Immunological Aspects of Renal System Flashcards
Which of the following would meet the criteria for Acute Kidney injury?
A. GFR greater than or equal to 60mL/min with stable serum creatine
B. Kidney damage seen for greater than 3 months
C. GFR less than 60mL/min for 3 months with an increase in SCr by 50% w/in 7 days
D. Increase in SCr by 50% within 7 days, or 0.3mg/dL in 2 days
Increase in SCr by 50% within 7 days, or 0.3mg/dL in 2 days
also oliguria (abnormally small amounts of urine produced)
In most cases, which of the following is the cause of an AKI (acute kidney injury)?
A. Inflammation brought on by an infection
B. Sterile Inflammation
C. Graft vs. Host Disease
D. Type I Hypersenstivity reaction
Sterile Inflammation
CRPs have 5 subunits like IgM, allowing it to bind DAMPs and activate complement. Which of the following binds to CRPs the same as IgM allowing the classical complement pathway to be activated?
A. C1
B. C2
C. Mannose
D. C3
C1
PAMPs are released from exogenous pathogens, and DAMPs are from endogenous damaged cells that both include Nucleic acids, lipids and proteins that bind to PRRs and cause release of pro-inflammatory mediators. Which of the following are some of the pro-inflammatory mediators?
A. TGF and IL-10
B. IL-4, IL-6, IL-1B
C. TNF-a
D. TNF-a, IL-1B, and IL-6
TNF-a, IL-1B, and IL-6
All of the following are PAMPs released from pathogens, except for which of the following that are DAMPs?
A. CpG and ds DNA
B. Lipid A
C. ATP and oxLDL
D. PGN
ATP and oxLDL
All of the following DAMPs activateNF-kB when they bind to their respective receptors. Which of the following DAMPs is released from the nucleus of a damage cell and binds the RAGE receptor?
A. HMGB1
B. Uric Acid
C. HSP
D. S100
HMGB1
NOTE: RAGE= Receptor of Advanced Glycation End products
All of the following DAMPs activateNF-kB when they bind to their respective receptors. Which of the following DAMPs is released from the nucleus of a damage cell and binds the NLR-P3 receptor?
A. HMGB1
B. Uric Acid
C. HSP
D. S100
Uric Acid
NOTE: HSP binds to scavenger receptor A
Damage to kidneys causes release og chemokines and cytokines via the activation of resident renal cells like DCs, Macrophages, and endothelial cells. According to Dr. Shnyra’s cahrt, activation of which of the following cells is a related response to Ischemia Induced Glomerulonephritis, Diabetes, and sepsis?
A. Endothelial Cell release of TNF, IL-6, and IFN-a
B. DC release of IL-12, CXCL2, IL-1B, and Type I IFNs
C. Macrophage release of ROS, IL-1B, TNF, IL-6, and chemokines
D. None of the above
Endothelial Cell release of TNF, IL-6, and IFN-a
The presence of certain cells and cytokines varies between early and late stages of an AKI. Which of the following are you most likely to see at the early stages of an AKI?
A. High concentration of Th17 releasing IFN-y, IL-6 and IL-4
B. Th1 predominating causing an increase in levels of IL-12 and IL-6
C. Th17 predominating causing an increase in levels of IL-12 and IL-6
D. High level of Alternatively activated M2 macrophages promoting anti-inflamation and wound repair
Th17 predominating causing an increase in levels of IL-12 and IL-6
NOTE: Th1 predominate the late phase and give off: IFN-y, IL-6 and IL-4
Macrophages play a role in AKI response as well. Which of the following correctly describes the role of the classical and/or alternatively activated Macrophages?
A. M1s are reprogrammed M2s that have changed their phenotype after exposure to M-CSF, IL-4 and IL-13
B. M2s release IL-10, TGF-B and proline polyamines for anti-inflammatory actions and wound repair
C. Classically activated Macrophages show up and release IL-1, IL-12, and IL-23 to promote inflammation
D. All of the above
E. A and C
F. B and C
B and C
B. M2s release IL-10, TGF-B and proline polyamines for anti-inflammatory actions and wound repair
C. Classically activated Macrophages show up and release IL-1, IL-12, and IL-23 to promote inflammation
NOTE: M2s are reprogrammed M1s
Which of the following subset of T cells releases or promotes the release of CCL20 (MIP-3) which leads to recruitment of neurtrophils, monocytes, and other mediators of inflammation that ultimately leads to the progression of immune mediate kidney damage?
A. Th1
B. Th2
C. Th17
D. Treg
Th17
Why are kidneys so susceptible to complement induced damage?
Filtration favors the deposisiton of immune complexs on the tissues
Which of the following stimualte proinflammatory response in neurtrophils and macrophages leading to inflammation that relates to the eventual necrosis of kidney cells?
A. C3b and C5b
B. Bb and C4a
C. MAC complex
D. C3a and C5a
C3a and C5a
T/F: Complement activation may occur downstream as a result of Type I and Type IV hypersensitivity reactions
False; Type II (Ab-mediated injury) and Type III (immune complex deposition)
What are the 4 main variables that determine the outcome of transplantation?
- Allographs condition
- Disparity betwen host and donors antigens
- Strength of hosts response to donors Ags
- Immunosupressive regimen