renal mak Flashcards
nephrotic syndrome characteristics
edema, intial normal GFR, >3.5g/d proteinuria, lipiduria
if these foot processes which were there are now effaced, why then do we get so much leakage of protein
effacement changes the BM, making it more permeable to allow proteins to leak across
the major EM finding on a renal biopsy of a 5y/o w/ nephrotic syndrome who responded to corticotherapy is
fusion of foot processes (minimal change glomerulopathy)
- 10yo Girl was brough by her parents to their family physician. History revealed that the child had a sore throat for about 10d prior to the office visit. Initial laboratory tests ordered by the family physician revealed an elevated BUN and creatinine. A microscopic urinalysis showed hematuria w/ dysmorphic RBC’s. The light microscopic appearance of the renal biopsy showed hypercellularity, w/ PMN’s present, and there were subepithelial electron dense “humps” seen by electron microscopy. What additional laboratory finding is most likely to be present in this setting:
c. Elevated anti-streptolysin O titer
focal seqmental glomerulosclerosis of the kidney characteristics
b. It is not as common as minimal change disease in children
c. There is effacement of podocytes plus segmental scarring
d. It tends to recur after transplantation
e. Less than half of patients have some response to corticosteroids
light microscopic findings on renal biopsy suggests the worst immediate prognosis
d. Glomerular crescents (proliferation of parietal epithelium)
Major clinical feature associated w/ the renal biopsy finding on immunofluorescence microscopy of mesangial IgA deposistion in a 35yo man following a “flulike” illness is: (IgA nephropathy)
hematuria
Hyaline arteriolosclerosis of the kidney is most likely to be associated with which of the following conditions
Renal artery stenosis in the opposite kidney
The microscopic findings at autopsy of hyalinized glomeruli, interstitial fibrosis and focal tubular atrophy, and arteriolar thickening in a 75yo woman w/ normal renal function most strongly suggests:
d. Benign nephrosclerosis
Nephritic Sx Pathogenesis
inflammatory rupture of glomerular capillaries w/ bleeding into the urinary space
Nephritic Sx Clinical
mild to mod proteinuria and edema
- *gross hematuria**
- red cell casts*
Nephritic Sx Diseases
- Acute Proliferative
- Nonstrep Acute
- Rapidly Progressive (RPGN)
Glomerulonephritis
Acute Proliferative
1-4 weeks post GAS (kids)
immune complex mediated–> coarse IF
Acute Proliferative Morph
LM: proliferation w/ neutrophils and monocyte infiltration
IF: Granular deposits
EM: “humps” in epithelial side of BM
Acute Proliferative clinical
kids 6-10yo, 1-2 weeks post sore throat
hematuria, oliguria, periorbital edema, HTN, mild proteinuria and red cell casts
Nonstrep Acute
same as Acute, just after another disease
RPGN
severe, death w/in weeks if untreated
RPGN path
ruptures in GBM triggers Crescent formation
immunologically mediated
Crescent
proliferation of parietal epithelia cells lining Bowman’s capsule due to infiltration by monocytes and macrophages
contain fibrin
Type I RPGN
Anti-GBM antibody, linear IF
Goodpasture’s Sx
Goodpasture’s Syndrome
anti-GBM ab also xreact with pulmonary alveolar BM
Type II RPGN
immune complex deposition granular IF
lupus, post infections, Henroch Scheloin
Type III RPGN
NO anti-GBM or immune complexes
circulating ANCA
RPGN gross
large, pale kidneys with cortical petechial hemes
RPGN clinical
hematuria, RBC, proteinuria, htn , edema
Nephrotic Syndrome
increased BM permeability leading to loss of plasma protein
Nephrotic Syndrome clinical
severe proteinuria >3.5g/day, hyperlipidemia, edema
Nephrotic Syndrome diseases
Membranous nephropathy, minimal-change disease, Focal Segmental Glomerulosclerosis, Membranoproliferative Glomerulonephritis
Membranous Nephropathy
idiopathic, autoimmune
immune complex mediated with diffuse thickening of glomerular capillary wall
Membranous Nephropathy EM
- deposits btwn GBM and epithelial cells
- spikes protruding from GBM
- spikes and domes
Membranous Nephropathy clinical
INITIAL mild proteinuria, hematuria, mild HTN –> severe goes to sclerosis, inc Creatinine, HTN worse
Minimal Change disease
kids in 2-6 following RI selective to albumin
Minimal change disease
no immune complexes seen, but responds to steroids
effacement of foot processes of visceral epithelial cells on EM
Focal Segmental Glomerulosclerosis (FSGS)
idiopathic, adaptive response to loss of renal tissue
poor steroid response
FSGS path
visceral epithelial damage
w/ hyalinosis and sclerosis
FSGS light microscopy
focal sclerosing, segmental, affected capillary loops collapse
FSGS EM
effacement of foot processes, detachment of epithelial cells and denudation of GM
MPGN Type I
immune complexes in glomerulus w/ activation of both complement pathways
secondary is always Type I
MPGN Type II
dense deposit disease
alternative complement only (C3 only)
MPGN LM
proliferation of mesangial cells and capillary endothelium
**tramtrack splitting*
MPGN Type I EM
subdendothelial deposits
MPGN Type II EM
ribbonlike dense material in GM
MPGN clinical
nephrotic syndrome + hematuria
bad reoccurrence