308 - Glomerular Diseases (nephritic) Flashcards
Glomerular disease are usually accompanied by ___ and ___
hematuria
proteinuria
In most cases hematuria will not be macroscopic, beside in the case of ___ and ___
IgA nephropathy
sickle cell anemia
When microscopic anemia is found, we should rule out: (5). Also remember- kidney cysts and vascular kidney injury
BPH IS nephritis papillary necrosis hypercalciuria nephrolithiasis
When dysmorphic RBC or RBC ____ are found, there is a high chance for ____
casts
glomerulonephritis
Common symptoms of proteinuria include: ___ and ____
edema
foamy urine
Transient proteinuria is usually < ___ g/24hr. It is more common in situations such as: (5)
1 Fever physical activity obesity OSA CHF
Glomerular proteinuria in the adult is non selective, while in ___ in children the proteinuria is selective- mostly for ____
MCD
albumin
Pyuria is more common in ___ disease, such as: ___ or ____
inflammatory glomerular
post acute strep
MPGN
Acute nephritic syndrome is define by proteinuria of ___g/24hr, ____, ___, ___, ____, ____ (5).
1-2 hematuria (with RBC casts) pyuria HTN edema decreased GFR
Extreme acute nephritic syndrome may lead to ___ (RPGN) within days. The histopathological expression is called ____
Rapidly progressive glomerulonephritis
Crescentic glomerulonephritis
Pulmonary renal syndrome is the combination of ___ and ___
RPGN
pulmonary bleeding
Pulmonary renal syndrome may be caused by: (4)
Goodpasture’s syndrome
ANCA associated small vessel vasculitis
SLE
cryoglobulinemia
Nephrotic syndrome is defined by massive proteinuria > ___ gr/24hr, ___,___,___,___,____ (5)
3 HTN hypercholesterolemia hypoalbuminemia edema microscopic anemia
Basement membrane syndrome may be caused by a genetic mutation (___), or autoimmune process harming the GBM (___).
Alport’s syndrome
Goodpasture’s syndrome
Basement membrane syndrome manifestations include: (4)
microscopic hematuria
proteinuria
HTN
decreased renal function
Glomerular vascular syndrome may lead to ____ or ___
hematuria
proteinuria
Glomerular vascular syndrome may be caused by: (5)
vasculitis thrombotic microangiopathy atherosclerosis cholesterol thrombi HTN
Common causes for infectious disease associated syndrome include: (5)
SBE malaria schistosomiasis HIV HBV/HCV
Name 6 clinical glomerular syndromes: (6)
acute nephritic syndrome pulmonary renal syndrome nephrotic syndrome basement membrane syndrome glomerular vascular syndrome infectious disease associated syndrome
When classifying acute vs chronic state we can notice that in the acute state it is more common to see ___ and uremic symptoms (___,___,___,___)
lethargy nausea vomiting fluid edema drowsiness
In chronic cases the patients may be ____
asymptomatic
In acute nephritic syndrome there is an extensive damage to the ___, leading to a decrease in ___ therefor ___ and ___
glomeruli
GFR
fluid retention
electrolytes
PSGN appears after cutaneous infection (___)- 2-6 weeks after, or throat infection (____) 1-3 weeks after
impetigo
pharyngitis
PSGN more common in ___ countries, in the ages of ___ and in ___ countries in ___ population with comorbidities. Generally it is more common in ___
developing 2-14 developed elder men
The pathology of PSGN includes ___ of the ___ and ___ cells
hypocellularity
mesangial
endothelial
In PSGN we can find glomerular infiltration of ___, subendothelial granular sediments of ___ and ___ (C3-9, IgM, IgG)
PMN
immunoglobulins
complements
Systemic symptoms of PSGN include in 50%- (4)
headache
malaise
anorexia
flan pain (due to capsule swelling)
In PSGN patients lab work, 90% of patients will have a depressed ___ test and low levels of ___ together with normal levels of ___
CH50
C3
C4
Testimony of strep infection in PSGN can be: ____ (10-70%), ___ (30%), ___ (70%), ___ (40%). Sometimes RF will be positive together with p-ANCA
Positive culture
ASO
anti DNAase
anti hyaluronidase
Treatment for PSGN includes supportive care- controlling ___ and ___, sometimes to the point of dialysis. Treat also with ___ both the patients and relatives.
HTN
edema
Abx
SBE (___)
subacute endocarditis
SBE patients mechanism is ___ sediments from circulation with ___ activation
immune complexes
complement
SBE clinic includes ___ (micro/macro), ____, and light ___.
hematuria
pyuria
proteinuria
Lab work of SBE may reveal: (5)
normocytic anemia Cr ESR complement decrease ANCA
Treatment of SBE should be focused on ___ the pathogen with prolonged Abx (___ weeks)
eradication
4-6
In lupus nephritis there is a high correlation between the ___ and the ___ of the disease
pathology
stage
Lupus nephritis can be classified into __ stags: (6)
6 minimal mesangial mesangial proliferation focal nephritis diffuse nephritis membranous nephritis sclerotic nephritis
The mechanism in lupus nephritis is based on ____ sediments, leading to an ____ reaction
immune complexes
inflammatory immune
The clinical presentation of lupus nephritis includes mostly ___, but also ___
proteinuria
nephritic symptoms
The best lab result for diagnosing lupus nephritis is ___. Other values may include ___ (70-90%). ___ should be performed only after we see a pathological picture in ____
anti ds- DNA
hypocomplementemia
biopsy
urine sample
class 1/2 (minimal mesangial\ mesangial proliferation) of lupus nephritis: (2)
Good prognosis
no treatment is needed
class 3 of lupus nephritis (focal nephritis)- symptoms may include (4). Mild proliferation usually respond to ___
HTN urine casts proteinuria Cr increase steroids
class 4 of lupus nephritis (diffuse nephritis) is usually with high titer of ___, low levels ___, hematuria, ___ casts, proteinuria, ___, and renal dysfunction. treatment include: ____+___/____ for 2-6 months
anti DNA complement RBC HTN High dose steroids cyclophosphamide mycophenolate
class 6 of lupus nephritis (sclerotic nephritis)- most patients will need ____ or ____
kidney transplantation
dialysis
Anti GBM (___) is an autoimmune disease in which antibodies are formed against component of __ in the GBM. In some cases they show together with lung bleeding- ____ syndrome.
glomerular BM disease
collagen
Goodpasture’s
In anti GBM disease when performing biopsy, we can see focal or segment ___ followed by ___ and crescent formation in the bowman space, meanwhile development of ___ and ___. In immunofluorescence ___ will show.
necrosis proliferation nephritis IS fibrosis IgG
A typical anti GBM patient could be a ___ years old ___ with a sharp drop of ___ levels, ___, dyspnea, and ___.
20
man
hemoglobin
hematuria
Beside young men, other typical anti-GBM patients may be in their ___ decade of life. In this case the disease is ___ with __ renal prognosis. Oliguria usually suggest ___ prognosis.
6-7
asymptomatic
worse
bad
Anti GBM calls for an urgent kidney ___ . Serum AB against GBM- mostly ___________.
biopsy
alpha 3 NC1 domain of collagen type 4
In vasculitis associated variant of anti GBM 10-15% of patients will have ____ AB against ___- it is a vasculitis variant of ___. ____ levels will be normal
pANCA
MPO
Goodpasture’s
complement
Treatment for anti GBM includes 8-10 courses of __, in the first 2 weeks ___ should be given as well.
plasmapheresis
prednisone
cyclophosphamide
Anti GBM has a bad prognosis when the patients has >___% of and advanced ___ in the biopsy, ___>5-6 mg/dL, ___, a need for urgent dialysis.
crescents
fibrosis
Cr
oliguria
IgA nephropathy is defined by an episodic ___ and mesangial deposition of ___. It is one of the most common forms of ___. More common in ___ in their __ decade of life
hematuria IgA GN men 2-3
The mechanism of IgA nephropathy is ___ deposition in the ___
IgA
glomeruli
IgA nephropathy can present in 2 ways: ____ episodes during/after ___ (usually also with ___). or- prolonged ___ ____
macrohematuria URTI proteinuria asymptomatic microhematuria
Diagnosis of IgA nephropathy requires kidney ___
biopsy
Treating IgA nephropathy includes ___. When RPGN-> ___,___,___
ACEi
steroids
cytotoxic
plasmapheresis
In benign IgA nephropathy __% of patients will go through complete remission. When the disease is progressive- renal failure will occur in ___% of patients ___ years after. Risk factors include: (5)
5-30 25-30 20-25 HTN proteinuria>6 months sex old age bad biopsy
ANCA small vessel vasculitis is defined by ___ with ___ and positive ___
GN
vasculitis
ANCA
In ___ it is more common to see ____ and in ____ and ___ it is more common to see ___
Wegener's cANCA microscopic polyangiitis Churg Strauss syndrome pANCA
In all of the ANCA small vessel vasculitis treatment includes a combination of ___, ___, and ___ in the acute phase, followed by maintenance of ___/___ for a year.
plasmapheresis steroids cyclophosphamide cyclophosphamide azathioprine
Wegner’s granulomatosis = _____
granulomatosis with polyangiitis
in granulomatosis with polyangiitis patients are usually with: ___, purulent rhinorrhea, nasal ulcers, ___, polyarthralgia/____, cough, ___, dyspnea, micro-____ and proteinuria.
fever sinusitis arthritis hemoptysis hematuria
In Wegener’s CXr we may see- ___, ___ and sometimes ___
Pulmonary nodules
infiltrations
cavitation
In granulomatosis with polyangiitis biopsy we will see a mixed tissue of: ____ and ____
noncaseating granulomas
small vessel vasculitis
When Wegner’s is active the biopsy will show- ____ without immune deposition
segmental necrotizing glomerulonephritis
Risk factors for granulomatosis with polyangiitis include: ___ exposure and ___ deficiency
Silica
alpha 1 antitrypsin
Microscopic polyangiitis is similar to WG but without ___/___ involvement. Also, we will not find ___ in biopsy and the damage is limited to the ____
lung
sinusitis
granulomas
capillary/venules
Churg Strauss syndrome is defined by ___ with ___. Other symptoms may include: (4)
small vessel vasculitis eosinophilia purpura mononeuritis multiplex allergic rhinitis/asthma
MPGN= ____
membranoproliferative glomerulonephritis
MPGN is defined by GN mediated by the ___ system, characterized by thickening of the ___ with ___ changes. in 70% we will see ____. The idiopathic forms are usually seen in young adults or ___
immune GBM mesangial proliferative hypocomplementemia children
How many types of MPGN are there?
3
Type 1 MPGN is associated with prolonged infection of ___, autoimmune disease (___/___), and ___. It is the most ___ form
HCV
SLE
cryoglobulinemia
proliferative
In type 1 MPGN biopsy we may find ___+____ , ____ between the BM and the endothelial cells (double contour). In 50% of cases there will be low levels of ___
lobular segmentation
mesangial proliferation
mesangial interposition
C3
Type 2 MPGN is mostly ___. There is a ___ of the GBM with ribbons of dense deposits of ___
Idiopathic
dense thickening
C3
Type 3 MPGN is usually ___, possibly with ____ deposition along the widened segments of the ___
Focal
sub epithelial
GBM
Type 1 MPGN is caused by ___ deposition from a circular/in situ source. Type 2/3 are associated with ___- Ab activating ___
immune complex
nephritic factors
C3
The clinical presentation of MPGN includes: (5)
proteinuria hematuria pyuria systemic symptoms low C3
Treating MPGN includes- ___ in patients with proteinuria. ___ or ___could also be benefitable
RAAS inhibitors
steroids
plasmapheresis
The prognosis of MPGN- __% of patients will develop ESRD within __ years, 90% will reach CKD within ___ years. Risk factors- ___, ___, ___.
50 10 20 HTN nephrotic syndrome renal insufficiency
Class 5 of lupus nephritis is characterized as ___
membranous nephritis
In class 5 lupus nephritis there is an increased risk for___ complications including in the __
thromboembolic
renal vein
