·
Renal Artery Stenosis
↓ Blood flow
because of ↑ resistance d/t vasoconstriction from the Renin
system
o
Therefore, velocity ↑ in order to get
through occlusion, but the contralateral kidney is
not protected = Goldblatt’s kidney
Goldblatt’s Kidney
o
contralateral
kidney is destroyed first when you have renal artery stenosis
because renin will cause healthy kidney to be blasted
with blood, while the affected kidney will have a clot protecting it.
·
Ischemia and
heavy metals primarily damage the epithelial cells of the proximal straight
tubules, while aminoglycosides primarily affect the
proximal convoluted tubule.
·
Hyperaldosteronism (Conn's
syndrome) is associated with hypertension, alkalosis, and hypokalemia due to increased aldosterone
action.
Liddle's syndrome,
which is due to a mutation in the sodium channel, results in a similar picture.
Sjögren's syndrome causes renal tubular acidosis and hypokalemia.
Barrter's syndrome
is due to a defect in a transporter in the loop of Henle
and simulates a patient taking loop diuretics; because volume expansion does
not occur, the patient is normotensive.
·
7 patterns in the kidney of vasculitis:
- partial clot in renal artery à renal stenosis
- Complete clot inrenal artery à renal failure
- Inflammed glomerulus à glomerular nephritis
- Clot off medulla à interstisial nephritis
- Clot off Papilla à. papillary necrosis
- Clott of pieces of nephron à focal segmental glomerulo nephritis
- Clot off all the nephrons à RPGN = rapid progressive glomerulo nephritis
·
IMMUNOFLORESCENCE
1. Linear deposits - Antiglomerular basement memb
along capillary wall membrane disease (IgG, C3) (Good Pasteur syndrome)
- Diabetic nephropathy (IgG, Albumin)
- Dense deposit disease (C3)
2. Granular mesangial
- IgA nephropathy (IgA)
- Lupus nephritis (Full house = All type of immunoglobulins)
3. Granular deposits -
Membranous glomerulonephritis
- Membranoproliferative glomerulonephritis
- Lupus nephritis
- Post streptococcal glomerulonephritis (IgG & C3)
4. Diffuse “Smudgy ”
mesangial and capi llary wall deposits (IgG)
-
Primary amyloidosis (λ chain)
- - Fibrillary glomerulonephritis
·
ELECTRON
MICROSCOPY:
Site of deposits Disease
1. Subepithelial
- Membranous GN, Lupus nephritis, Post infectious GN (Humps)
2. Intramembranous
- Dense deposit disease (MPGN II), GN related to endocarditis
3. Subendothelial
- Membrano proliferative GNI, Lupus nephritis
4. Mesangial
- IgA nephropathy, Henoch Schonlein purpura, C1q
nephropathy
5. Combined subendo
& subepithelial - - Lupus nephritis, Membrano proliferative and mesangial
glomerulonephritis
In membranous lupus GN,
the deposits are in a subepithelial location, while
in diffuse proliferative lupus GN (WHO class IV) the deposits are mainly in a subendothelial location and produce a characteristic “wire-loop”
appearance due to thickening of the capillary wall. None of these changes
are specific for lupus. In contrast to the “wire-loop” appearance of the glomerular capillaries with lupus nephritis, “holly
leaf” mesangial deposits are seen with focal segmental GN (IgA
deposits suggests Berger disease), a “string of popcorn” immunofluorescence
pattern is also seen with membranous glomerulonephropathy, “tram-track” splitting
of the basement membrane is seen with both types of membranoproliferative GN, and a “spike and dome” appearance
of the basement membrane is seen with membranous
glomerulonephropathy.
·
markedly elevated
levels of hCG are associated with choriocarcinomas,
while elevated levels of AFP are most characteristic of yolk sac tumors and embryonal carcinomas. But there are many areas of overlap
between tumors, and many tumors are composed of multiple types of germ cell
cancers. The only definitive statement that can be made is that elevated serum
levels of AFP cannot be seen in a tumor that is a pure seminoma.
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