Glomerulonephritis. Large Group 4 -Barnes Flashcards
What are some primary causes of nephritic syndrome? (2)
Acute proliferative GN (acute post-infectious)
crescentic GN
What are some primary causes of Nephrotic syndrome? (4)
Membranous GN
Minimal change disease
focal segmental glomerulosclerosis
Membranoproliferative GN
What can a dysmorphic RBC in the urine indicate?
it came from the glomerulus–> glomerular injury
can look like mickey mouse ears
What 3 things make up the glomerular filtration barrier?
endothelial cells (fenestrated)
Glomerular basement membrane (3 layers)
podocytes (with filtration slits and a diaphragm)
What are the major indications of nephritic syndromes?
hematuria (RBC casts)
HTN
azotemia
oliguria
proteinuria <3.5g/day
inflammatory glom injury
vasculitis or IC deposits
What are the major indications of nephrotic syndromes?
severe proteinuria (>3.5g/day)
hypoalbuminemia (<3g/dL)
generalized edema
hyperlipidemia
lipiduria
non-inflammatory glom injury
podocyte and basement membrane damage
What is the most common glomerulonephritis worldwide?
IgA nephropathy
“Berger’s Disease”
How long after URI will IgA nephropathy symptoms appear? What will be the main presenting symptom?
1-2 days after URI
microscopic/macroscopic hematuria
How is Alport’s Syndrome diagnosed?
biopsy kidney
thinned basement membrane with “splitting” of the lamina densa on EM
What are the symptoms that will appear with Alport’s syndrome?
sensorineural deafness and lenticonus of the lens capsule
X-linked defect in type IV collagen (mutation in C0L4A3)
What is the main problem in Benign Familial Hematuria? What are the symptoms? What will this look like on EM?
Type IV collagen genetic defect, similar to Alport’s
symptoms: hematuria, normal BP, very little proteinuria. rarely progresses to ESRD
line through the basement membrane in EM
What is the treatment for Alport’s?
ARBs and ACE Inhibitors
What are the different classifications of SLE? Which ones are nephritic vs nephrotic?
I=Minimal mesangial
II=Mesangial proliferation
III=focal proliferative
IV=diffuse proliferative
V=membranous
VI=advanced sclerotic
I and II are mild
V is nephrotic
I can progress to IV (nephritic)
and all can end at VI =RPGN
How long after an URI will symptoms from post-strep GN appear?
2-4 weeks after a URI
children infected > adults
What studies must be done on a sample from a kidney biopsy?
light microscopy
immunoflorescence
Electron microscopy
What blood tests are associated with SLE?
ANA
anti-ds DNA* specific
What are the presenting symptoms of SLE GN?
Can present as isolated Lupus Nephritis Proteinuria Hematuria Hypertension RBC casts or dysmorphic RBCs Varying degrees of renal failure
What lab results are consistent with Post-strep GN?
+ ASO antibody
low serum complement
How does Post-Strep GN appear in EM?
Lumpy bumpy sub-epithelial deposits
What is causing the damage in Post-strep GN?
the body’s reaction to an infection (not the bacteria!!)
What are the typical lab and microscopic findings for Membranoproliferative GN Type I?
Tram tracking basement membrane (“splitting”) on PAS
low complement
lobulated light microscopy due to IC deposit between the mesangium and endothelium of BM
What are the risk factors for Membranoproliferative GN Type I?
IV drug abuse
endocarditis, SLE, hepatitis B and C, cryoglouminemia
How does Wegner’s granulomatosis present?
fever recurrent sinusitis (nasal ulcers) hemoptysis micro or macroscopic hematuria RBC casts
What biopsy findings are present in Wegner’s?
anti-PR3 Ab (c-ANCA)
small vessel vasculitis
non-caseating granulomas
