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Nephrosis I and II Flashcards

1
Q

indicators of a nephritic state

A

hematuria

proteinuria

azotemia

oliguria

hypertension

edema

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2
Q

podocalyxin

A

a protein that covers the podocyte cell surface associated with sialoglycoprotein, SGP

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3
Q

components of the slit diaphragm

A

nephrin

P-cadherin

ZO-1

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4
Q

mesangial cells

A

centrally located phagocytic and contractile cells

contain angiotensin-II receptors, and thereby regulate intraglomerular blood flow, and lastly, they respond to various cytokines (IL-1) by producing reactive oxygen species, proteases, and growth factors

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5
Q

What are the four factors regulating ultrafiltration?

A

intrarenal blood flow

transcapillary hydraulic pressure difference

colloid concentration

capillary sieving coefficient

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6
Q

What proteins in the slit diaphragm determine charge selectivity?

A

HS-PG and SPGs

type IV collagen

laminin

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7
Q

minimal change disease

A

most common cause of nephrotic syndrome in children

normal glomeruli by light microscopy

podoctye process alterations by electron microscopy

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8
Q

What are the histological features of minimal change disease?

A

normal glomerular morphology

tubular protein absorption droplets

tubular lipid droplets (oil red o stain)

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9
Q

What are the electron micrograph features of minimal change disease?

A

fusion of podocyte foot processes

villous transformation

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10
Q

mechanisms of proteinuria

A

may be related to the loss of size and/or charge selectivity of the ultrafiltration unit

may be due to the injury to the capillary by antigen, antibody, immune complex, complement, proteolytic enzymes and reactive oygen species (ROS) or nascent oxygen radicals

may be related to the adverse influences of high protein diet damaging the glomerular mesangial cells

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11
Q

selective proteinuria

A

leakage of albumin only, seen in minimal change disease

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12
Q

nonselective proteinuria

A

leakage of albumin and globulins, seen in other nephritides

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13
Q

mechanism of nephrotic edema

A

glomerular injury (loss of charge/size selectivity) increases permeability to proteins

results in albuminuria and hypoalbuminemia

decreased plasma oncotic pressure

increase in interstitial fluid volume (anasarca)

edema

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14
Q

mechanism of nephritic edema

A

glomerular injury

decrease in ultrafiltration coefficient

decrease in GFR

decrease in fluid delivery to renal tubules

constant or increased distal tubular resorption (response to humoral factors

decrease in urinary Na while dietary Na is constant

sodium retention

increased extracellular volume

edema

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15
Q

diabteic nephropathy

A

10-15% of adult onset diabetes

higher among juvenile diabetics

superhyperfiltration (elevated GFR)

followed by nephrotic-range proteinuria and then declining GFR

may be initially slective with microalbuminuria

progression of disease becomes non-selective due to loss of both the charge- and size- selective properties of the renal glomerulus

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16
Q

mechanismtic findings in diabetes nephropathy

A

diffuse and/or nodular glomerulosclerosis

non-enzymatic glycations of proteins and decreased synthesis of proteoglycans

increased activity of TGF-beta and increased generation of reactive oxygen species (ROS)

thickening of renal basement membranes - non-specific trapping of proteins

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17
Q

morphological types of renal lesions in diabetes nephropathy

A

diffuse intercapillary glomerulosclerosis - characterized by thickened GBMs and increased nesangial matrix

nodular glomerulosclerosis (Kimmelstiel Wilson lesions) - characterized by nodularity with cellular

in advanced cases marked diabetic glomerulosclarosis is observed

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18
Q

Describe the histologicla features of diabetic nephropathy.

A

increased mesangial cells

extracellular mesangial matrix

thickened GBMs

four stages

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19
Q

Describe the electron micrograph findings of diabetic nephropathy.

A

thickened GBM

nodules in the mesangium

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20
Q

What is the result of non-enzymatic glycation in diabetes mellitus?

A

resistance to collagenase digestion

change in physiochemical properties

defective cross-linking of proteins

trapping of proteins in circulation

defective ECMs

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21
Q

What is the role of proteoglycans in diabetes mellitus?

A

decreased synthesis of PGs

decreased sulfation of PGs

excessive release of PGs

poor deposition of PGs and defective GBM

increased pore size, decreased negative charge in the GBM

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22
Q

What is the range of proteinuria for microalbuminuria?

A

30-300

high levels of damage and loss of negative charge allows large amounts of albumin to be released

23
Q

hereditary nephritis (Alport’s Syndrome)

A

a disease with autosomal dominant inheritance, and mutations in gene encoding alpha5 chain of type-IV collagen

abnormalities in other chains of type IV-collagen may be seen

associated with hematuria and aminoaciduria

sensorineural deafness and occular abnormalities

24
Q

morphology of hereditary nephritis (alport’s syndrome)

A

laminated-trabeculated appearance of the GBM, fetal glomeruli and foam cells

25
types of amyloidotic nephropathy
primary - nephrotic range proteinuria, related to multiple myeloma (cancer of the plasma cells - high Ig production), 75% of cases Secondary - chronic infections, degenerative diseases, alzheimers, mutant proteins, renal lesions indistinguishable from secondary amyloidosis no hypercellularity
26
histological findings of amyloidotic nephropathy
congo red stain birefringent deposits
27
histological findings of amylodotic nephropathy under polarizing microscopy
birefringent nodules with two colors due to the presence of beta-pleated sheets
28
electron micrograph findings of amyloidotic nephropathy
amyloid deposits in mesangium and capillary wall amyloid fibril deposits in capillary wall fibrils are **8-10 nm in diameter** and randomly arranged
29
immune-complex-mediated glomerular diseases
a disease state that results from the deposition of antigen-antibody complexes formed in situ or in circulation, and followed by activation of complement, elaboration of mediators of inflammation, and consequential glomerular injury
30
factors influencing the deposition of immune-complexes
valence of the antigen, affinity of the antibody, molar ratio, and reduction and alkylation status of the complex charge on the complex size hemodynamics monocytic regulation (Fc receptor-mediated immune-complex phagocytosis)
31
mechanism of immune-complex deposition
circulating immune-complex deposition in situ immune-complex formation (2 scenarios)
32
circulating immune complex deposition
immune-complexes are formed in circulation and subsequently trapped in various regions of the glomerulus best exemplified by lupus nephritis
33
in situ immune-complex formation
complexes are not formed in circulation but within the glomerular capillary wall 1) the antigen may be an intrinsic component of the glomerular capillary, the antibody or autoantibody in circulation complexes within the intrinsic agents of the glomerular capillary wall 2) the non-intrinsic foreign tissue antigen implants itself in the glomerular capillary, evokes an immune response, and subsequently the circulating antbody binds to the already implanted antigen
34
elements influencing the outcome of immune-complex mediated injury
complement PMNs and monocytes platelets and coagulation system glomerular cells
35
How does the complement system influence the outcome of immune complex-mediated injury?
classical pathway is involved in glomerulonephritis in some and alternate in others the terminal portion of the complement (C5-C9) causes lysis of glomerular cells via membrane attack complex (MAC) and results in the detachment of hte pithelial foot processes and proteinuria
36
Dense Deposit Disease (DDD)
an autoantibody to C3 convertase, nephritic factor (C3NeF), is found in the serum causes slow and continued activation of complement and resultant hypocomplementemia
37
How doe PMNs and monocytes affect the outcome of immune-complex mediated injury?
releases proteases, metalloenzymes, lysosomes, cytokines, and free O2 radicals these all damage the glomerulus and cause proteinuria
38
How do platelets and the coagulation system influence the outcome of immune-complex mediated injury?
aggregation of platelets and activation of coagulation system are seen in crescentic form of glomerulonephritis
39
How do glomerular cells influence the outcome of immune-complex mediated injury?
paracrine and autocrine effects of various cytokines and growth factors accentuate the extent of glomerular injury by stimulating the mesangial cells which in turn produce inflammatory mediators
40
general characteristics of focal segmental glomerulo-sclerosis (FSGS)
history of minimal change disease, heroin addiction, HIV, ureteral reflux uropathy nephrotic - nonselective proteinuria juxtamedullary glomeruli - FSGS, segmental hyalinosis, foam cells effacement of foot processes and detachment segmental deposits of IgM and C1q in hyalinotic segments
41
histologic findings of FSGS
predominant sclerosis of deeper glomeruli loss of capillaries in segments and hyalinosis of the glomerulus
42
electron micrograph findings of FSGS
segmental large deposit in the glomerulus foam cells in the glomerulus
43
general characteristics of idiopathic membranous nephropathy
most coommon cause of nephrotic syndrome in adults history of neoplasms, prescriptions of gold or penicillamine, hepatitis antigen excess disease, Heyman antigen complex subepithelial deposits in various stages, IgG and C3 immune-complex deposits
44
What locations can immune complexes be deposited in the glomerulus?
subendothelial mesangial subepithelial
45
histological findings of IMN
thick capillary basement membranes without proliferation of cells capillary deposits with granular appearance of IgG deposits
46
electron micrograph findings of IMN
subepithelial deposits no deposits in mesangial matrix
47
membrane intrinsic-fluid-current hypothesis
more sheer forces in the inner layers of the capillary compared to the outer layers since the sheer forces are much less in the outer layer, if the immune complexes are stuck on the outer layer, the inner layer becomes washed own
48
Heymann nephritis antigenic complex
related to the autoantibody directed against the Heymann Nephritis Antigen Complex pathogenic epitope located in the smaller subunit the epitope there is residing in the N-terminal 86 amino acids these patients also have autoantibodies against the PLA2 receptor thiscauses subepithelial deposits
49
redistribution-capping-shedding hypothesis
binding of ligand to a binding protein on a cell causes redistribution and shedding of the complexes on the cell
50
major diagnositc criteria for SLE
antinuclear and other antibodies **butterfly rash**, photosensitivity, discoid lesions migratory arthralgia **proteinuria/hematuria/casts** anemia/leukopenia/thrombocytopenia Raynaud's phenomenon circulating mimmune complexes pleuritis/pericarditis/endocarditis psychosis/convulsions alpecia
51
diffuse vs. membranous lupus nephritis
the nephritic form is minimal -\> diffuse proliferative form the nephrotic form is the membranous form
52
histologic findings of membranous lupus glomerulo-nephritis (MLGN)
thick membranes, karyorrhexis, and immune deposits
53
antibody - immunofluorescence of MLGN
electron-dense subepithelial and mesangial regions IgG/C3 beaded immune complex disorders
54
electron micrograph findings of MLGN
membrane bound spherical virus C type particles tubulo-vesicular myxovirus like elements to make it a lupus disease - have a 90% of deposits in subepithelial space and 10% in the mesangium and also tubular vesicular elements

Renal (28 decks)

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