elevated BUN and Cr
from decreased GFR
13
Q
Uremia
A
Azotemia that has sx
uremic frosting can be seen
14
Q
BUN is made how
A
Urea N broken down in liver from protein making BUN
it then goes to the kidneys
15
Q
ideal BUN : Cr ratio
A
10:1 - 20:1
16
Q
prerenal azotemia
A
CHF burns GI hemorrage Shock, stress dehydration
17
Q
renal level azotemia
A
GN Pylo DM Nephrotoxic drugs renal failure anabolic steroids
18
Q
Post renal azotemia
A
stones , neoplasm
bladder urethral abnormality
bladder outlet obstruction (BPH)
19
Q
GFR is what and normal
A
how much blood passes glomeruli each minute
- estimated from serum cr
= 90mL/min/1.73m2 or higher
20
Q
proteinuria Nephritic syndrome SX
A
- hematuria + RBC casts
- HTN
- low GFR
- mild proteinuria
21
Q
Proteinuria Nephrotic Syndrome
A
- heavy proteinuria
- hypoalbuminuria = edema
- hyperlipidemia, lipiduria
22
Q
dip stick use
A
usually only in EM
23
Q
AKI
A
rapid decline in GFR (hours to days)
= fluid electrolyte dysregulation
= high CR and BUN
= low or no urine can happen (ATI)
24
CKD
low GFR under 60 for at least 3mos,
| = also albuminuria can happen
25
CKD is end stage of what
chronic renal parenchymal disease
26
CKD usually effects what pts
DM and HTN
27
Wilms tumor effects
developmental abnormalities in kidney and urinary tract
28
most common cause of chronic kidney disease in children
renal dysplasias and hypoplasias
29
Prune Belly Syndrome prevalence and 5 common SX
male
1. Hydroureteronephrosis
2. Vesicourereral reflux (VUR) bilateral
3. renal dysplasia
4. cryptochidism bilateral
5. UTIs common
30
Bilateral agenesis
usually un stillborn infants
| only compatible with life if unilateral
31
unilateral agenesis of kidney can progress to what
glomerular sclerosis or hypertrophy nephrons
32
renal hypoplasia is common when
in low birth weight infants
33
ectopic kidney can be found where
pelvis, iliac fossa, abd or thoracic cavities, contralateral positions
34
Vesicoureteral reflux (VUR)
most common and serious anomaly
= high chance of pylo + loss of renal function
= can cause congenital vesicouterine fistulae (dilation of ureter)
35
Ureteropelvic Junction Obstruction (UPJ) SX children
most common cause of hydronephrosis in infants
1. UTI
2. Hematuria
3. FTT
4. Sepsis
5. azotemia
6. Hydronephrosis
36
Ureteropelvic Junction Obstruction (UPJ) what happens
ureter gets obstructed and compressed by a renal artery like the inferior segmental artery
37
Ureteropelvic Junction Obstruction (UPJ) SX adults
women
1. UTI
2. hematuria
3. ABD pain or V from intermittent obstruction
38
3 sites that have high risk of constriction of the ureter
Ureteropelvic junction (as it exits kidney)
Crossing the iliac artery and pelvic brim
When entering bladder
39
renal diverticuli
pouches forming in bladder or ureter
= 1cm-10cm
= can cause infection and rare carcinoma
40
Extrophy of bladder
NO anterior wall development for abd and bladder
| = exposed bladder mucosa
41
Extrophy of bladder can cause what
the exposed mucosa can go through colonic glandular metaplasia (adenocarcinoma) + infections to upper GU
42
urachal cyst
the urachal canal and bladder is connected by allantois that is obliterated however if not it makes the urachus cyst (metaplastic glandular epithelium cyst on umbilicus)
43
urachal cyst can become
adenocarcinoma
44
Malformation of urethral groove
ventral (Hypospadias) or dorsal (epispadias) opening of penis
45
Hypospadias and epispadias can cause what
ascending infection of urinary tracts
| or if as base of penis can cause X ejactulation
46
Cryptorchidism
partial or complete failure of testes to descend into scrotal sac
= usually unilateral
47
Cryptorchidism can cause what
testicular cancer
| = also can at times present in hypospadias
48
4 diseases that usually effect the glomerulous
1. DM
2. HTN
3. SLE
4. Fabry disease
49
Basement membrane layers
1. Lamina rara interna (loose)
2. Central Lamina densa
3. Lamina rara externa (loose)
50
layers from capillary to urine lumen (tubule)
1. capillary fenestrated endothelium
2. BM (3 layers)
3. Podocytes and foot processes (visceral epithelial cells)
51
Acute response to glomerular injury is what
1. mesangial and endothelial cells swell and proliferate + WBCs come proliferate = Endocapillary proliferation
2. glomerular epithelial cells proliferation from injury that causes plasma proteins leakage into urine ----> activate coagulation = CRESCENTS formation + WBCs go into these
52
Chronic Response to glomerular injury
THICKENING OF BM or CAPILLARY WALLS :
1. immune complexes deposition, fibrin, amyloid, cryoglobulins deposition in GBM
2. Protein synthesis in GBM= Diabetic Glomerulosclerosis
3. More layers (matrixes) form in BM = Membranoproliferative Glomerulonephritis (MPGN)
53
Hyalinosis
ECM amorphous material leak into glomerulous
= can obliterate capillary lumens if glomerular tuft
= usually from endothelial or epithelial injury + end stage
54
Sclerosis
EXM collagenous matrix leak deposition in mesangial cells or capillary loops
= in Diabetic Glomerulosclerosis
= can obliterate capillaries
54
Sclerosis
EXM collagenous matrix leak deposition in mesangial cells or capillary loops
= in Diabetic Glomerulosclerosis
= can obliterate capillaries
55
Podocytopathy
loss of podocytes which have limited replication capability
= seen in FSGF and diabetic neuropathy
= causes proteinuria
56
Podocytopathy can happen from what things happening
immune complex deposition
57
when does progressive renal disease happen
once nephrons are destroyed so GFR is 30%-50% normal = progression starts independent or original disease
58
progressive renal disease causes what 2 things to happen
1. Sclerosis : secondary FSGS, after many renal injuries (proteinuria + loss of renal function)
2. Tubulointerstitial Injury : interstitial inflammation (in GN) + Tubulointerstitial fibrosis (Diabetic nephropathy)
59
decline in renal function is more correlated to what
extent of tubulointerstitial damage then glomerular damage
60
Acute Proliferative (Post-infectious and Infection-Associated) GN is what and caused by
immune complexes + glomerular cell proliferation
| = most common for strep (Group A B-hemolytic Strep (GABH)
61
Acute Proliferative (Post-infectious and Infection-Associated) GN immunoflorescent staining
speckles from granular deposits of C3 (N that cause "humps")
62
Rapidly Progressive GN (Crescentic) is what
fast loss of renal function (NEPHRITIC) + oliguria
63
Rapidly Progressive GN (Crescentic) Immunoflorescent stain
crescents glomeruli seen (know what this looks like) from PAS
= proliferating epithelial cells and WBS in BC
64
Type 1 Anti-GMB Abs is what
GOODPASTURE SYNDROME
= AB against a3 of collagen4
= can effect lungs (pulmonary hemorrhage)
65
Type 1 Anti-GMB Abs prevalence
male 20yo, often smokers
| = autoimmune
66
glomerular lesions are formed from what 3 autoimmune diseases and what is seen in this
1. Goodpasture
2. Microscopic polyangiitis
3. Granulomatosis with polyangiitis (Wegner's)
= glomerular necrosis + crescent formation**** + scarring sclerosis
67
Rapid Progressing GN (RPGN) types
1. Type 1 Anti-GMB Abs = (GP syndrome)
2. Type 2 Immune complex = (SLE, Henoch - Schönlein Purpura, IgA nephropathy BERGER, post-infectious GN)
3. Type 3 Pauci- Immune = (Wegner GPA + Microscopic PA, Membranous nephropathy, Minimal change disease, FSGS, MPGN)
68
Type 2 Immune complex RPGN is what and SX
SLE
- fever
- skin, jonts, kidney , serous membranes
- hematuria, RBC casts, htn (NEPHRITIC)
69
DX SLE
AB to dsDNA (Smith Ag = Sm Ag)
70
SLE and kidney
50% pts
GN and Tubulointerstitial nephritis
= immune complex deposit on BM ----> WIRE LOOP when cap wall thickens
= crescents in BC
71
Henoch - Schönlein Purpura SX
1. ABD pain + GI bleeding, V
2. blood + protein urine
3. RASH : pupuric rash (Vesicles) on legs, butt, arms
4. joint pain
72
Henoch - Schönlein Purpura and kidney
nephritic or nephrotic, RPGN + many crescents
= IGA deposited mesagial cells (like in IgA nephropathy)
= usually follows URI
= atrophy
73
Henoch - Schönlein Purpura prevalence
3yo -9yo children syndrome
| can happen in adults = more severe
74
fibrillary GN SX
1. blood + protein in urine
2. BUN and Cr high
3. edema
4. granular IgG, C3, kappa + lambda light chains SEEN ****
5. + DNAJB9**
75
IgA nephropathy is also called
Bergers disease
76
IgA Nephropahty (Bergers)
IgA deposits in the mesangial regions
| - hematuria
77
IgA Nephropahty (Bergers) is very similar to what disease
Henoch-Schönlein purpura
78
IgA Nephropahty (Bergers) is associated to what diseases
Celiacs
| Hepatobiliary clearance of IGA problems (Liver disease)
79
IgA Nephropahty (Bergers) immunoflorescents stain
grandular IgA deposition on mesangial cells
80
RPGN Type 3 Pauci- Immune SX
WEGNER (GPA)
1. necrotizing granuloma of URT
2. necrotizing grnulomatous vasculitis (lungs, airways)
81
RPGN Type 3 Pauci- Immune happens from
T-cells responding to inhaled or other envir thing
| = PR3- ANCA
82
RPGN Type 3 Pauci- Immune TX
immunosuppression
83
post strep GN deposition location
immune complexes deposition on subepithelial spaces + many N and glomerular cells proliferate
84
RPGN nephritic or nephrotic
nephritic
85
highest molecular weight protein
immunoglobulins only in non-selective proteinuria
86
most common causes of secondary nephrotic syndrome
DM
SLE
Amyloidosis
87
most common primary nephrotic syndrome causes
1. FSGS (all ages)
2. Minimal change disease (children)
3. membranous nephropathy (adults)
88
Membranous nephropathy happens how
75% primary = autoimmune
(other causes)
- drugs like gold, NSAIDS, Penicillin
- tumors
- SLE
- HEP B, HEPC, schistosomiasis
89
Primary Membranous nephropathy causes
anutoABs to M-type Phospholipase A 2 Receptor (PLA2R)
90
Membranous nephropathy immunoflorescents staining and deposition location
thickening of capillary wall**
| Ig deposits on subepithelial side of BM (IgG)
91
Minimal change disease what happens
diffuse effacement of foot processes (flattening)
| = minimal changes to glomerulus
92
Membranous nephropathy associated with what 5 diseases
1. respiratory infections
2. corticosteroids
3. eczema, rhinitis
4. HLA haplotypes for atrophy
5. Hogdkin lymphoma
93
Focal Segmental Glomerulosclerosis prevalence
most common nephrotic syndrome
| esp in AA and hispanic
94
Focal Segmental Glomerulosclerosis secondary causes for this
1. HIV , heroin, Sickle cell, morbid obese
2. other necrotizing lesions like IgA nephropathy, focal GN
3. slit diaphragm protein mutation
95
Focal Segmental Glomerulosclerosis what happens
1. effacement of foot processes
2. proteins accumulate in mesangial matrix
3. focal + segmental sclerosis (TGF-B fibrosis)
96
Focal Segmental Glomerulosclerosis immunoflorescence stain and location
1. collapse of cap loops, increase matrix, plasma protein on cap walls ----> hyalinosis
2. foam cells + lipids
3. IgM + C3 can be deposited in mesangium
97
Focal Segmental Glomerulosclerosis can lead to
tubular atrophy and interstitial fibrosis
98
2 diseases that can lead to FSGS and difference
1. DM = global mesangial sclerosis
| 2. HIV = focal segmental GN
99
Membranoproliferative GN type 1 and type 2
TYPE 1 : deposition of IgG**** + Complement
| TYPE 2 : dense deposite disease**, C3 GLOMERULOPATHY (complement activation and excretion)
100
Membranoproliferative GN type 1 and type 2 is associated with
1. SLE, HEP B, HEP C, schistosomiasis, HIV
2. a-1 antitrypsin def
3. hodgkins
101
Membranoproliferative GN type 1 and type 2 immunoflorescence
WBC to mesangium
= double-contour**, tram track appearance** (split membrane appearance)
=lobular look glomeruli
=
102
Membranoproliferative GN type 2 WHAT is seen
LOW C3 , only normal C1 and C4
LOW Factor B, Properdin
(C3 nephritic factor in circulation C3NeF)****
103
Alport Syndrome SX
hematuria ----> Chronic RF
nerve deafness
eye disorders
104
Alport Syndrome what causes this
mutation in collagen 4 subunits (in GBM, lens, cochlea)
| esp subunits a3, a4, a5
105
Alport Syndrome inheritance
X linked most common
| can be AD or AR
106
Alport Syndrome staining look
thickening and thinning spots on the BM of glomeruli + lamina densa splitting
= basket-weave apperance
107
Alport Syndrome can progress to what
global or focal segmental Glomerulosclerosis , vascular sclerosis, tubular atrophy, interstitial fibrosis
108
Thin Basement Membrane Nephropathy (Benign Familial Hematuria)
asymptomatic hematuria
| diffuse thinning of GBMm however normal renal function
109
Diabetic Nephropathy first sign
low amounts of albumin in urine (30mg-300mg/day) (which will show - dip stick, you need urine microscopy)
110
Diabetic nephropathy prevalence
more in T1D, however still in T2D AA, native americans, hispanic
= can progress to ESRD
111
glomerulus in Diabetes
most in T1D
| Glomerular capillary BM (GBM) thickening) + mesangial widening + tubular BM thickening
112
Diabetic Nephropathy is also called what
intercapillary glomerulosclerosis OR Kimmelstiel- Wilson disease
113
Diabetic Nephropathy what is seen in the arteries and tubules
hyalinosis in capillaries
| tubular atrophy + interstitial fibrosis (glomerulosclerosis)
114
acute kidney injury (AKI) Ischemic vs nephrotoxic
Ischemic : from low BF
| Nephrotoxic : from endogenous agents
115
muddy brown granular casts are seen when
AKI on microscopes
116
Initiation Phase of AKI
decrease of Urine output and increase BUN (oliguria can happen, from low BF + low GFR)
117
Maintenance Phase AKI
decrease urine (40-400ml/day = oliguria), NA and Water overload, rising BUN, hyperkalemia, metabolic acidosis,
118
Recovery Phase AKI
increase in urine V up to 3L/day (from still damaged tubules), HYPOkalemia, tubules recover over time, BUN and Cr decrease
119
HALLMARKS of tubulointerstitial disorders
1. X nephritic X nephrotic syndrome
2. X concentration in urine (polyuria or nocturia), salt wasting,
3. metabolic acidosis = cant excrete acids
120
acute pyelonephritis
bacterial infection
usually from UTI
= suppurative inflammation
121
Chronic pyelonephritis
usually also bacterial infection + vesicoureteral reflux, obstruction
122
acute pyelonephritis SX
CVA tenderness
fever, high WBCs
Dysuria, polyuria
123
pyelonephritis is usually from what
E. Coli
124
TX pyelonephritis
E. Coli Cystitis :
= 1 dose AB FOSFOMYCIN
= 3day TMP/SMZ
= nitrofurantoin
125
kidney viral infection happens from what usually
Polyomavirus usually from allograft kidney from immunosuppression = Polyomavirus-associated-nephropathy(PVAN)
126
other viral infections of kidneys primary
BK virus
| JC virus
127
complications of pyelonephritis
1. Papillary necrosis : coagulative necrosis of pyramids (yellow grey-white)
2. Pyonephrosis: almost or complete obstruction usually high in GU tract
3. Perinephric abscess : suppurative inflammation through renal capsule to perinephric tissue
128
Papillary necrosis is seen in what patients with pyelonephritis
1. DM
2. Sickle cell
3. Obstruction
129
Pyonephrosis is what
almost or complete obstruction of GU tract esp high up
| = suppurative exudate cant drain and fills pelvis, calyces, ureter + pus
130
what diseases effect chronic tubulointersititial inflammation and scarring of CALYCES + pelvis
Chronic pyelonephritis + Analgesic nephropathy
131
dilation of calyces Vesicoureteral reflux vs obstruction
obstruction dilates more and basically all calyces from the high P backflow
132
blood agar and MacConkey agar is used when
for pus or urine samples
133
Proteus Mirabilis on blood agar
thin waves of concentric circles form
134
Proteus Mirabilis UTI TX
UTI : 3day trimethoprim/sulfamethoxazole (TMP/SMZ)
| or 3day fluroquinolone (ciprofloxacin)
135
complicated UTI TX
ABs for 10-21 days
136
TX acute Pyelonephritis uncomplicated
```
(Gentamycin or ceftriaxone can be given 1 time before starting)
1. Fluoroquinolone**
OR
2. TMP/SMZ
OR
3. cephalosporin
(7-14days)
```
137
acute kidney injury top causes
1. Pyelonephritis
| 2. toxin or drug induced tubulointerstitial nephritis
138
Drug or Toxin induced Tubulointerstitial nephritis happens from what
Sulfonamides, synthetic penicillin (methicillin, ampicillin), synthetic AB (Rifampin), diuretics, NSAIDS, allopurinol, cimetidine
139
Drug or Toxin induced Tubulointerstitial nephritis injury happens how
1. cause interstitial inflammation (acute hypersensitive nephritis)
2. cause ATI
3. injuries cumulate take years to become CKD (goes unrecognized)
140
Drug induced ACUTE Tubulointerstitial nephritis SX
2-40days after
1. fever
2. high E
3. rash 25%
4. renal problems (blood, protein, WBCs esp E)
5. high Cr or AKI (50%)
141
NSAIDS and kidney
inhibits COX2 including in the kidney
| = can cause several renal injuries
142
nephropathy with hyperuricemia happens in which 3 diseases
1. Acute uric acid nephropathy
2. Chronic urate nephropathy
3. Nepholithiasis (stones)
4. Tumor Lysis Syndrome (effecting tubules and high uric acid, usually from tumor cells undergoing chemo)
143
hypercalcemia and kidney
diseases like hyperPTH
| can lead to stones and chronic tubulointerstitial disease
144
ADTKD (AD Tubulointerstitial Kidney Disease)
also called
causes
(medullary cystic kidney disease)
| = progressive renal failure in adults inherited as AD
145
ADTKD (AD Tubulointerstitial Kidney Disease) MUTATIONS 4
1. MUC1 (distal nephrons)
2. UMOD (thick ascending LOH)
3. REN (Juxtaglomerular apparatus)
4. HNF1B (hepatocyte TF regulating other genes)
146
multiple myeloma and kidney + 4 reasons effects happen
renal insufficiency due to
1. Bence- Jones proteinuria + nephropathy
2. Amyloidosis
3. Light Chain deposition disease
4. Hypercalcemia + Hyperuricemia
147
cancer that can cause membranoproliferative GN
leukemia and lymphoma
148
cancer that can cause minimal change disease
Hodgkins
149
cancer that can cause membranous nephropathy
carcinomas
150
cancer that can cause monoclonal immunoglobin / light chain deposition disease
Multiple Myeloma
151
Uromodulin (Tamm-Horsfall protein) function
protein in kidney (guardian)
1. modulate ion channel activity + balance
2. systemic inflammatory responce
3. tubular communication
4. bacterial adhesion protection
5. mineral crystallization
152
Uromodulin (Tamm-Horsfall protein) THP mutation can cause
1. UTI recurrent
2. kidney stones
3. htn
4. hyperuricemia
5. AKI / CKD
153
organ that can impair renal function
LIVER DISEASE ****
| also Heart Disease
154
Hepatorenal syndrome steps
1. PORTAL HTN (from liver disease)
2. vasodilators made
3. lower renal BF
4. renin/angiotensin activation
5. lower renal BF more = renal failure
155
Hepatorenal syndrome is usually from what
Portal HTN from cirrhosis, severe alcoholic hep, or tumor at times, fulminant hepatic failure
156
most common disease or system in body that effects
vascular disease (HTN, vasculitis)
157
Nephrosclerosis strong association
HTN (DM makes it worse)
158
Nephrosclerosis kidney looks like
```
grain leather (sugar coating) look on surface
+ reduced size from cortical scarring
```
159
renal artery stenosis causes what
HTN from the renin production activated (when ischemia in kidney)
160
Fibromuscular Dysplasia (FMD)
thickening in medium and large As (renal, carotid, splanchnic, vertebral) = hyperplasia + fibrosis ----> luminal stenosis
161
Fibromuscular Dysplasia (FMD) in renal artery can be caused by + angiography look
renovascular htn
| = beads on string on adjacent vessels ----> vascular outpouching (aneurysms) that can rupture
162
Focal FMD vs Multifocal FMD
Focal FMD : tubular narrowing (stenosis), focal lesions
= intimal fibroplasia
Multifocal FMD : 90%, many lesions + STRING ON BEADS
163
thrombotic microangiopathy is what
syndrome that includes TTP/HUS and thrombi on caps and arterioles (including in kidney) = MICROANGIOPATHIC HEMOLYTIC ANEMIA
164
thrombotic microangiopathy is what
| is caused by what
1. Shiga toxin- mediated HUS (E. coli H0517)
2. Atypical HUS
3. TTP (ADAMTS13)
165
Typical Hemolytic Uremic Syndrome is what and from what
Epidemic, Classic, +Diarrhea
| 1. GI E. Coli O157:H7 infection
166
Typical HUS SX
hematemesis, melena, oliguria, hematuria, thrombocytopenis, hemolytic anemia, HTN, neurologic changes
167
Atyical Hemolytic Uremic Syndrome is what and caused by 4
Non-Epidemic, -Diarrhea
1. Factor H def. Factor I def, def CD46 (prevent complement)
2. Anti-phospholipid syndrome (can be from SLE)
3. post-pregnancy complications
4. systemic sclerosis, malignant htn
168
TTP PENTAT
1. fever
2. neurologic changes, headache
3. thrombocytopenia
4. microangiopathic hemolytic anemia
5. renal problems (renal failure)
169
TTP happens because of
ADAMT13 mutation of ABs against it** (cleaves vWF for proper plt aggregation)
170
TTP looks like what in kidney
massive ischemic necrosis in CORTEX
171
Bilateral renal artery disease can cause what and important to recognize for
see in angiography
can cause chronic ischemia + renal insufficiency (even with no htn)
= surgery to revascularize to prevent more renal decline
172
3 renal problems that can occur in sickle cell pts
1. hematuria
2. poor concentrated urine = hyposthenuria
3. Patchy papillary necrosis
