Nephrotic syndrome

Question 1

significant proteinuria

Answer 1

nephrotic syndrome

Question 2

hematuria and glomerulonephritis

Answer 2

nephritic syndrome

Question 3

definition of proteinuria

Answer 3

> 3.5 gm in 24 hr

Question 4

definition of hypoalbuminemia in salbumin

Answer 4

< 3.5 gm/dl

Question 5

what do we see in nephrotic syndrome

Answer 5

1. proteinuria
2. hypoalbuminemia
3. Edema
4. hyperlipidemia and lipiduria

Question 6

urine sediment in nephrotic syndrome

Answer 6

negative- non-active nl kidney function and blood pressure

Question 7

Morbidity associated with Nephrotic syndrome

Answer 7

1. Edema and effusions
2. loss of IgG and complement
3. Loss of ATIII
4. loss of Vitamin D
5. Hyperlipidemia and vascular disease

Question 8

pathogenesis of proteinuria

Answer 8

injury to podocytes by either genetics, depositions or direct injury by ab, cytokines and toxins

Question 9

3 primary glomerular diseases with nephrotic syndrome

Answer 9

1. MCD- minimal change disease
2. FSGS- focal segmental glomerulosclerosis
3. MN- membranous glomerulopathy

Question 10

secondary glomerular diseases with nephrotic syndrome

Answer 10

1. diabetes
2. SLE
3. Amyloidosis
4. medications- NSAIDS + Lithium
5. Tumors/ infections/ vaccinations

Question 11

three major causes of ESRD

Answer 11

1. diabetes
2. HTN
3. Glomerular disorders

Question 12

what are the advantages and disadvantages of dipstick ruine

Answer 12

• Pro:
  1. quick
  2. semi-quantitive
  3. detects mainly labumin
• Cons:
  1. does not detect microalbumin
  2. does not detect abnormal proteins

Question 13

spot urine

Answer 13

protein to creatinine ratio

Question 14

what do we expect to see in light microscopy for a pt. that has minimal change disease?

Answer 14

normal glomerulous

Question 15

what do we see in electron microscopy with a pt. that hasa minimal change disease

Answer 15

abnormal podocytes: flat and unhappy

Question 16

MCD:

1. most common cause of
2. peak incidence in children occur at ages
3. in adults it is caused by the use of _____ which lead to immune dysfunction and cytokine/ direct toxicity
4. hereditary chances
5. response to steroids?
6. prognosis?

Answer 16

1. most common cause of NS in children
2. peak incidence in children occur at ages 2-6
3. in adults it is caused by the use of NSAIDS which lead to immune dysfunction and cytokine/ direct toxicity
4. hereditary cases are rare and they are due to nephrin mutations
5. responsive to steroids 6. good prognosis

Question 17

FSGS:

1. most frequent in
2. at risk populations
3. possible genetic component?
4. most common cause of
5. primary form is
6. secondary form is ________ due to
7. prognosis?
8. recurrence?

Answer 17

1. most frequent in adults
2. at risk populations- hispanics/ high BMI/ African Americans/ HIV +
3. possible genetic component- yep
4. most common cause of NS in the US
5. primary form is idiopathic with some semblance to MCD
6. secondary form is hyperfiltration due to obesity/solitary kidney/ transplant kidney
7. prognosis is poor with progression to ESRD
8. recurrence is possible in transplants

Question 18

Membranous nephropathy:

1. occurs mostly in
2. _____ renal function at presentation
3. autoimmune disease
4. rare cases associated with __________ (1 in 10 pt) , ___________ and _____________
5. disease is acute or chronic
6. response to steroids

Answer 18

1. occurs mostly in adults 4-5th decade
2. normal renal function at presentation
3. autoimmune disease: most cases IgG class 4 against phospholipase A2-receptor (anti-PLA2R)
4. rare cases associated with cancer associated ab (1 in 10 pt) , collagen- vascular disease and infection
5. disease chronic
6. response to steroids is poor

Question 19

Diabetic nephropathy:

1. most common cause of
2. up to 1/3 of DMI and DMII will
3. first sign of diabetic nephropathy
4. ________ develops in about 20yr

Answer 19

1. most common cause of ESRD in the US (diabetes mellitus)
2. up to 1/3 of DMI and DMII will develop diabetic nephropathy and kidney failure
3. first sign of diabetic nephropathy is microalbuminuria

4 overt proteinuria develops in about 20yr

Question 20

course of Diabetic glomerulosclerosis

Answer 20

1. hyperglycemia related to insulin deficiency
2. non-enzymatic glycosylation of proteins
3. biochemical changes of GBM
4. increased synthesis of collagen IV
5. GBM thickening and increased mesangial matrix
6. Glomerulosclerosis

Question 21

apple green Birefringence

Answer 21

amyloidosis

Question 22

amyloidosis:

1. deposition of
2. disease of
3. deposition in the glomeruli leads to
4. deposition in heart leads to
5. major types: ______ associated with lymphoma and _______ associated with Liver

Answer 22

1. deposition of abnormally folded proteins- amyloid
2. disease of adults
3. deposition in the glomeruli leads to NS and kidney failure
4. deposition in heart leads to CHF
5. major types: AL which is deposition of immunoglobulin light chains associated with lymphoma and AA- deposition of serum amyloid-A-protein associated with Liver

Question 23

Answer 23

oval fat bodies

Question 24

Answer 24

focal segmental glomerulosclerosis-FSGS

Question 25

Answer 25

focal segmental glomerulosclerosis-FSGS

Question 26

Answer 26

membranous nephropathy- uniformly thick GBM

Question 27

Answer 27

silver stain for collagen 4- not really distinct pt. has membranous

Question 28

Answer 28

immunofluorescence with IgG showing capillary loops in patient with membranous n

Question 29

Answer 29

notice the subepithelial electron dense deposits- membranous nephropathy

Question 30

Answer 30

membranous nephropathy pathogenesis

Question 31

Answer 31

nodular sclerosis seen in patients with advanced diabetes- nodular diabetic glomerulosclerosis

Question 32

Answer 32

nodular diabetic glomerulosclerosis- kimmelstiel wilson disease

Question 33

Answer 33

EM of Diabetic nephropathy

Question 34

Answer 34

pt. with amyloidosis

Question 35

Answer 35

congo red stain of pt. with amyloidosis

Question 36

Answer 36

polarized light of amyloidosis

Question 37

Answer 37

fibrillary deposits in EM seen in amyloidos