Renal Pathology part 1 Flashcards Preview

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Flashcards in Renal Pathology part 1 Deck (64)
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31

Basement membrane like mesangila matrix forms

a meshwork in which the mesangial cells are embedded
-these cells, of mesangial origin are contractile, phagocytic and capable of proliferation of laying down both matrix collagen and of secreting several biologically active mediators

32

Normal glomerulus is highly permeable to

water and small solutes because of the fenestrated nature of the endothelium and impermeable to proteins of the size of albumin or larger

33

Permeability characteristics of the glomerular filtration barrier allow

discrimination among various protein molecules, depending on their size (the larger, the less permeable) and charge (the more cationic, the more permeable)

34

Visceral epithelial cell is important for

maintenance of glomerular barrier function; its slit diaphragm presents a size-selective distal diffusion barrier to the filtration of proteins, and it is the cell type that is largely responsible for synthesis of GBM components

35

Nephrin

-a transmembrane protein with a large extracellular portion made up of immunoglobulin like domains
-molecules extend toward each other from neighboring foot processes and dimerize across the slit diaphragm

36

Within the cytoplasm of the foot processes, nephrin forms

molecular connections with podocin, Cd-2 associated protein, and ulitmately the actin cytoskeleton of the visceral epithelial cells

37

Mutations in genes encoding slit diaphragm proteins lead to

defects in protein permeability and the nephrotic syndrome

38

Some inflammatory diseases of the glomerulus are characterized by

an increase in the number of cells in the glomerular tufts

39

Hypercellularity of glomerular tufts results from

-proliferation of mesangial or endothelial cells
-infiltration of leukocytes, including neutrophils, monocytes, and in some diseases, lymphocytes
-formation of crescents

40

Endocapillary proliferation

-combination of infiltration of leukocytes and swelling and proliferation of mesangial and/or endothelial cells

41

Crescents

-accumulations of cells composed of proliferating glomerular epithelial cells and infiltrating leukocytes
-epithelial cell proliferation that characterizes crescent formation occurs following an immune/inflammatory injury involving capillary walls
-plasma proteins leak into the urinary space, where it is believed that exposure to procoagulants leads to fibrin deposition

42

Suspected of being a trigger for crescent formation

activation of coagulation factors such as thrombin

43

By light microscopy, basement membrane thickening appears as

thickening of capillary walls, best seen in sections with PAS

44

By electron microscopy, basement membrane thickening takes one of these forms

-deposition of amorphous electron dense material, most often immune complexes, on the endothelial or epithelial side of the membranes or within the GBM itself. Fibrin, amyloid, cryoglobulins, and abnormal fibrillary proteins may also deposit in the GBM
-increased synthesis of the protein components of the basement membrane as occurs in diabetic glomerulosclerosis
-formation of addiional layers of BM matrices, which most often occupy subendohelial locations and may range from poorly organized matrix to duplicated lamina densa, as occurs in membranoproliferative glomerulonephritis

45

Hyalinosis

-the accumulation of material that is homogenous and eosinophilic by light microscopy
-usually a consequence of endothelial or capillary wall injury and typically the end result of various forms of glomerular damage

46

Hyalin

-an extracellular, amorphous material composed of plasma proteins that have insulated from the circulation into glomerular structures
-when extensive, these deposits may obliterate the capillary lumens of the glomerular tuft

47

Sclerosis

-characterized by deposition of extracellular collagenous matrix
-may be confined to mesangial areas as is often the case in diabetic glomerulosclerosis, involve the capillary loops, or both

48

Sclerosing process may also result in

obliteration of some or all of the capillary lumens in affected glomeruli

49

Histologic glomerular change categories

-diffuse, involving all of the glomeruli in the kidney
-global, involving the entirety of individual glomeruli
-focal, involving only a fraction of the glomeruli in the kidney
-segmental affecting a part of each glomerulus
-capillary loop or mesangial affecting predominantly capillary or mesangial regions

50

Glomerulonephritis can be readily induced experimentally by

Ag-Ab reactions

51

Found in the majority of individuals with glomerulonephritis

-glomerular deposits of immunoglobulins often with components of complement

52

Two forms of antibody associated injury in glomerulonephritis have been estabilshed

-injury by Abs reacting in situ within the glomerulus, either binding to insoluble fixed glomerular Ags or extrinsic molecules planted within the glomerulus
-injury results from deposition of circulating Ag-Ab complexes in the glomerulus

53

The major cause of glomerulonephritis resulting from formation of Ag-Ab complexes is the consequence of

in situ immune complex formation

54

in glomerular injury from in situ formation of immune complexes

immune complexes are formed locally by Abs that react with intrinsic tissue Ag or with extrinsic Ags "planted" in the glomerulus from the circulation

55

Membranous nephropathy

-classic example of glomerular injury resulting from local formation of immune complexes

56

Heymann Nephritis rat model of glomerulonephritis

-induced by immunizing rats with an Ag, megalin that is present in epithelial cell foot processes
-rats develop Abs to this Ag and disease develops from the reaction of Ab with the megalin-containing protein complex located on the basal surface of visceral epithelial cells, leading to localized immune complex formation

57

Ag that underlies most cases of primary human membranous nephropathy

-M-type phospolipase A2 receptor (PLA2R)

58

Ab binding to PLA2R present in the glomerular epithelial cell membrane is followed by

complement activation and then shedding of the immune aggregates from the cell surface to form characterisitic deposits of immune complexes along with the sub epithelial aspect of the BM

59

On EM, glomerulopathy is characterized by

presence of numerous discrete subepithelial electron dense deposits (made up largely of immune reactants)

60

In glomerulopathy the pattern of immune deposition by IF microscopy is

granular rather than linear, reflective of the very localized Ag-Ab interaction