Renal Pathology I Flashcards by she ign

4 histologic alterations due to glomerular injury

hypercellularity, BM thickening, mesangial expansion, sclerosis

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where can new cells grow in response to injury?

glomerular capillaries, urinary space, mesangium

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BM thickening aka

duplication or double contours

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mesangial widening due to –

increased mesangial matrix and cells (mesangial proliferation)

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crescents

cellular proliferation in urinary space

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crescents in urinary space is due to –

basement membrane rupture

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what cells are present in crescents?

macrophages, neutrophils, epithelial cells

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T/F: crescents contain fibrin and are seen in severe glomerular injury

true

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pathogenesis of glomerular injury (immunologic injury)

immune complex-mediated injury, cytotoxic antibodies, cell mediated autoimmunity

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how can you detect immune complex deposits?

immunofluorescence (most sensitive method)

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immunofluorescence can be used to characterized – of immune complex deposits

type of immunoglobulin

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How can you determine the precise location of immune complex deposits?

electron microscopy

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what color is immune complex deposits in immunofluorescence?

green

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where can immune deposits be found?

subepithelial, subendothelial, mesangial

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which type of immune deposits elicits more inflammation?

subendothelial

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deposits activate – which lead to inflammation

complement

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4 types of glomerular syndromes

asymptomatic hematuria and/or proteinuria, nephrotic syndrome, acute nephritic syndrome, chronic renal failure

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T/F: most glomerular diseases present with one particular syndrome

true

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T/F: some patients present with a mixed syndrome

true

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T/F: some diseases have variable presentation

true

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features of nephrotic syndrome

proteinuria (at least 3.5 g/day)
hypoalbuminemia
generalized edema
hyperlipidemia, hyperlipiduria

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hypoalbuminemia

low albumin in blood because you lost albumin to urine

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edema in nephrotic syndrome is the result of –

lost albumin

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major causes of nephrotic syndrome

membranous nephropathy, minimal change nephropathy, focal and segmental glomerulosclerosis

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nephrotic syndrome is due to -- abnormality

podocyte (visceral epithelial cell)

what causes membranous nephropathy (one cause of nephrotic syndrome)?

immune complex formation on subepithelial side of BM

in membranous nephropathy (one cause of nephrotic syndrome), epithelial cells respond to injury by --

making more BM in form of spikes

why do epithelial cells make spikes in membranous nephropathy?

try to wall off immune complex deposits

immunofluorescence of membranous nephropathy show --

granular deposits of IgG and complement along BM

types of membranous glomerulonephritis

primary (idiopathic) or secondary

features of minimal change nephropathy (one cause of nephrotic syndrome)

most common cause of proteinuria in children, can develop at any age, normal glomeruli by lumen, diffuse loss of podocytes by EM

how to treat minimal change nephropathy?

steroids

focal affects

some but not all glomeruli

segmental affects

only a portion of glomerulus

focal and segmental glomerulosclerosis (one cause of nephrotic syndrome) is often found in --

older kids, young adults

types of focal and segmental glomerulosclerosis

primary (idiopathic) or secondary

FSGS -->

leaky glomeruli - -> lose ability to filter blood - -> need more compensatory nephrons

features of nephritic syndrome

hematuria, oliguria (decreased urine), hypertension, proteinuria (less than nephrotic syndrome)

types of nephritic syndrome

acute proliferative or rapidly progressive glomerulonephritis

acute proliferative glomerulonephritis is -- process

immune complex mediated

causes of acute proliferative GN

exogenous or endogenous antigens

exogenous antigens of acute proliferative GN

post infectious/post-streptococcal

endogenous antigens of acute proliferative GN

lupus (autoimmunity)

in acute proliferative GN, -- are trapped in the glomerulus

circulating immune complexes

acute proliferative GN: circulating immune complexes --

bind/fix complement

acute proliferative GN: complement and cytokines --

recruit leukocytes

acute proliferative GN: proliferations of --

endothelial and circulating cells in capillaries (may include mesangial and epithelial cells)

most post infectious GN (acute proliferative GN) cases are resolves with --

supportive care

deposits of post infectious GN (acute proliferative GN) resolve within --

a few months

is there scarring in post infectious GN (acute proliferative GN)

who easily recovers from post infectious GN (acute proliferative GN)?

children

most adults with post infectious GN (acute proliferative GN) develop --

end stage renal disease

post infectious GN (acute proliferative GN) prevalence

developing countries

If circulating immune complex mediated GN is transient then --

deposits are phagocytized and/or degraded and inflammatory changes resolve

if circulating immune complex mediated GN is continuous then --

chronic progressive GN

lupus is -- circulating immune complex mediated GN

continuous

post streptococcal GN is -- circulating immune complex mediated GN

transient

all rapidly progressive glomerulonephritis are have this morphological characteristics

crescents

crescent is -- within urinary space

fibrin

crescent: fibrin within urinary space incites --

marked proliferation/accumulation of macrophages and epithelial cells

isolated hematuria -- nephropathy

IgA and thin basement membrane nephropathy

most common primary glomerular disease

IgA nephropathy

IgA nephropathy prevalence

Asian and Hispanic patients

most common presentation of IgA nephropathy

hematuria

1/3 of patients with IgA nephropathy

progress to end stage renal disease

IgA has variable appearance in light microscopy but the most common finding is --

mesangial proliferation

T/F: when extensive loss of nephrons occurs, end stage renal disease continues to progress regardless of initial cause of injury

true

progression of renal disease results in glomerular injury which morphologically resembles --

FSGS and tubulointerstitial scarring

tubulointerstitial scarring includes

tubular atrophy and interstitial fibrosis

renal disease progression to FSGS results in --

proteinuria

features of renal disease progression to FSGS

segmental scarring and eventually global scarring

as more glomeruli become sclerotic --> GFR

decreases

T/F: hyperfiltration increases as renal disease progresses to FSGS

true

what causes nephritic syndrome?

endothelial cell injury

what causes nephrotic syndrome?

podocyte injury

diseases that potentially cause endothelial injury

post-infectious GN lupus nephritis RPGN