Nephrology Flashcards

1
Q

What genetic pattern of inheritance does Polycystic Kidney Disease have? What are the main genetic mutations?

A

Autosomal Dominant

PKD1/PKD2 - polycystic (ciliopathies)

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2
Q

Which mutations convey a poorer prognosis in PCKD

A

Truncating mutations

PKD1

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3
Q

Early manifestation of PCKD

A

Hypertension (with normal eGFR)

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4
Q

Extra-renal manifestation of PCKD

A
CNS: Cerebral aneurysm
CVS: Valvular disease, cardiomyopathy, AF, aortic dissection and aneurysm 
Hepatic Cysts
Pancreatic Cysts (IPMN) 
Seminal vesicle cysts
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5
Q

Main risk factor for progression/poor prognostic factors for PKCD

A
Male
Early onset of symptoms 
Kidney size
PKD1/Truncating mutations 
Proteinuria
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6
Q

Diagnostic Criteria for PKCD (with and without family history)?

A
\+ Family history 
>/= 3 cysts ( 15-39) 
>/= 2 cysts in both kidneys (40-59) 
- Family history 
>/= 10 cysts each kidney 
\+ bilateral kidney enlargement 

Can use CT/MRI if needed

Can use genetic testing if necessary

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7
Q

Pharmacological management in PCKD
> CVS
> Targeted

A

RAAS Blocker (Ace inhibitor/ARB)
Tolvaptan (V2 vasopressin antagonist)
> Earlier treatment associated with more benefit
> eGFR <90, + eGFR progressively worsening by 2.5-5ml/min/yr over 5 years.
Main adverse effects of tolvaptan include: Polydipsia, polyuria/nocturia and LFT derangement

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8
Q

Thiazide induce hyponatraemia time frame

A

Most commonly occurs within 2 weeks of commencing or with intercurrent illness.

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9
Q

Treatment for PCKD

A

BP control <110/75
Reduce NA
Increase fluid intake
Tolvaptan

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10
Q

IGA nephropathy secondary causes

A

ETOH

Coeliac Disease

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11
Q

Treatment for IGA nephropathy

A

ACE to decrease proteinuria - BP target <130/80
Transplant

No benefit to immunosuppression

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12
Q

Acute allograft dysfunction

A

First 7 days: Ureteric obstruction/HLA mismatch

1-12 weeks: Acute rejection

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13
Q

AIN findings

A
Raised Cr
Eosinophilia
Urine sediment: WCC/RCC/WC casts 
Evidence of tubulointerstital damage
Raised fractional sodium
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14
Q

Resistant Hypertension

Not complete

A
A
C
D 
> Not within limits despite triple therapy 
Add in 

Note refractory, not response to 5 drugs.

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15
Q

RTA

Not complete

A

1: Hypokalaemia. Impaired hydrogen secretion (distal)
2: Hypokalaemia (Proximal). Impaired Bicarb reabsorption. Raised urinary PH.
4: Hypoaldosteronism

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16
Q

Histological finding of Amyloidosis affecting the kidney

A

Proteinuria only
Nodular Glomerulosclerosis
Congo red staining

Note often stem with cardiac involvement

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17
Q

Rapidly progressive glomerulonephritis causes

A

Anti-GBM
Small vessel vasculitis (ANCA)
Cryoglobulinaemia
Lupus Nephritis

RPGN is a clinical syndrome characterised by evidence of GN (haematuria/proteinuria/leukocytes in urine) and progression to kidney failure in a short period of time.

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18
Q

Most common causes of Nephrotic Syndrome in adults?

A

Secondary causes
Diabetes (Also most common overall)
Infection
Autoimmune disease

Primary causes
Minimal change disease
Focal segmental glomerulosclerosis (most common)
Membranous nephropathy (most common)
Membranoproliferative glomerulonephritis:

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19
Q

Nephrotic Syndrome

A

Nephrotic range proteinuria: 3500mg/24 hr or P:Cr 3000mg/g
Hypoalbuminaemia: <35
Oedema
Hyperlidipidaemia

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20
Q

Treatment for neprhotic syndrome

A

Treat cause
Statins (Hyperlipidaemia +/- treatment for triglycerides)
Anticoagulant in patients with additional risk factors or low risk with albumin <28 (prothrombotic tendency)
Low salt diet and diuretics (oedema)

Note patients with nephrotic syndrome are also more likely to develop infections ? due to loss of immunoglobulins through the glomerulus.

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21
Q

Nephritic Syndrome

A

Haematuria (+/- dysmorphic eryhtrocyte casts)
Proteinuria
+/- leukocytes

Clinically
Hypertension
Oedema
Kidney Failure

Reflects proliferation in the glomeruli.

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22
Q

Investigation for nephrotic syndrome?

A

Usually requires a kidney biopsy to diagnose
●Glycated hemoglobin (HbA1C, to diagnose diabetes)
●Antinuclear antibody and anti-double stranded DNA (dsDNA) antibody
●Anti-PLA2R autoantibody
●In patients older than 50 years – Serum free light chains and serum protein immunofixation
●Tests for hepatitis B and C viruses and HIV
●Serum C3 and C4 complement levels

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23
Q

Which cause of nephrotic syndrome is most likely to cause renal vein thrombosis>?

A

Membranous nephropathy

Seek secondary causes particularly occult malignancy

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24
Q

Treatment options for Membranous Nephropathy

A
1/3 spontaneous remission 
Persistent disease after 6-12 months or thromboembolic event 
RAS blockade 
Immunsuppression 
Rituximab (esp if PLAR2 +)
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25
Q

Secondary causes of minimal change disease

A
Malignancy
- Hodgkins lymphoma
- Thymoma 
Medications
- NSAID's
- Lithium 
- Pamidronate
- Interferons
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26
Q

Treatment of minimal change disease

A

Initially: Glucocorticoids
Relapsing: Cyclophosphamide, calcinuerin inhibitors, mycophenolate or rituximab

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27
Q

Risk factors for progression of renal impairment

A

1) Renal impairment i.e GFR <90
2) Proteinuria (predicts ESRF and reducing it delays ESRF)
3) Diabetes
4) Hypertension

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28
Q

Mainstay of treatment for proteinuria in non-diabetic patients

A

Ace Inhibitor and salt restriction

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29
Q

Which anti-hypertensives reduce proteinuria and thus progression to renal failure

A

ACE inhibitor or ARB

  • Reduce progression to ESRF
  • Reduced cardiovascular death
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30
Q

Target BP in diabetic patients (no-nephropathy and nephropathy?)

A

No nephropathy: <130/85
Nephropathy: <125/75

Note blood pressure control has the greatest effect on delaying progression to ESRF in diabetics. Microvascular endpoints tight BP control is better than glycemic control.

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31
Q

Target BP in proteinuria?

A

<125/75

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32
Q

What is the most likely cause of death in a patient commencing dialysis?

A

Cardiovascular event

Need to monitor and control cardiovascular risk factors

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33
Q

Kidney biopsy findings in RPGN

A

Crescent formation

Specific diagnosis of cause is made with IF

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34
Q

Treatment of patient’s with non-infectious cause of RPGN

A

High dose pulse IV steroids then transition to oral steroids

  • Pauci-immune GN: Cyclophosphamide/Rituximab
  • ANti-GBM: Plasmapharesis in the context of pulmonary haemorrhage or rapid kidney failure to remove circulating antibodies
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35
Q

RPGN + Pulmonary Haemorrhage

A

Anti-GBM disease (Goodpastures)

Antibody against type IV collagen –> bind –> inflammatory response.

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36
Q

RPGN + Pulmonary Haemorrhage

A

Anti-GBM disease (Goodpastures). Cause of RPGN in young patients.

Antibody against type IV collagen –> bind –> inflammatory response.

Positive antibody for Anti-GBM 1

Kidney biopsy: crescents with linear deposition of immunoglobulin

Complement level = normal

Treatment: Plasmapharesis (to remove circulating antibodies), steroids and cyclophosphamide.

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37
Q

Pauci-immune glomerulonephritis causes and associations

A

Caused by microscopic vessel vasculitis affecting the kidney –> necrotising lesions but no immune deposits.

+/- systemic vasculitis

Complement levels normal.

Associated with
Granulomatosis Polyangitis (URT - C-ANCA (Pr3ANCA) +
Granulomatosis Polyangitis with eosinophils (Asthma/eosinophils)
Microscopic Polyangitis (Haematuria - PANCA (MPO ANCA) +

Treatment
Induction: Steroids + Cyclophosphamide +/- plasmapheresis
Rituximab for mild disease
Maintenance with azathioprine/mycophenolate/methotrexate

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38
Q

Pathophysiology of IGA Nephropathy

A

Abnormal IGA (Galactose deficient) –> Body forming antibodies against same –> immune complex formation –> inflammatory lesions in the glomerulus (or extra-renal sites in the context of HSP).

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39
Q

Classical presentations of IGA Nephropathy (two)

A

1) Asymptomatic microscopic haematuria

2) Haematuria post URTI (synpharyngitic nephritis)

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40
Q

Finding on microscopy of IGA Nephropthy

A

Mesangial proliferation and deposition of IGA

Crecent formation may be occasionally seen –> RPGN

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41
Q

Treatment for IgA Nephropathy

A

If proteinuria then commence on ACE

Can use steroids for six months

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42
Q

Which classes of lupus nephritis do you commence steroids for?

A

Most of III: Focal, proliferative <50% gloms involved
All IV: Diffuse, proliferagtive >50% gloms involved
V: Membranous LN If neprhotic range proteinuria

Induction: glucocorticoids + cyclophosphamide/mycophenolate

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43
Q

Infection related glomerulonephritis causative organisms

A

Streptococcus (onset 1-6 weeks post)
Staphylococcus (onset at time of infection)
Rarely gram negative organisms

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44
Q

Infection related glomerulonephritis diagnosis

A

Strep related: Anti-streptolysin-O antibodies or Anti-DNAase antibodies
Other
- Cultures to identify potential inciting organism
- Depressed complement levels, esp C3
- Kidney biopsy: diffuse endocapillary proliferation and exudative glomerulonephritis and C3 dominant IF staining (forming humps in a subepithelial location)

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45
Q

Membranoproliferative glomerulonephritis causes

A
Immune complex deposition
- Monoclonal gammopathy 
- Autoimmune disease (SLE) 
- Hepatitis C 
Activation of the alternative pathway 
- Dense deposit disease
- C3 glomerulonephritis
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46
Q

Membranoproliferative glomerulonephritis findings on biopsy

A

Immunoglobulin deposition +/- complement deposition

Mesangial and endocapillary proliferation with thickening of the basement membrane.

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47
Q

Glomerulonephritis with reduced complement levels

A

Infection related glomerulonephritis
Lupus nephritis
Membrano proliferative nephritis

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48
Q

Glomerulonephritis with normal complement levels

A
IgA Nephropathy
Membranous nephropathy
Anti-GBM1 
Pauci-immune glomerulonephritis 
Minimal change disease
FSGS
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49
Q

Hallmark of FSGS

A

Segmental scars in some glomeruli. Podocyte effacement but no immune deposits.

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50
Q

What type of collagen is affected in all port syndrome?

A

Type IV (similar as that affected in Anti-GBM disease or good pastures syndrome).

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51
Q

Elevation of which parameter carries this highest risk of mortality in dialysis patients?

A

Phosphate

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52
Q

How to reduce phosphate in dialysis patients?

A

1) Phosphate binder with food
2) Prevent hyperparathyroidism
- giving vitamin D
- Consider calcimimetics or PTH

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53
Q

Main reason to treat elevated phosphate in dialysis patients?

A

Reduce the risk of cardiovascular disease

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54
Q

Blood pressure targets

A

<140/90

<130/80 (diabetics)

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55
Q

Treatment for hypertension

A

1) ACE/ARB
2) Calcium channel blocker
3) Diuretic

*can individualised based on patient profile i.e for patient with BPH consider using prazosin.

Note: Three drugs at half standard dose will be more effective than one drug at maximal dose

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56
Q

Which anti-hypertensive to consider adding in context of resistant hypertension (hypertensive despite 3 agents)

A

Spironolactone (Rehot study) best add in if already on 2/3 agents.

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57
Q

Most common presentation of Conn’s

A

Hypertension and normokalaemia

Note severe = hypertension and hypokalaemia

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58
Q

HB target for patients on dialysis

A

110-130

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59
Q

When to given iron replacement therapy in CKD patients

A

HB <110
TSAT <30%
Ferritin <500

Given IV iron rather than oral iron as GIT absorption of iron insufficient to keep up with demand

In dialysis patients aim;
Ferritin >200
TSAT > 20%

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60
Q

What effect does vitamin D have on calcium and phosphate?

A

Gut absorption:
- Increase absorption of calcium and phosphate
Urinary losses:
- Reduces urinary losses of calcium and phosphate

Vitamin D = interested in building bone

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61
Q

What effect does Parathyroid hormone have on calcium and phosphate?

A

Urinary losses:

  • Reduced urinary losses of calcium
  • Increased urinary loss of phosphate

PTH is concerned with maintaining serum calcium homeostasis.

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62
Q

Initial investigation for primary hyperaldosteronism (conn’s syndrome)

A

Morning blood sample in seated patient

  • Plasma aldosterone concentration
  • Plasma renin activity
  • ensure patient off eplenerone/aldosterone blockade/ amiloride

PAC/PRA >555 pmol/ng/ml = further investigation for primary hyperaldosteronism

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63
Q

Confirmatory test for primary hyperaldosteronism (conn’s syndrome) on finding of elevated PAC/PRA

A

1) Saline suppression test
(Normally bolus of salty water would decrease renin and thus aldosterone production)

2) Adrenal CT scan
3) Adrenal venous sampling to determine if unilateral or bilateral

64
Q

Treatment for primary hyperaldosteronism

A

1) Unilteral: Surgical resection

2) Bilateral: Mineralocorticoid receptor antagonist.

65
Q

Indications that increase in Cr is due to AKI rather than CKD

A
Time frame <3 months 
Absence of 
1) anaemia 
2) elevated phosphate 
3) elevated parathyroid hormone
4) small kidneys
66
Q

KDIGO staging of AKI

A

Stage 1) 1.5-1.9 reference value
Stage 2) 2.0-2.9 reference value
Stage 3) >3.0 times reference value

67
Q

Causes of ATN

A

1) Ischaemia
2) Nephrotoxins
3) Pigment nephropahty
- Hb
- Myoglobin
- Bili

68
Q

Treatment for AKI

A

1) Balanced crystalloid (Hartmanns)
- Less dialysis
- Lower K
- Less acidosis
2) Treat the cause

69
Q

Tumor Lysis Syndrome

A

1) Elevated phosphate
2) Elevated potassium
3) Low Calcium
4) High urate
5) High LDH

70
Q

Prevention of TLS

A

1) Hydration
2) Allopurinol (xanthine oxidase inhibitor)
3) Urinary alkalisation
4) Rasburicase

71
Q

Hepato-renal syndrome

A

1) Urinary sodium <10
2) Falling GFR
3) No blood or protein in urine
4) Normal RUS

72
Q

Treatment for hepatorenal syndrome

A

1) Trial of volume (cease diuretics, give fluid)
2) Terlipressin
3) Dialysis then liver transplantation

73
Q

When does serum creatinine in radio-contrast nephropathy peak?

A

Peaks 5-7 days post bolus

Resolves within 14 days

74
Q

Main cause of nephrotic syndrome in childhood?

A

Minimal Change Disease

Flattening of podocytes on EM

Responds well to oral steroids (not so in adults)

75
Q

Treatment for Minimal Change Disease in adults?

A

Steroids

If no response then consider cyclophosphamide or cyclosporine

76
Q

Poor prognostic factors in FSGS

A

1) Nephrotic range proteinuria
2) Hypertension
3) Decreased GFR
4) Interstitial fibrosis on biopsy

77
Q

Which GN has the highest recurrent rate in transplant

A

FSGS

78
Q

Treatment for FSGS

A

1) Prednisolone 3 months

2) Cyclophosphamide or cyclosporin for steroid non-responsive

79
Q

Primary Membranous Nephropthy finding on histology

A

Thickened GBM

Intra-membranous Ig deposits and spikes

80
Q

Utility of PLA2R antibody in Membranous Nephropathy

A

1) Diagnostically: does not remove

2) Recurrence: In treated or transplanted.

81
Q

Most common cause of nephritic syndrome?

A

IgA Nephropathy

82
Q

Most common cause of RPGN

A

Anca associated vasculitis

83
Q

Investigations in RPGN

A

1) Renal biopsy
2) SLE serology
3) ANCA
4) Anti-GBM antibodies

84
Q

A-HUS diagnosis

A
1) Thrombocytopenia 
\+
2) Haemolysis 
\+ 
3) End organ damage: kidney/neurological/GIT/cardiac
85
Q

A-HUS treatment

A

1) Ecluzilmab MAB to C5a

86
Q

Scleroderma renal crisis

A

1) Acute onset Hypertension
- Hypertensive encephalopathy
- Hypertensive retinopathy
2) Acute onset Renal failure

87
Q

Scleroderma renal crisis risk factors

A

Risk factors

  • More common in diffuse cutaneous SSc
  • within 5 years of diagnosis (early manifestation of disease)
  • anti-RNA polymerase III
  • Glucocorticoid use
  • Cyclosporin use
88
Q

Scleroderma renal crisis treatment

A

1) Captopril
- low dose 6.25 if normotensive
- high dose 12.5 if hypertensive

89
Q

Which immunosuppressant used in kidney transplants has the highest risk of diabetes?

A

Tacrolimus (Beta cell toxin - impairs pancreatic production)

90
Q

Which GN do you use steroids post transplant?

A

IgA nephropathy

91
Q

Induction therapy for kidney transplant

A

Basiliximab (Anti-CD25, bind to IL2 receptor)

Found to reduce acute rejection

92
Q

Main use of ATG in kidney transplant

A

Steroid resistant rejection

Note increased risk of post transplant lymphoproliferative disorders with ATG if EBV donor positive but recipient negative

93
Q

Mechanism of action of Tacrolimus/Cyclosporin

A

Calcinuerin Inhibitor

Note significant nephrotoxicity

94
Q

Which immunosuppressant can you use in kidney transplant patient with neutropenia

A
Calcineurin Inhibitors (do not suppress bone marrow) 
Cytopenias common with Mycophenolate (approx 2-6 months)
95
Q

Combination of immunosuppressives used in pregnancy

A

Calcineurin inhibitor (Tac or Cyclo), Azathrioprine (Switch Mycophenolate for Aza) and Prednisolone

96
Q

Mechanism of action of Sirolimus/Everolimus

A

mTOR inhibitors
Note benefits include
- Reduced risk of cancers particularly reduced skin cancer risk

97
Q

Causes of death in patient with kidney transplant (1st year then after the 1st year)?

Nb: Death with kidney graft loss is the main cause of graft loss overall

A

1) 1st year
- Cardiovascular
- Infection
- Cancer
2) After 1st year
- Cancer
- Cardiovascular
- Infection

98
Q

Causes of death censored kidney graft loss (1st year then after the 1st year)?

A
1st Year
1) Graft thrombosis/technical graft loss
2) Rejection
3) GN
After 1st T=Year 
1) Chronic allograft nephropathy 
2) GN
99
Q

Risk factors for ATN post transplant

A

1) Deceased donor (very uncommon with live donor)
2) AKI in donor
3) Increasing age of donor
4) Length of cold ischaemia time

100
Q

Investigation for suspected graft thrombosis

A
  • Doppler ultrasound

- MAG-3 scan (nuclear medicine investigation)

101
Q

Causes of worsening kidney graft function in 1st year

A

1) Acute rejection
2) CNI toxicity
3) BK virus
4) Renal artery stenosis
5) Obstruction/leak
6) Recurrence of disease

102
Q

Which nephropathies are most likely to recur early post transplant

A

1) MPGN
2) aHUS
3) FSGS
4) IGA Nephropahty
5) ANCA associated

103
Q

Investigation for suspected acute rejection

A

1) Biopsy

104
Q

Risk factor for acute kidney graft rejection

A

1) Prior sensitisation
- transfusion
- pregnancy
- previous transplant
2) Young recipient older donor
3) Ischaemia time
4) Higher HLA mismatch

105
Q

Treatment of acute kidney graft rejection

A

1) T-Cell Mediated
- Pulse methylprednisone
- Optimise immunosuppression
- ATG if steroid resistant
2) Antibody mediated
- Exchange transfusions
- IVIG

106
Q

Treatment for BK associated nephropathy

A

1) Reduce immunosuppression

2) Consider IVIG/Steroids if element of acute rejection from biopsy

107
Q

Prophylaxis for CMV in kidney transplant based on Donor and Recipient CMV status

A

1) D+R-: 6 months prophylaxis
2) D-R+ or D+R+: 3 months
3) D-R-: None required unless giving ATG

108
Q

Malignancies with the highest incidence post transplant

A

1) NHL

2) Melanoma

109
Q

Pathophysiology underlying ATN

A

ATP depletion which leads to hypoxia/oxidative stress which leads to necrosis/apoptosis.

110
Q

Drugs that most commonly cause AIN

A
NSAIDs
penicillins and cephalosporins, antimicrobial sulfonamides, ciprofloxacin and other quinolones,
rifampicin
diuretics
cimetidine
allopurinol
proton pump inhibitors (PPIs)
indinavir, and 5-aminosalicylates
111
Q

Treatment for calcium oxalate stones

A

1) Hypercacliuria
Thiazide diuretics (induce hyponatraemia –> increased reabsorption of calcium)
2) Hyperoxaluria
Reduce oxalate consumption (rhubarb, chocolate and spinach)
Commence on calcium citrate or colestyramine

112
Q

Treatment for low urinary citrate

A

Reduce animal protein

Alkalise serum with potassium citrate or sodibic

113
Q

Treatment for struvite stones

A
Treat UTI (UTI predisposes to stone formation) 
Surgical removal if stone formed
114
Q

Uric acid stones treatment

A

Maitain urine output 2L/day

Alaklise urine

115
Q

Treatment for cysteine stone

A

Urinary alkalisation

116
Q

Indication for kidney biopsy in diabetes with pre-existing diabetic nephropathy.

A

Dependent on the stem

  • Persistent haematuria (looking for alternative causes of nephritic syndrome)
  • ANCA with active urinary sediment and or features of vasculitis.

Note: Main prognostic element of diabetic nephropathy is progression of proteinuria while on RAS blockade.

117
Q

Biopsy in acute rejection of allo-graft in kidney transplant

A

T-cell

118
Q

Criteria for Acute renal allograft rejections

A

1) Deterioration in allograft function
+
2) Specific pathological changes in the graft

119
Q

Two principal histological forms of acute rejection

A

1) Acute T cell-mediated cellular rejection
- Can develop at any time
- Lymphocytic infiltration of the tubules and interstitium (CD4/CD8)
2) Antibody mediated rejection (3-10% all transplants)
- Morpholgic evidence of acute tissue injury
- Circulating donor-specific antibodies
- Immunological evidence of antibody-mediated rejections including C4d deposition in the allograft

120
Q

Main cause of EPO resistance in ESRD

A

Inflammation

121
Q

Indication for Iron Infusion in patients with ESRD

A

1) Hb <100 TSAT <30 and Ferritin <300
2) Hb >100 TSAT <20 Ferritin <200
* Generally TSTA >30 Ferritin >300 = iron replete. If anaemia then use ESA.

Note: high circulating PTH may cause inhibition of early erythroid precursors/RBC survival

122
Q

At what Hb threshold should you not give EPO?

A

Hb >120 (increased risk of stroke)

123
Q

The main benefit for using EPO analogues in the management of CKD

A

Decrease in left ventricular hypertrophy.

Not clearly shown to improve QOL.

124
Q

Most common cause of secondary FSGS

A

Malignancy

125
Q

Treatment for IgA nephropathy

A

Aggressive RAS blockade and hypertensive treatment

Unless Crescentic disease then immunosuppression.

126
Q

AD PKD more common in younger individuals

A

PKD 1 Age <50

127
Q

AD PKD more common in older individuals

A

PKD 2 Age >50

128
Q

PD membrane survival

A

1) Preservation of residual renal function - RAAS blockade
2) Preventing infection
3) Protecting peritoneal membrane integrity with low glucose concentrations

129
Q

Which SGLT2 inhibitor is best to use in a patient with impaired renal function?

A

Canagliflozin (Can use eGFR<30) - Credence trial

130
Q

Types of renal tubular acidosis, location of deficiency and key diagnostic clues

A

Type 2: Proximal tubule defect of reabsorption of HCO3. Mild metabolic acidosis with low urine PH
Type 4: Aldosterone deficiency or resistance
Type 1: Cortical collecting duct defect of H+ excretion, metabolic acidosis with high urinary PH, hypercalciuria and propensity to develop renal calculi.

131
Q

Does dialysis improve Restless legs syndrome associated with end stage renal failure?

A

No

132
Q

Definition of Acute Kidney Injury

A

KDIGO Guidelines

  • Increase in serum creatinine by > or = 0.3mg/dl within 48 hours
  • Increase in serum creatinine to > or = to 1.5 times baseline within 7 days
  • Urine volume <0.5ml/kg/h for 6 hours

Nb: You cannot use EGFR in to context of AKI.

133
Q

Staging of AKI by KDIGO guidelines based on serum creatinine

A

1: 1.5-1.9 times the baseline
2: 2.0-2.9 times the baseline
3: 3.0 times the baseline or initiation of renal replacement therapy

134
Q

Drugs that can cause AIN

A

Beta Lactams
PPI
NSAIDs
Immunotherapy

135
Q

How to use the urinary sodium in AKI

A

Low urinary sodium <40 = Renal Hypo-perfusion
High urinary sodium >40 = ATN

Note fractional excretion of sodium is better than urinary sodium.

136
Q

Features of autoimmune polyglandular syndrome

A

Hypoadrenal (autoantibodies to 21-OH)
Hypothyroid (autoantibodies to Anti-TPO)
Hypoovarian (ovarian autoantibodies)

Pathogenesis involves the failure of AIRE leading to auto reactive T-Cells escaping to the periphery

137
Q

ACTH levels for adrenal cause or pituitary/ectopic cause of Cushing’s syndrome

A

<1.1 = Undetectable = Adrenal

>3.3 - Pituitary/Ectopic cause

138
Q

Test to differentiate between pituitary and ectopic causes of cushings syndrome

A
High dose dexamethasone suppression test 
ACTH surpasses (>50%) = likely pituitary (as the pituitary tumours retain some features of normal regulation of ACTH secretion) 
ACTH not surpassed (<50%) = likely ectopic
139
Q

Next test if a pituitary source (cushings disease) is thought likely
i.e high cortisol –> ACTH high –> suppression with high dose dexamethasone –> MRI brain

A

Bilateral inferior petrosal sinus sampling with measurement of ACTH (unless MRI shows tutor >6mm)

139
Q

Next test if a pituitary source (cushings disease) is thought likely
i.e high cortisol –> ACTH high –> suppression with high dose dexamethasone –> MRI brain

A

Bilateral inferior petrosal sinus sampling with measurement of ACTH (unless MRI shows tutor >6mm)

140
Q

What hormones do each of the zones of the adrenal cortex produce

A

Reticularis: Androgens
Fasiculata: Cortisol
Glomerulosa: Mineralcorticoids

141
Q

Features of Conn’s Syndrome (Aldosterone producing adenoma)

A

Hypertension
Hypokalaemia
Low renin
Metabolic alkalosis (due to loss of H+ ions by the intercalated cells)

142
Q

Investigations for suspected hyperaldosteronism

A

Note: need to stop beta-blockers and diuretics for at least 4 weeks

1) Aldosterone Renin Ratio
2) Suppression test such as the saline infusion test or stimulation test with captopril
3) Adrenal CT
4) Adrenal Vein Sampling

143
Q

Initial treatment for phaeochromocytoma hypertension and tachycardi

A

1) Alpha Blocker: Phenoxybenamine preferred (non competitive alpha antagonist)
2) Beta blocker: Only to be commenced once alpha blocker started due to risk of precipitating unopposed alpha vasoconstriction

144
Q

Genetic conditions linked with phaecochromocytoma

A

1) VHL
2) MEN 2/Men 3
3) NF1

145
Q

Features consistent with an adrenal incidentaloma

A

Size: <4cm
Shape: Round with regular margins
Attenuation: Houndsfield units <10
Rapid washout of contrast: >50% at 10 minutes

146
Q

Which cells produce LH and FSH in males

A

LH “libido” –> Leydig cells –> Testosterone

FHS “sperm” –> Sertoli cells –> Spermatogensis

147
Q

Main benefit of testosterone treatment on young hypogonadal men?

A

Improved libido and erectile function (although erectile function not different from phosphodiesterase inhibitors).

148
Q

Congenital adrenal hyperplasia most common pathogenesis

A

AR inherited deficiency of 21-hydroxylasewhich results in impaired synthesis of cortisol and aldosterone and accumulation of 17-OH progesterone –> androgens

149
Q

Clinical features of 21-hydroxylase deficiency

A

Excess androgens: ambiguous genetalia in women, amenorrhea or hirsutism
Deficiency of mineralcorticoids: Salt wasting crisis and hypotension
Deficiency of glucocorticoids: Adrenal crisis

150
Q

Investigations and treatment for 21-Hydroxylase deficiency

A

Elevated 17-OH-progesterone levels (including after administration of ACTH)
Elevated renin levels

Treatment: Corticosteroid treatment and anti-androgens

151
Q

Features of Graves Disease on investigation

A
Clinical exam
- Diffuse goitre with bruit
- Opthalmopathy
- Pretibial myxodema
TSH receptor antibodies: elevated
Technetium 99 scan: Diffuse uptake
152
Q

Treatment options for Graves Disease

A

1) Symptom Control: Propanolol
2) Control Hyperthyroidism
- Thionamides: PTU or Carbimazole: Caution in those with LFT derrangements
- Radioactive Iodine: Caution in young women or those with eye disease
- Surgical resection:L Can lead to parathyroid injury and graves can recur if there is any remnant of disease

153
Q

Proposed pathogenesis of Graves orbitopathy

A

TSH receptors expressed on the surface of orbital fibroblasts –> Adipogenesis + Hyaluronic acid synthesis –> Expanded orbital muscles and adipose tissue

154
Q

Main adverse effects of the thionamides (PTU and carbimazole)

A

PTU: Fulminant inflammatory hepatitis (rare), Safe in first trimester of pregnancy
Carbimazole: Non threatening cholestasis. Not safe in the first trimester of pregnancy but can be used in the trimesters thereafter. Increased risk of alopecia cutis, Ompahloecele and other birth defects

155
Q

Graves orbitopathy risk factors for progression and treatment

A
Risk factors for progression
- Smoking
- Hypothyroidism from overtreatment with thionamides
- Radioactive iodine treatments 
Treatment 
- Ophthalmologist review: pulse steroids 
- Radiotherapy int he acute phase
- Debulking in the chronic phase
\+/- Selenium treatment
156
Q

What is thyrotoxic periodic paralysis?

A

Usually occurs in Asian individuals with thyrotoxicosis post high carbohydrate meal