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Renal 2 Test 1 > Renal Pathology part 1 > Flashcards

Renal Pathology part 1 Flashcards

1
Q

Most glomerular diseases are

A

immunologically mediated

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2
Q

Tubular and interstitial disorders are

A

frequently caused by toxic or infectious agents

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3
Q

Severe glomerular damage impaires

A

flow through the peritubular vascular system

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4
Q

Tubular destruction

A

-may induce glomerular injury by increasing intraglomerular pressure

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5
Q

Azotemia

A
  • biochemical abnormality that refers to an elevation of BUN and creatinine levels and is related largely to a decreased glomerular filtration rate (GFR)
  • consequence of renal and external disorders
  • typical feature of both acute and chronic injury
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6
Q

Prerenal azotemia

A

Encountered where there is hypoperfusion of the kidneys (hypertension or excessive fluid losses from any cause, or if the effective intravascular volume is decreased due to shock, volume depletion, congestive heart failure or cirrhosis of the liver) that impairs renal function in the absence of parenchymal damage

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7
Q

Postrenal azotemia

A
  • seen whenever renal flow is obstructed distal to kidney

- relief of obstruction followed by correction of the azotemia

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8
Q

Uremia

A
  • when azotemia becomes associated with clinical signs/symptoms and biochemical abnormalities
  • failure of excretory function and a host of metabolic and endocrine alterations resulting from renal damage
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9
Q

Uremic patients frequently have secondary involvement of

A
  • GI system (uremic gastroenteritis)
  • peripheral nerves (peripheral neuropathy)
  • heart (uremic fibrinous pericarditis)
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10
Q

Nephritic syndrome

A
  • clinical entity caused by glomerular disease and is dominated by the acute onset of either grossly visible hematuria (RBCs in urine) or microscopic hematuria with dysmorphic red cells and red cell casts on urinalysis, diminished GFR, mild to moderate proteinuria, and hypertension
  • classic presentation of acute post streptococcal glomerulonephritis
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11
Q

Rapidly progressive glomerulonephritis

A

-nephritic syndrome with rapid decline in GFR (within hours to days)

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12
Q

Nephrotic syndrome

A
  • due to glomerular disease

- heavy proteinuria, hypoalbuminemia, severe edema, hyperlipidemia, and lipiduria

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13
Q

Asymptomatic hematuria/proteinuria

A

usually a manifestation of subtle or mild glomerular abnormalities

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14
Q

Acute kidney injury

A
  • Rapid decline in GFR (within hours to days), with concurrent dysregulation of fluid and electrolyte balance, and retntion of metabolic waste products normally excreted by the kidney including urea and creatinine
  • In most severe forms, manifested by oliguria or anuria (reduced or no urine flow)
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15
Q

Acute kidney injury can result from

A

-glomerular, interstitial, vascular or acute tubular injury

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16
Q

Chronic kidney disease

A
  • the presence of a diminished GFR that is persistently less than 60mL/min/ 1.73 m2 for at least 3 months, from any cause, and/or persistent albuminuria
  • may present with clinically silent decline in renal excretory function in milder forms and in more severe cases by prolonged symptoms and signs of uremia
  • end result of all chronic renal parenchymal diseases
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17
Q

end stage renal disease (ESRD)

A

-GFR less than 5% of normal; terminal state of uremia

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18
Q

Renal tubular defects are dominated by

A

polyuria (excessive urine formation), nocturia, and electrolyte disorders (metbolic acidosis)
-result of diseases that with either directly affect tubular structures or cause defects in specific tubular functions (can be inherited or acquired)

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19
Q

Urinary tract infection

A
  • bacteriuria and pyuria

- may be symptomatic or asymptomatic, may affect the kidney or the bladder

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20
Q

Nephrolithiasis

A
  • renal stones

- spasms of severe pain (renal colic) and hematuria,often with recurrent stone formation

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21
Q

Secondary glomerular disease causes

A

-systemic immunologic diseases such as systemic lupus erythmatous, vascular disorders such as hypertension, metabolic diseases such as diabetes mellitus, and some heriditary conditions such as Fabry disease often affect glomerulus

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22
Q

The glomerulus consists of

A
  • an anastomosing network of capillaries lined by fenestrated endothelium invested by 2 layers of epithelial cells
  • visceral epithelial cells (podocytes) are incorporated into and become an intrinsic part of the capillary wall, separated from endothelial cells by a basement membrane
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23
Q

Glomerulus parietal epithelium

A
  • situated on Bowman’s capusule

- lines the urinary space, the cavity in which plasma filtrate first collects

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24
Q

The glomerular capillary wall is

A

-the filtering membrane and consists of a thin layer of fenestrated endothelial cells, a glomerular basement membrane (GBM) with a thick electron-dense layer, the lamina densa, and thinner electron-lucent peripheral layers, the lamina rara internal and lamina rara external

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25
Q

GBM consists of

A

-collagen type IV, laminin, polyanionic proteoglycans (mostly heparin sulfate), fibronectin, entactin, and several other glycoproteins

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26
Q

Type IV collagen forms

A
  • a network suprastructure to which other glycoproteins attach
  • building block of this network is a triple-helical molecular composed of one or more of 6 types of alpha chains
  • each molecule consists of a 7s domain at the N terminus, a triple-helical domain in the middle, and a globular non collagenous domain (NC1) at the C terminus
27
Q

NC1 domain

A
  • importain for helix formation and for assembly of collagen monomers into the basement membrane superstructure
  • glycoproteins and proteoglycans attach to the collagenous superstructure
28
Q

Antigens in the NC1 domain are

A

the targets of Abs in the anti-GBM nephritis; genetic defects in the alpha chains underly some forms of heriditary nephritis; and the proteoglycans content of the GBM may contribute to its permeability characteristics

29
Q

Visceral epithelial cells (podocytes)

A
  • possess interdigitating processes embedded in and adherent to the lamina rara externa of the basement membrane
  • adjacent foot processes are separated by filtration slits, which are bridged by a thin diaphragm
30
Q

Glomerular tuft is supported by

A

mesangial cells lying between the capillaries

31
Q

Basement membrane like mesangila matrix forms

A

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
Q

Normal glomerulus is highly permeable to

A

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

33
Q

Permeability characteristics of the glomerular filtration barrier allow

A

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

34
Q

Visceral epithelial cell is important for

A

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
Q

Nephrin

A
  • 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
Q

Within the cytoplasm of the foot processes, nephrin forms

A

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

37
Q

Mutations in genes encoding slit diaphragm proteins lead to

A

defects in protein permeability and the nephrotic syndrome

38
Q

Some inflammatory diseases of the glomerulus are characterized by

A

an increase in the number of cells in the glomerular tufts

39
Q

Hypercellularity of glomerular tufts results from

A
  • proliferation of mesangial or endothelial cells
  • infiltration of leukocytes, including neutrophils, monocytes, and in some diseases, lymphocytes
  • formation of crescents
40
Q

Endocapillary proliferation

A

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

41
Q

Crescents

A
  • 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
Q

Suspected of being a trigger for crescent formation

A

activation of coagulation factors such as thrombin

43
Q

By light microscopy, basement membrane thickening appears as

A

thickening of capillary walls, best seen in sections with PAS

44
Q

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

A
  • 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
Q

Hyalinosis

A
  • 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
Q

Hyalin

A
  • 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
Q

Sclerosis

A
  • 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
Q

Sclerosing process may also result in

A

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

49
Q

Histologic glomerular change categories

A
  • 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
Q

Glomerulonephritis can be readily induced experimentally by

A

Ag-Ab reactions

51
Q

Found in the majority of individuals with glomerulonephritis

A

-glomerular deposits of immunoglobulins often with components of complement

52
Q

Two forms of antibody associated injury in glomerulonephritis have been estabilshed

A
  • 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
Q

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

A

in situ immune complex formation

54
Q

in glomerular injury from in situ formation of immune complexes

A

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
Q

Membranous nephropathy

A

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

56
Q

Heymann Nephritis rat model of glomerulonephritis

A
  • 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
Q

Ag that underlies most cases of primary human membranous nephropathy

A

-M-type phospolipase A2 receptor (PLA2R)

58
Q

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

A

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
Q

On EM, glomerulopathy is characterized by

A

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

60
Q

In glomerulopathy the pattern of immune deposition by IF microscopy is

A

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

61
Q

In glomerulopathy, sub-epithelial complexes with resultant host responses can result in

A

a thickened basement membrane apearance by LM–membranous nephropathy

62
Q

In humans, primary membranous nephropathy is

A

an autoimmune disease caused by Abs to endogenous tissue componenets

63
Q

Secondary forms of membranous nephropathy can be experimentally induced by

A

drugs (mercuric chloride) and graft vs host disease

64
Q

In some situations of membranous nephropathy

A

there may be uncontrolled B cell activation leading to the production of autoantibodies that react with renal Ags

Renal 2 Test 1 (16 decks)

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