GUT Pathology

·         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:

1. partial clot in renal artery à renal stenosis
2. Complete clot inrenal artery à renal failure
3. Inflammed glomerulus à glomerular nephritis
4. Clot off medulla à interstisial nephritis
5. Clot off Papilla à. papillary necrosis
6. Clott of pieces of nephron à focal segmental glomerulo nephritis
7. 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.