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FRACP Shuyu > RPA nephrology > Flashcards

RPA nephrology Flashcards

1
Q

Kidney donor risk index; and what is the best predictor of future graft function

A

Donor age - best predictor of future graft function Hypertension Diabetes Last creatinine Cause of death BMI DCD status

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2
Q

risk of ESKD in live kidney donor

A

increased risk compared with healthy non donors but still 100 in 100,000 (small absolute risk)

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3
Q

what GN is likely to recur after transplant

A

FSGS

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4
Q

absolute contraindication to transplant

A

active malignancy

uncontrolled infection (E.g. bronchiectasis)

chronic infections

unacceptable anaesthetic risk

smoking, alcohol, psychological

relative risks: severe sun damage, severe calcular disease, non adherence

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5
Q

what alleles are assessed in renal transplant

A

A, B, DR

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6
Q

what is the universa plasma donor

A

AB

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7
Q

what is a more sensitive test than Complement dependent cytotoxicity crossmatch

A

Lminex > Flow cross match > CDC crossmatch

CDC crossmatch only involves adding complement, look for lysis. It is crude and subjective

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8
Q

acute cellular kidney rejection histology

A

cellular - tubulitis, intersitital infiltrate

vascular - endothelialitis, glomerulitis, haemorrhage

antibody-mediated - PMNs, C4D+, PTC

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9
Q

chronic kidney rejection histology

A

glomerulopathy, chronic interstitial inflammation

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10
Q

type of kidney rejection

A

vascular kidney rejection

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11
Q

treatment of acute kidney rejection

A
  1. IV methylpred (90% effective)
  2. lymphocyte depleting antibody (ATG)
    1. steroid resistant OR vascular rejection
  3. Adjust immunosuppressants
  4. PLEX, IVIG (for Ab-mediated rejection)
  5. Rescue (high dose tac/myco)
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12
Q

how does the activated T cell signal for more T cell proliferation (in the context of kidney transplant rejection)

A

release of IL-2

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13
Q

where does belatacept work

A

fusion protein composed of the Fc fragment of a human IgG1 immunoglobulin linked to the extracellular domain of CTLA-4

blocks the co-stimulation of CD40 to CD40L (between the antigen presenting cell and T cell)

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14
Q

basiliximab MOA

A

a chimeric (mouse/human) monoclonal antibody which acts as an immunosuppressant by blocking the interleukin-2 receptor

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15
Q

what immunosuppresion is better for malignancy or Interstitial fibrosis and tubular atrophy (chronic scarred kidney)

A

mTOR

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16
Q

main adverse effects of mTOR

A

proteinuria

wound healing problems

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17
Q

main adverse effect of mycophenolate

A

bone marrow suppression

GIT symptoms (myfortic may be a slightly better alternative for GI symptoms)

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18
Q

which transplant immunosuppressant is assoc with a tremor

A

mTOR

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19
Q

which transplant immunosuppressant is the worst for lipids

A

mTOR

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20
Q

what transplant immuno are ok/not ok for pregnancy

A

pred/tac ok

myco and mTOR contraindicated in pregnancy

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21
Q

primary cells involved in acute kidney rejection

A

CD4T cells - main target of medications as well

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22
Q

what does glomuerlar scerosis and tubular atrophy suggest

A

dead and chronic changes in glom

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23
Q

anatomical abnormality for nephrotic syndrome

A

podocyte

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24
Q

Nephrotic Ddx

A

minimal change

FSGS

Membranous

Lupus class V

diabetic nephropathy

Amyloid

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25
causes of nephritic syndrome
anca vasculitis anti GMB post strep GN lupus III/IV TMA
26
causes of nephritic/nephrotic overlap
IgA MPGN Lupus Myeloma/MGRS
27
GN histological classification
1. Glomerular involvement 1. Diffuse or focal; segmental or generalised 2. Cell involvement 3. Changes in non-cellular components of the glomerulus
28
GNs that have a mesangial predominance
IgA Mesangioproliferative GN ImG nephropathy Clas II lupus nephritis diabetic nephropathy
29
is the podocyte on the urine or blood side
urine
30
what GNs affect the podocytes/epilepthium
minimal change membranous FSGS
31
what GNs affect the endothelial cells
these proccesses are usually immune sytem +++ see slides
32
nephrotic ++++ syndrome in young person with acute onset (sometimes with preceeding allergic rhinitis)
minimal change disease
33
minimal change histology
light microscopy look normal EM - flattened podocytes
34
minimal change disease treatment
steroid (second line cyclophosphamide, cyclo/tac, ritux if not steroid responsive - consider other Ddx ?FSGS
35
FSGS histology
focal & segmental glomerulosclerosis and hyalinosis
36
secondary causes of FSGS
secondary FSGS (obesity, HTN, previous damage to kidney)
37
FSGS management
steroids (less responsive than minimal change) high dose (60mg) for 6 months 2nd line - cyclophosphamide; cyclo/tac
38
suPAR use
to predict FSGS recurrence in transplant
39
most common cause of nephrotic syndrome that's secondary to a GN
primary membranous nephropathy
40
Primary membranous nephropathy histology
LM: membranous IF: granular IgG +/- C3 EM: subepithelial deposits; silver stain has intra-membranous Ig deposits, spikes
41
what are the proteinuria cut offs for risk stratification for membranous GN
\>8g/day high risk 4.5-8 med risk
42
pathophysiology of primary membranous GN
podocyte specific antigen that some people develop an antibody for causal biomarker is auto Ab to PLA2R. Titre antibody corresponds to the disease activity. immune deposits on epithelial side
43
anti-PLA2R in GN
membranous nephropathy used for: diagnosis risk stratification differentiating between primary vs secondary **do not need kidney biospy; and only in primary**
44
aside from the anti PLA2R, what other antibody is ass with membranous nephropathy
TSHD7A Ab (might be assos with malignancies)
45
primary membranous nephropathy treatment
cyclophshamide + pred anticoagulation (warfarin if serum albumin \<20mg/day) HOWEVER, NEJM 2019 compared rituximab with cyclosporine in treatment membraneous nephropathy. Rituximab was superior (although non inferiority trial). Awaiting PBS
46
secondary membranous GN causes
drugs, hepatitis, malignancy
47
most common form of GN worldwide
IgA nephropathy
48
pathogenesis of IgA nephropathy
O-linked glycans on IgAs are abnormal the body recognises the abnromality and forms an IgG to this abnormal hinge region. The immune complex deposits on the mesangium in IgA nephropathy. (it deposits on the endothelium in Henloch Purpura) Not all people with this O-linked glycans develop IgA
49
treatment of IgA nephropathy
ACE-I +/- steroids
50
rapidly progressing glomerunonephriti vs crescentic glomerulonephriti
RPGN id the clinical syndrome and crescentic GN is the pathology
51
what is the most common type of RPGN and what age group does that syndrome occur in
anca vasculitis older people 60-70
52
ANCA vs GBM histology
LM: - eosinophils + neutrophils IF: pauciimmune (no immune deposits) GBM: IF: linear IgG
53
pathology if the crescents
disruption of GBM with proliferation of inflammatory cells and fibrin around the glom and decreases filtering capacity of the glomerulus
54
Treatment of rapidly progressing GN
Pred cyclophosphamide +/- PLEX (use in pulmonary haemorrhage; anti GBM)
55
ANCA assoc vasculitis
small vessel vasculitis, crescentic pauci-immune
56
variants of ANCA vasculitis
GPA (Wegner's) - granulomas - PR3 EGPA (Churg-strauss) - **asthma** + eosinophilia + granulomas (PR3/MPO) MPA - no granulomas MPO PR3 = cANCA (worse prognosis) MPO = pANCA
57
ANCA assos vasculitis treatment
pred + cyclo or ritux (ritux can only be given if there's a contraindication to cyclo or they failed cyclo)
58
ANCA vasculitis maintainence
ritux or aza
59
what lupus nephritis to immunosuppress
III + IV (diffuse or focal proliferative disease) Corticosteroids + cyclo/mycophenolate refractory: steroids + MMF + CNI
60
EM: subepithelial hump diagnosis
post-infectious GN
61
membranoproliferative GN histology
(same as mesangiocapillary) describes a histological pattern due to some cause of immune deposition that causes inflammation and the development of a second membrane. "double coutor" (reduplicaiton of membrane) cellular proliferation, interstitial damage if there is positive staining for complement and immunoglobins, look for causes of complexment/immune deposition
62
secondary causes of membranoproliferative GN
hep C SLE monoclonal gammopathy
63
CLassificaiton of TMA
histological diagnosis classification primary: hereditary - normally abnormality in complement regulatory genes Acquired TMA - antibodies to something
64
pregnancy + fragments on blood film
HUS
65
diagnosis of atypical HUS
observable TMA + end organ damage ddx TTP
66
eculizumab MOA
blocks C5 to stop the conversion to C5b and membrane attack complex
67
kimmelstiel wilson nodules on histology
diabetic nephropathy
68
when is eGFR not accurate
AKI Children extremes of body weight patients taking extra creatinine/creatining caution with drug dosing
69
when is the eGFR most useful
monitoring in CKD
70
stages of CKD
71
what antihypertensives have additional albuminuria reduction properties
ACE I/ARB Non-dihydropyride CCB Spironolactone
72
daily sodium restriction
1500-2000mg/day
73
MOA of thiazides
inhibiting reabsorption of sodium (Na+) and chloride (Cl−) ions from the distal convoluted tubules in the kidneys by blocking the thiazide-sensitive Na+-Cl− symporter. they are vasodilating - but they are more likely to cause diluting hypontraemia
74
75
Iron study cut off for iron def in kidney disease
TSAT \<20% Ferritin \<100
76
most common reason for refractory anaemia to EPO in CKD
iron deficiency (other: chronic inflammation, high PTH, B12/folate, hypothyroid, marrow disorder, malignancy)
77
protein intake recommendations in CKD
0.6-0.8g/kg/day mild reduction in protein is good for kidneys
78
bicarb aim in CKD
\>21 oral sodibic replacement
79
Ca+, Phos and PTH management in CKD
no evidence that any intervention has mortality benefit in RCTs phosphate binders are only on PBS for dialysis
80
81
tolvaptan indications
autosomal dominant PCKD improves eGFR by 1mL/year compared to placebo PBS for eGFR 30-89
82
resistant hypertension already max dose 3 drugs including diuretic, next step
spironolactone
83
which RTA is assos with hyperkalaemia
Type 4 RTA found in hypoaldosteronism which is common in DM
84
Dialysis dysequilibrium syndrome
due to the reduction of plasma solute level over a limited time. Plasma becomes hypotonic compared to brain cells and water shifts from the plasma into the brain tissue
85
what drug is assos w SSc renal crisis
corticosteroids
86
alport syndrome genetics
COL4A5 mostl likely X-linked
87
ATN urinary sodium
sodium wasting (as opposed to hepatorenal - low sodium \<10)
88
expect pCO2
0.7 [HCO3] + 20 (range: +/- 5) (or similar to the last 2 digits of the pH)
89

FRACP Shuyu (65 decks)

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