Henry Lectures

Question 1

unexplained swelling in the face, abdomen, etc. (edema/ascites)?

Answer 1

-need a URINALYSIS to look for PROTEIN in urine

Question 2

when is the only time you get blood clots in the urine?

Answer 2

-when bleeding from the ureter/bladder

Question 3

when do you see RBCs, RBC casts, dysmorphic RBCs?

Answer 3

in Nephritic syndrome (hematuria) - bleeding from the glomerulus

Question 4

how do you diagnose GN?

Answer 4

renal biopsy -> light microscopy, IF, EM

-do NOT need biopsy in children w/ minimal change disease

Question 5

what do you see in membranous GN?

Answer 5

• SUBEPITHELIAL immune complex deposits-> SPIKES and DOMES
• thickening of the GBM

-test for HBV, HCV, and Syphilis

Question 6

what do you see with proliferation of cells due to inflammatory response?

Answer 6

CRESCENT formation

-capillaries burst -> hypercellularity -> crescent formation filling Bowman space and impinge on capillaries

Question 7

Nephrotic syndrome

Answer 7

• proteinuria (>3g/day)
• NO inflammation
• NORMAL creatinine
• FEW RBCs

Question 8

Nephritic syndrome

Answer 8

• less proteinuria (<3g/day)
• HIGH inflammation
• more WBCs and RBCs (hematuria)
• Coca-cola urine
• HIGH creatinine

Question 9

Minimal change disease

Answer 9

• nephrotic
• most common type in CHILDREN
• EM -> efface podocytes -> proteinuria
• treat w/ STEROIDS
• 75-80% of adults respond -> some progress to FSGS
• SLE, parvovirus, HIV, NSAIDs

Question 10

FSGS

Answer 10

• nephrotic
• more common in ADULTS - African Americans
• light microscopy -> podocyte effacement -> proteinuria
• less response to steroids

-heroin, HIV, sickle cell

Question 11

collapsing GN

Answer 11

• nephrotic
• MALIGNANT form of FSGS
• RAPID progression to renal failure
• capillary loop collapse
• APOL1 mutation in African Am.

-HIV, parvovirus B19

Question 12

Membranous GN

Answer 12

• nephrotic
• thick GBM
• SUBEPITHELIAL deposits -> SPIKES and DOMES
• Malignancy in 20-30% of patients >60 y/o**
• complexes bind to PLA2R on podocytes
• hypercoagulable w/ loss of ATIII and PROTEIN C,S

-HBV, HCV, SLE, malignancy, drugs

Question 13

Membranoproliferative GN

Answer 13

• thick GBM
• overactive complement (C3)
• type I -> SUBENDOTHELIAL deposits in HBV, HCV -> treat w/ steroids
• type II -> INTRAMEMBRANOUS deposits due to C3 nephritic factor -> NO treatment

Question 14

IgA nephropathy

Answer 14

• nephritic
• most common GN worldwide
• IgA deposits in MESANGIUM**
• increase matrix deposition
• high IgA due to mucosal immunity
• hematuria at the ONSET of pharyngitis** (synpharyngitic syndrome)

Question 15

Henoch-Shonlein Purpura

Answer 15

• nephritic
• IgA mediated vasculitis
• PURPLE lesions
• CRESCENTS if severe

Question 16

post strep GN

Answer 16

• nephritic
• after GAS infection
• children 2-6 y/o
• hematuria AFTER resolution of the GAS (pharyngitis)
• CRESCENT moon
• SUBEPITHELIAL HUMPS
• test w/ anti-streptolysin O titer

Question 17

Rapidly progressive GN

Answer 17

• nephritic
• CLINICAL syndrome -> rapid loss of renal function
• CRESCENT formation**

3 categories

1. anti-GBM disease (ex. Goodpastures) -> Abs attack alpha 3 chain on type 4 collagen
2. Immune complex crescentic GN
3. paci-immune GN (most common) -> no immune complex -> ANCA + and vasculitis

Question 18

Alport Syndrome

Answer 18

• X linked
• defective type 4 collagen (COL4A5, COL4A3, COL4A4 genes)
• THINNING and SPLITTING of GBM

Question 19

Apolipoprotein 1

Answer 19

• serum factor in trypanosome lysis
• protects from trypanosome brucei
• cause renal disease