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RACP Written Exam > Renal > Flashcards

Renal Flashcards

1
Q

Horeshoe kidney complications

A

hydronephrosis
nephrolithiasis
infection
increased renal ca

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2
Q

Difference between CrCl and GFR

A

CrCl estimates GFR
CrCl slightly overestimates as creatinine is moderately secreted by renal tubules

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3
Q

Where do loop diuretics act

A

Ascending loop of henle
Blocks Na/K/Cl transporter

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4
Q

Where to thiazide diuretics act

A

early DCT
blocks Na/Cl transporter

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5
Q

Where is majority of Na and water reabsorped in nephron

A

early PCT

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6
Q

Aldosterone effect on principal cells vs alpha-intercalated cells

A

principal cells - promotes Na and water reabsoprtion, K secretion
alpha intercalated cells - promotes K reabsorption and H secretion

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7
Q

Fanconi syndrome mechanism

A

generlised reabsorption defect in PCT
- increased excretion of AA, glucose, HCO3, PO4

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8
Q

Fanconi syndrome lab findings

A

metabolic acidosis (type 2 RTA)
low phosphate and K

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9
Q

What can cause Fanconi syndrome?

A

hereditary -> wilsons, glycogen storage disease
ischaemia
multiple myeloma
drugs (tenofovir, isofosfamide, cisplatin, lead poisening)

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10
Q

What is Bartter syndrome and lab findings

A

autosomal recessive reabsorption defect in thick ascending loop of henle
Like being on chronic loop diuretics
metabolic alkalosis, low K and high Ca

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11
Q

What is Gitelman syndrome and lab findings

A

AR defect of NA/CL transporter in DCT
causes metabolic alkalosis, low Mg K and Ca
similar to chronic thiazide use

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12
Q

What is Liddle’s syndrome and lab findings

A

Gain of function mutation to reduce Na channel degradation -> increased Na reabsorption
Metabolic alkalosism, low K, low aldosterone and HTN

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13
Q

What is SAME (syndrome of apparent mineralocorticoid excess) pathophys

A

AR 11beta-HSD deficiency leads to higher cortisol (rather than cortisone) which increased mineralocorticoid activity
Caused metabolic alkalosis, low K, low aldosterone and HTN

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14
Q

Actions of angiotensin 2

A

vasocontricts arterioles -> increase BP
contricts efferent arteriole -> increased GFR when renal blood flow low
Increases Na/H transporter activity in PCT
Secretes aldosterone -> H2O net absorption
Posterior pit to secrete ADH

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15
Q

Inhibitor for RAAS

A

ANP and BNP -> dilates afferent arteriole increasing renal blood flow and reducing renin
promotes naturesis

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16
Q

Most common cause of GN in developed countries

A

IgA nephropathy

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17
Q

IgA nephropathy presentation

A

40-50% macroscopic haematuria, flank pain and fever
30-40% microscopic haematuria plus mold proteinuria
10% rapid progressive GN
Rare to have malignant HTN or AKI

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18
Q

IgA nephropathy clinical associations

A

Cirrhosis
Coeliac disease in 1/3
Dermatitis hepatiformis
HIV
Minimal change and membranous
GPA when in remission
Small cell carcinoma
Bronchiolitis obliterans
Lymphoma
TB
IBD

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19
Q

Indications for Bx in IgA nephropathy

A

Protein >1g
Elevated creat
New HTN
Elevation in BP above previous stable baseline

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20
Q

Characteristic IF finding in immune complex GN

A

granular deposits of polyclonal Ig

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21
Q

Predictors of outcome in IgA nephropathy

A

reduced GFR worse
HTN worse
degree of proteinuria most important predictor in one study

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22
Q

what is considered remission in IgA nephropathy

A

protinuria < 1g/day

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23
Q

treatment of IgA nephropathy

A

aim ACEi, BP control, lifestyle for 6 months
if protein >1g/day or other factors (minimal change disease, AKI, RPGN) consider immunosuppresion with glucocorticoids

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24
Q

Characteristic histo findings in lupus nephritis

A

“full house” IF pattern
glomerular deposits that stain for IgG, IgA, IgM, C3 and C1q
seen everywhere

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25
Q

therapy immunosuppression for lupus nephritis

A

Induction: MMF or cyclophosphamide
Maintence: AZA

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26
Q

How to Dx infection related GN

A

kidney bx in those with preceeding or current infection and low C3

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27
Q

Most common GN in adults >50yo

A

pauci immune (ANCA associated)

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28
Q

Which ANCA is GPA

A

PR3

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29
Q

Which ANCA is MPA

A

MPO

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30
Q

Genes associated with ANCA vasculitis

A

MHC
PRTN3 gene

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31
Q

SNPs associated with PR3

A

HLA-DP
SERPINA1
PRTN3

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32
Q

SNP asscoiated with MPO

A

HLA-DQ

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33
Q

Most likely type of ANAC vasculitis to have replapsing renal disease

A

GPA and PR3

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34
Q

Better treatment for relapsing ANCA vasculitis renal disease

A

rituximab is superior to cyclophosphamide

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35
Q

Treatment with rituximab is better in what subgroup of ANCA vasculitis

A

PR3

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36
Q

Avacopan use in ANCA vasculitis trial findings

A

ADVOCATE study
avacopan non-inferior but not superior to tapered pred at 26 weeks, but superior at 52 weeks for sustained remission

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37
Q

Bx findings in pauci immune GN best and worse outcomes

A

focal -> best
sclerotic -> worse

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38
Q

Characterstic IF findigs in anti-GBM

A

linear deposits of IgG and frequently with C3

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39
Q

Histo findings of anti-GBM

A

severe necrotising and crescenteric pattern if active

40
Q

Anti-GM antigen

A

alpha 3 chain of type 4 collagen

41
Q

Assocations with anti-GBM

A

smoking and lung haemorrhage
hydrocarbons
alemtuzumab
HLA-DR2

42
Q

anti-GBM presentation

A

rapidly progressive GBM
40% have alveolar haemorrhage

43
Q

anti-GBM treatment

A

PLEX
steriods
cytotoxic therapy (cyclophosphamide)

44
Q

What can occur after transplant for alport syndrome

A

de novo anti-GBM

45
Q

How common is relapse of anti-GBM after transplant

A

uncommon

46
Q

Proliferative GN with monoclonal Ig deposits most common Ig deposit

A

IgG
rarely IgA
less common IgM

47
Q

Most common pattern of pathology in fibrillary GN

A

mesangial proliferative GN in 70%
IgG in all pt with C3 deposits

48
Q

cryoglobulinemic GN histo findings

A

membranoproliferative pattern with infiltrating macrophages and PAS deposits
deposits most often IgM

49
Q

Can differenciate between C3GN and dense deposit disease based on what

A

EM findings

50
Q

Pathophys difference between dense deposit disease and C3GN

A

Both lead to C3 convertase activity increasing
C3GN -> C3 mutation so is not inhibited by factor H
DDD -> C3 mutation leading to functional factor H deficiency

51
Q

treatment of membranoproliferative (C3GN)

A

mild - supportive
moderate >1.5g/day -> steriods, MMF
RPGN -> steriods plus cyclophosphamide or MMF +/- eculizumab +/- PLEX
refractory - eculizumab

52
Q

Mutations of Bartter syndrome

A

NA-K-Cl type 1
ROMK T2
CIC kb type 3
barttin T4
upregulation of CaSR t5

53
Q

frusemide effects on Ca

A

inhibits all downstream events, reduced Ca reabsorption

54
Q

thiazide effect on Ca

A

compensatory increase in NAKCl, increases Ca reabsorption

55
Q

Familial hypercalcaemia hypocaluria mutation and bloods

A

mutation in CaSR
slightly high Ca, high or inappropriate normal PTH
urinary Ca/Cr ratio <0.01 or low 24 hr urine Ca

56
Q

Pathology of lithium and hypercalcaemia

A

damaged CaSR
same as FHH
15-20% of people on lithium have high Ca

57
Q

Target Hb in CKD

A

> 100

58
Q

New therapies for anaemia in CKD

A

hypoxia inducible factor inhibitors or stabilisers

59
Q

Target for acidosis in CKD

A

aim HCO3 23-29
sodium bicarb
issue with fluid retention

60
Q

Most common causes of renovascular disease

A

atheroscelrotic disease 60-80%
fibromuscular disease 10-20%

61
Q

Difference physiologically between bilateral and unilateral renal artery stenosis

A

both have HTN
unilateral -> normal volume, high renin
bilateral -> hypervolaemia, normal renin

62
Q

When is stenting beneficial in renovascular HTN

A

in FMD
high risk atheroscleosis - recurrent flash APO, advancing renal impairment

63
Q

Most common cause of KD in dialysis

A

in decreasing order
diabetic nephropathy
GN
HTN

64
Q

most common side effects of dialysis catheter

A

infection

65
Q

Most common cause of death of dialysis

A

CVD

66
Q

Mortality benefit patter in renal transplant

A

higher early, but lower in longer term

67
Q

Causes of HLA sensitisation (difficult to match for transplant)

A

Previous transplant
Pregnancy
blood transfusions in past

68
Q

Most used induction agent for transplant

A

Basilixumab (anti CD25 and IL2 receptor)

69
Q

Most common immunosuppression regime for renal transplant

A

pred
tacro
MMF

70
Q

What immunosuppressant to use for induction if high immunological risk group

A

ATG (rabbit thymoglobulin polyclonal Ab)

71
Q

Major interactions between renal transplant immunosuppressants

A

cyclosporin lowers MMF levels but tacrolimus doesnt

72
Q

Side effects of mTOR inhibitors

A

wound complications
proteniuria

73
Q

Most common cause of renal graft loss in early (1st year)

A

infection 33%
cardiovascular 29%
cancer 7%

74
Q

Most common cause of renal graft loss in late (beyond 1st year)

A

cancer 29%
cardiovascular 22%
infection 13%

75
Q

Most common cause of graft loss (due to graft failure)

A

early: graft thrombosis (technical)
late: chronic allograft nephropathy

76
Q

Most common cause of delayed graft function

A

native kidney ATN (decease donor 30-40%)

77
Q

Causes of early graft rejection

A

acute rejection
CNI toxicity
renal artery stenosis
recurrent disease in early: primary FSGS and aHUS (late more IgA)

78
Q

Underlying physiology behind acute graft rejection

A

can be T cell mediated or Ab mediated

79
Q

Treatment for acute graft rejection

A

t-cell mediated: IV methylpred, ATG (if steriod resistant)
Ab mediated: PLEX, IVIG

80
Q

Features of BK virus on Bx

A

intranuclear viral inclusions and SV40 staining (only in medulla)

81
Q

Rule of thumb for infection post transplant

A

first 1 month - donor derived and nocicomal
first 6 months - reactivation, oppurtunistic
langer term - sommunity acquired (CMV, PJP)

82
Q

Most risk profile for CMV in kidney donation

A

donor +ve recipient -ve

83
Q

prophylaxis for CMV in renal transplant

A

D+R- : prophylaxis for 6 months, valgancyclovir
D-R+ or D+R+ : prophylaxis for 3 months

84
Q

Cancers which are higher risk in renal transplant

A

NHL
lung
colorectal

85
Q

Best combo of immunosuppression in renal transplant for lowest skin cancer risk

A

reduced dose CNI with no MMF

86
Q

most common inhereted renal disease

A

polycystic kidney disease

87
Q

mode of inheretance PCKD

A

AD

88
Q

Most common mutation type PCKD

A

PKD1 (polycystin1) 78%
PKD2 15%
mostly monoalleleic
complete penetrance

89
Q

Which are the most severe PCKD mutations?

A

PKD1 worst than PKD2
if non-truncating mutation -> less severe

90
Q

CNS extrarenal manifestation of PCKD

A

cerebral aneursyms - most in MCA
5% in younger, 20% in >60yo
only screen high risk pt

91
Q

hepatic manifestations of PCKD

A

hepatic cysts with severe PLD in 15%
avoid estrogen replacement in women if liver cysts

92
Q

Most common valvular disease in PCKD

A

MVP and AR

93
Q

DIagnostic criteria for PCKD

A

if positive Fhx: if 15-39yo need >3 cysts, if 40-59 need 2 cysts in both kidneys
if negative FHx, need bilat renal enlargement and >10 cysts in each kidney

94
Q

Tolvaptin MoA

A

vasopressin V2 receptor antagonist

95
Q

Tolvaptin use in PCKD

A

for every 4 years on the drug, delay dialysis for 1 year

RACP Written Exam (14 decks)

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