Renal 1106 Glomerular Diseases I

Front 1

What are the usual types of primary renal nephritic syndromes?

Back 1

postinfectious glomerulonephritis, IgA nephropathy

Front 2

What are the usual types of primary renal nephrotic syndromes?

Back 2

minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy

Front 3

What are the usual types of systemic disease causing nephritis?

Back 3

anti-GBM disease, Wegener's, SLE

Front 4

What are the types of systemic disease causing nephropathy?

Back 4

diabetic nephropathy, amyloid nephropathyWh

Front 5

What is the hereditary nephritic syndrome?

Back 5

Alport's Syndrome

Front 6

In what diseases do you usually see subendothelial glomerulonephritis?

Back 6

membranous glomerulonephritis, post-infectious glomerulonephritis

Front 7

What kind of deposits do you usually see in the subendothelium and mesangium?

Back 7

hgiher molecular weight, usually IgA nephropathy or SLE nephritis

Front 8

What is the result of subendothelial deposits?

Back 8

proliferation filling up the capillary loop, inflammation, very proximateto the circulation

Front 9

What is post-infectious glomerulonephritis?

Back 9

acute proliferative GN, usually after strep infection, produced by deposition of immune complexes in ghe glomeruli

Front 10

What are the clinical features preceding post-infectious glomerulonephritis?

Back 10

1-4 weeks after group A strep infection, antibiotic treatment of strep diminishes likelihood of illness

Front 11

What are the clinical features of post-streptococcal glomerulonephritis?

Back 11

coke-colored urine, red cell casts, mild proteinuria, oliguria, elevated BUN and creatinine, edema, fever, malaise, HTN, anti-strep antibody titers

Front 12

Which titers are elevated in post-strep glomerulonephritis?

Back 12

anti-streptolysin O ASO titers

Front 13

What kind of lesions do you get for post-strep glomerulonephritis?

Back 13

immune complex hump-like deposits on endothelial side of GBM, demonstratable by EM and immunofluorescence, containing IgG and complement

Front 14

What do you see in the capillaries with post-strep glomerulonephritis?

Back 14

lots of PMNs and monocytes, proliferation of cells, filling most of glomerular capillaries

Front 15

What is the pathogenesis of post-strep glomerulonephritis?

Back 15

antibody to strep antigens, leads to formation of circulating immune complexes which deposit in glomeruli, elicits an acute inflammatory response

Front 16

What is the prognosis of post-infectious glomerulonephritis in kids?

Back 16

transient and self-limited

Front 17

What is the prognosis of post-infectious glomerulonephritis in adults?

Back 17

less common, more likely to be persistent, may progress to end-stage renal disease

Front 18

What is IgA nephropathy?

Back 18

low-grade chronic glomerulonephritis produced by deposition of immune complexes in the mesangium

Front 19

What are the clinical features of IgA nephropathy?

Back 19

hematuria, proteinuria, ESRD

Front 20

What are the lesions in IgA nephropathy?

Back 20

immune complex deposits in mesangial regions by EM and IF
mostly IgA and C3

Front 21

What is the pathogenesis of IgA nephropathy?

Back 21

low grade immune complex disease of unknown etiology, can be after respiratory/GI/UTI
may involve acquired/genetic abnormal immune regulation of mucosal IgA production with abnormal hinge region glycosylation of IgA

Front 22

What is Henoch-Schonlein Purpura?

Back 22

purpuric skin lesions, abdominal pain, intestinal bleeding, arthralgias, nephritic syndrome

Front 23

How does Henoch-Schonlein Purpura compare to IgA nephropathy?

Back 23

renal lesions are the same, greater likelihood of severe injury iwth crescents in H-S P

Front 24

What is the prognosis of H-S P in kids?

Back 24

generally recover

Front 25

What is the prognosis of H-S P in adults?

Back 25

more severe injury may lead to renal failure

Front 26

What is membranous nephropathy?

Back 26

chornic glomerular disease produced by prolonged deposition of immune complexes on epithelial side of GBM, leading to proteinuria and nephrotic syndrome

Front 27

What are the clinical features of membranous nephropathy?

Back 27

nephrotic syndrome, mild hematuria maybe, impaired renal function late in the course

Front 28

In whom does membranous nephropathy usually occur?

Back 28

mostly adults, some in kids

Front 29

What do the lesions of membranous nephropathy look like?

Back 29

immune complex deposits on epithelial side of GBM in all glomerular capillaries
on H&E GBM looks thick with spikes

Front 30

What is the pathogenesis of membranous nephropathy?

Back 30

chronic immune complex injury, may be Phospholipase A2 receptor, present on many cells, can be congenital syphilis, malaria, hepatitis, chronic infections, drugs

Front 31

What is minimal change disease?

Back 31

unknown pathogenesis, increased permeability of GBM to albumin, effacement of foot processes in podocytes, nephrotic syndrome, reversible by corticosteroid therapy

Front 32

What are the clinical features of minimal change disease?

Back 32

nephrotic syndrome, minimal hematuria

Front 33

What are the lesions in minimal change diseaes?

Back 33

normal by light micro, foot processe effacement by EM

Front 34

Waht is the pathogenesis of minimal change disease?

Back 34

loss of anionic sites in basement membrane, altered foot processes with loss of slit diaphragm

Front 35

What is the prognosis of minimal change disease?

Back 35

steroid responsive, good

Front 36

What is focal segmental glomerulosclerosis?

Back 36

idiopathic focal segmental sclerosis of glomeruli, no immune complexes, foot process effacement, resistance to steroid therapy, progression to renal failure

Front 37

Why is it called focal?

Back 37

some, but not all glomeruli

Front 38

Why is it called segmental?

Back 38

involves a portiono f hte capillary tuft

Front 39

What are the clinical features of focal segmental glomerulosclerosis?

Back 39

nephrotic syndrome, can have hematuria, steroid resistant, can have increased creatinine and BUN

Front 40

What is the pathogenesis of focal segmental glomerulosclerosis?

Back 40

primary podocyte injury with consequent proteinuria and ECM production induced in response to injury,
can have secondary lesions from HIV infection or drug abuse
rare genetic forms from mutations

Front 41

What is the prognosis of focal segmental glomerulosclerosis?

Back 41

progression to ESRD in 5-10 years or less
may recur in transplants and cause graft loss

Front 42

What is the pathogenesis of focal segmental glomerulosclerosis?

Back 42

primary podocyte injury with consequent proteinuria and ECM production induced in response to injury,
can have secondary lesions from HIV infection or drug abuse
rare genetic forms from mutations

Front 43

What is the prognosis of focal segmental glomerulosclerosis?

Back 43

progression to ESRD in 5-10 years or less
may recur in transplants and cause graft loss