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GCUH FRACP Writtens 2020 > Renal > Flashcards

Renal Flashcards

1
Q

For diabetic patients receiving ACEi or ARB, how do they work?

A

Decreased afferent arteriole tone

Then

Decreased intraglomerular pressure

Then

Decreased GFR followed by stabilisation

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2
Q

Name 4 types of glomerular pathologies that arise from the trapping of circulating immune complexes?

A

Post-infectious

Membranoproliferative

Glomerulonephritis (chronic infection)

IgA nephropathy

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3
Q

Name 3 types of glomerular pathology that arise from in situ immune deposit formation from exogenous antigens.

A

Lupus nephritis

Post-infectious glomerulonephritis

Secondary membranous GN

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4
Q

Name two types of glomerular pathology that arise from in situ immune deposit formation from endogenous antigens.

A

Anti-GBM GN

Membranous

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5
Q

How is post-streptococcal GN treated?

A

Self-limiting

Clearance of infection = removal of circulating immune complexes

Of note - post-strep GN usually comes on 2 weeks or so after the infection; IgA nephropathy is more likely to be seen earlier on

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6
Q

What is the pathophysiology of post-streptococcal GN?

A

Activated immune-complexes and/or nephritogenic antigens circulating from strep infection

Attract and activate complement with injury as complexes contact endothelium - neutrophils recruited via chemotaxis

Proteases activated

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7
Q

What features would you see on microscopy for post-strep GN?

A

Diffuse endocapillary proliferation

“Hump” deposits

Effacement of podocyte foot processes

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8
Q

What is the pathophysiology of membranous GN?

A

Antibodies and complement inflict cytotoxic injury on the podocyte, resulting in a non-exudative non-proliferative capillary wall lesion

No influx of inflammatory cells or expansion of mesangium, but basement membrane is expanded

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9
Q

What features would you expect to see on microscopy for membranous GN? Name 2 features.

A

New basement

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10
Q

Which antibodies are implicated in primary membranous GN? Name 2.

A

Anti-PLA2R antibody - found on podocytes - 80% assoc with primary GN

IgG4 antibody specific for THSD7A (2-5%)

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11
Q

How is primary membranous GN treated?

A

1st line - steroid + cyclophosphamide based regimen

2nd line - ciclosporin if preserved eGFR, otherwise consider rituximab

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12
Q

In membranous GN, how many patients would be expected to have remission, and how many would progress to ESRD?

A

Spontaneous remission 5-20%

Partial remission 25-40%

ESRD

  • 14% at 5 years
  • 35% at 10 years
  • 41% at 15 years
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13
Q

Name two features in membranous GN that would suggest progress rather than remission in the future.

A

Heavy proteinuria

Renal dysfunction

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14
Q

What are the blood pressure and urine protein targets in membranous glomerulonephritis?

A

BP - 125/75

Urine protein - <1g/day

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15
Q

What drugs should be used in membranous GN to achieve BP/urine protein targets?

A

ACEi/ARB

Spironolactone

Loop diuretics +/- HCT

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16
Q

Membranous GN can pre-dispose to thrombotic events. Why is this, and how/when is this treated?

A

Loss of antithrombin III via urine

Warfarin if albumin <20; discontinue if albumin >20, or continue post-event for 3/12

No evidence for DOACs

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17
Q

What is the most common secondary cause of membranous GN, and how is it treated?

A

Malignancy

Treated by removal of tumour

Consider tumour work-up only if weight loss, +ve FOBT, anaemia etc.

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18
Q

What parameters are required for a diagnosis of nephrotic syndrome?

A

Proteinuria 3.5g/day

Albumin <30

Peripheral oedema

Assoc with raised protein:creatinine ratio, hyperlipidaemia and thrombotic disease

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19
Q

What are the BP and urine protein targets for IgA nephropathy?

A

BP - 130/80

Protein <1g/day

Use ACEi/ARB if protein >1g/day

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20
Q

For patients with persistent proteinuria in the context of IgA nephropathy, how should they be treated?

A

If proteinuria for 3-6 months without improvement - give steroids for 6 months

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21
Q

How should crescenteric rapid IgA nephropathy be treated?

A

Steroids + cyclophosphamide - however evidence is not great

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22
Q

Which glomerular pathologies are types of nephrotic syndome? Name 3.

A

Minimal change disease

Focal segmental glomerulosclerosis

Membranous GN

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23
Q

Which glomerular pathologies are types of nephritic syndome? Name 4.

A

IgA nephropathy

Lupus (most forms)

Pauci-immune

Anti-GBM

Post-strep

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24
Q

Which type of glomerular disease exhibits characteristics of both nephritic and nephrotic syndrome?

A

Membranoproliferative disorder (also known as mesangio-capillary GN)

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25
Q

What are the 4 different categories of mesangio-proliferative GN?

A

Immune-complex mediated MPGN

Complement-mediated MPGN/C3 glomerulopathies

Thrombotic microangiopathic MPGN

Idiopathic

Move away from type I and II; the first two are the main two categories, and C3 convertase is involved with both

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26
Q

Name 3 features you would expect to see on light microscopy with mesangio-proliferative GN.

A

Mesangial hypercellularity - mesangial cells and monocytes

Endocapillary proliferation - interpositioning of mesangial cell cytoplasm between GBM and endothelial cells

Thickened/double GBM due to complement (C3) deposition

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27
Q

Name 3 ways that immune-complex mediated MPGN can develop.

A

Chronic infection (hepatitis C, bacterial endocarditis)

Autoimmune (SLE, Sjogren’s, RA, mixed connective tissue disease)

Paraproteinaemias

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28
Q

Which gene/protein is implicated in congenital nephrotic syndrome?

A

NPHS1 - nephrin

No response to steroids

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29
Q

Which genes are implicated in familial FSGS?

A

NPHS2 - podocin

TRPC6

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30
Q

Name 5 causes of secondary focal segmental glomerulosclerosis.

A

Obesity

Heroin abuse

HIV

Malignancy

Loss of renal mass

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31
Q

Which receptor is found in elevated levels in patients with focal segmental glomerulosclerosis?

A

suPAR (serum soluble urokinase-type plasminogen activator receptor)

Found in 2/3s of FSGS patients

Renal disease only occurs when sufficient circulating suPAR activates podocyte B3 interim causing foot process effacement, proteinuria and FSGS-like glomerulopathy

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32
Q

Name 6 secondary causes of IgA nephropathy.

A

Alcoholic liver disease

Coeliac disease

IBD

Ankylosing spondylitis

Dermatitis heretofore is

Mycosis fungoides

Majority of cases are idiopathic

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33
Q

How many types of IgA are there, and which is typically implicated in IgA nephropathy?

A

IgA1 and IgA2

Glomerular deposition - polymeric IgA1

Bone marrow, lymph and spleen produce mainly IgA1. Plasma cells produce both.

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34
Q

What did the Stop-IgAN study look at, and what was the outcome?

A

Looked at immunosuppressive therapy to stop disease progression vs supportive care

No change in progression between groups, with much greater side effects in treatment arm - therefore intensive immunosuppressive regimens can not be recommended over and above maximal supportive care

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35
Q

Which epidemiological factors would predispose a patient towards developing lupus nephritis? Name 4.

A

Female

“Pigmented races”

Chinese

Polynesian

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36
Q

Name the 6 classifications of lupus nephritis.

A

I - minimal mesangial lupus nephritis

II - mesangial proliferative

III - <50% glomeruli (focal proliferative)

IV - >50% glomeruli (diffuse proliferative)

V - pure membranous

VI - advanced sclerosing

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37
Q

In lupus nephritis class III or IV (+/- V) disease in white or Asian populations, what are the stages of treatment?

A

Corticosteroids and MMF or reduced dose cyclophosphamide

If good response - maintenance with low dose steroids + MMF/azathioprine

If poor response - corticosteroids + high dose cyclophosphamide/rituximab/calcineurin inhibitor

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38
Q

In lupus nephritis class III or IV (+/- V) disease in black or Hispanic populations, what are the stages of treatment?

A

Corticosteroids + MMF

If good response - maintenance with low dose steroids + MMF/azathioprine

If poor response - Corticosteroids with high-dose cyclophosphamide/rituximab

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39
Q

In class V lupus nephritis with non-nephrotic range proteinuria, what is the treatment?

A

ACEi/ARB

40
Q

In class V lupus nephritis with nephrotic-range proteinuria, what are the treatment stages?

A

Corticosteroids and cyclophosphamide/MMF/azathioprine/calcineurin inhibitor

Maintenance immunosuppression with low-dose corticosteroids and MMF/azathioprine/calcineurin inhibitor

ACEi/ARB

41
Q

What 3 types of medication should be given in lupus nephritis as non-immunosuppressive therapy, and for what reason?

A

Antihypertensives

Lipid-lowering therapy

Anti-coagulation

Consider the above given increased risk of cardiovascular disease

42
Q

What are the 3 classifications of cryoglobulinaemia?

A

Type 1 - single monoclonal - haem malignancies

Type 2 - monoclonal antibody against polyclonal IgG (Hep C)

Type 3 - polyclonal antibodies

43
Q

How are factor H mutations involved in C3 nephropathies?

A

Factor H restrains complement activation on host surfaces that do not express other complement regulators, including exposed GBM (which express glycoaminoglycans) - endothelium is fenestrated.

44
Q

What association does C3 nephritic factor have with regard to adipocytes?

A

Partial lipodystrophy

45
Q

Name 6 triggers for atypical HUS?

A

Toxins

Infection

Pregnancy

Malignancy

Drugs

Malignancy hypertension

46
Q

Name 3 factors that may predispose towards atypical HUS.

A

Mutations in factor H, predominantly at C terminal

Autoantibodies binding to C terminal epitomes

C3 mutations prevent factor H binding

47
Q

What are the treatment options available for HUS? Name 4.

A

Eculizumab (complement inhibitor)

Plasma exchange

FFP

Transplantation (delay by 6 months following resolution of TMA and extra-renal manifestations)

48
Q

Name 2 diseases that polyarteritis nodosa is classically associated with.

A

Hepatitis B

Hepatitis C

49
Q

Which HLA allele is PR3 ANCA associated with?

A

HLA-DP

50
Q

Which genes is PR3 ANCA associated with?

A

SERPINA1 (a1 antitrypsin)

PRTN3 (proteinase 3)

51
Q

Which HLA allele is MPO ANCA associated with?

A

HLA-DQ

52
Q

PR3-ANCA is associated with which vasculitis?

A

Granulomatosis with polyangiitis

PR3-ANCA = c-ANCA

53
Q

MPO-ANCA is associated with which vasculitis?

A

Microscopic polyangiitis

54
Q

What immunosuppressive therapy is provided to patients receiving a renal transplant?

A

Induction - IL-2 monoclonal, polyclonal

Maintenance therapy

  • ciclosporin or tacrolimus
  • MMF or azathioprine
  • prednisolone
55
Q

What is betalacept, and how does it work?

A

Costimulation blocker binding to CD 80/86 on the APC

Prevents T cell activation

56
Q

In which patients is betalacept contraindicated, and why?

A

Patients who are EBV seronegative

10x increased risk of lymphoma

57
Q

What is the treatment for acute rejection in renal transplant patients?

A

Methylprednisolone 500mg-1g daily for 3 doses

Rescue dose MMF

Change ciclosporin to tacrolimus

Antithymocyte globulin

If antibody mediated, rituximab/PEx/IVIG

58
Q

What is the main factor resulting in patients requiring renal replacement therapy?

A

Diabetes

59
Q

Name 5 factors relating to mineral metabolism that can increase CVD risk in CKD patients.

A

FGF 23 mediated

Increased calcium and phosphate

Hyperparathyroidism

Vitamin D insufficiency

Vascular calcification

60
Q

What is the main factor resulting in patients requiring renal replacement therapy?

A

Diabetes

61
Q

Name 5 factors relating to mineral metabolism that can increase CVD risk in CKD patients.

A

FGF 23 mediated

Increased calcium and phosphate

Hyperparathyroidism

Vitamin D insufficiency

Vascular calcification

62
Q

Name 4 mechanisms that contribute towards having HTN in the setting of CKD.

A

Inability to excrete Na load with Na retention

RAAS activation

Increased sympathetic neural activity

Altered auto regulation of vascular factors

63
Q

What is the most potent predictor of ESKD and renal death?

A

Proteinuria

64
Q

What level of protein has been shown to potentially slow progression on CKD, and what level has been shown to increase mortality?

A
  1. 8g/kg/day may slow progression

0. 6g/kg/day increases mortality

65
Q

Name 5 factors that stimulates osteoblasts and osteocytes to secrete FGF23.

A

Increased dietary phosphate intake (mechanism unclear)

Increased 1,25 dihydroxyvitamin D

Increased parathyroid hormone

Less in response to high calcium

Possible response to iron deficiency

66
Q

What does FGF23 do?

A

Stimulates phosphaturia by down-regulating sodium phosphate co-transporters (proximal tubule)

Reduced 1,25 vit D by directly inhibiting 1a hydroxylase (renal) and stimulating 24 hydroxylase (catabolic)

Directly inhibits PTH secretion

67
Q

What happens to FGF32 in CKD?

A

FGF23 is progressively elevated in CKD to compensate for persistent phosphate retention

This is the driver for increased PTH secretion in CKD

68
Q

Name 5 methods of managing bone disease in ESKD

A

Optimise dialysis

Phosphate binders - non-calcium assoc with reduced mortality compared to calcium-containing binders

Vitamin D (1,25 vit D analogues effectively control PTH)

Calcimimetics

Bicarbonate (?)

69
Q

What is the target Hb for CKD?

A

Hb 110

Hb >125-130 in CKD is associated with increased CV mortality and stroke

70
Q

How does smoking impact upon overall survival and graft loss post-transplant?

A

2 x risk of graft loss

Half the overall survival

71
Q

What is the most common side effect of EPO?

A

Hypertension

72
Q

What type of cancer should be screened for more commonly in transplant patients?

A

Skin cancers, particularly SCC and BCC

73
Q

Name 2 phosphate binders you may consider using in a dialysis patient with high adjusted Ca and PO4.

A

Sevelamer

Lanthanum

74
Q

What accounts for the majority of deaths in haemodialysis patients over the age of 75?

A

Withdrawal of haemodialysis

75
Q

Name 7 indications for dialysis that are not considered absolute indications (in otherwise appropriate patients).

A

Declining nutritional status

Persistent or difficult to treat volume overload

Fatigue with no other reversible contributory pathologies

Mild cognitive impairment

Refractory acidosis

Refractory hyperkalaemia

Refractory hyperphosphataemia

76
Q

Name 3 absolute indications for dialysis

A

Uraemic pericarditis

Uraemic pleuritis

Uraemic encephalopathy

77
Q

Contraindications to living kidney donation include being incapable of making a decision (e.g. minor), coercion, illegal financial exchange and the hospital’s discretion. Name 6 others.

A

Uncontrolled HTN/history of HTN with end-organ damage

HIV infection

Diabetes mellitus

Active/incompletely treated cancer

Evidence of acute symptomatic infection

Uncontrolled, diagnosable psychiatric conditions

78
Q

Name 6 opportunistic infections that are most likely to occur after 6 months post-renal transplant.

A

Aspergillus

Nocardia

BK virus (polyoma)

Herpes zoster

Hepatitis B

Hepatitis C

79
Q

What histological features would you expect to see with lupus nephritis? Name 6.

A

Subendothelial immune deposits/wire loops

Hypercellularity

Leukocyte infiltration

Fibrinogen necrosis

Hyaline thrombi

Crescents in severe LN

80
Q

Name 6 opportunistic infections that are most likely to occur before 6 months post-renal transplant.

A

PJP

CMV

Legionella

Listeria

Hep B

Hep C

81
Q

Name 5 (groups of) drugs that can be cleared via dialysis.

A

“BLAST”

Barbiturates

Lithium

Alcohol

Salicylates

Theophylline

82
Q

What is the most sensitive and reliable indicator of possible rejection in renal transplant patients?

A

Rise in serum creatinine

83
Q

For patients looking to become pregnant who are on MMF for lupus nephritis, how should this be managed?

A

MMF should be changed to azathioprine 6 weeks prior to conception

84
Q

A prolonged course of immunosuppression in lupus nephritis helps to reduce relapse rates. How long should this be for?

A

> 2 years

85
Q

Which immunoglobulins/complement constituents could you expect to see deposits of in proliferative lupus nephritis?

A

IgG

C1q

C3

IgA

IgM

“Full house”

86
Q

Name 3 indications for PLEX in ANCA-positive vasculitis

A

Pulmonary haemorrhage

Anti-GBM

Haemoptysis

87
Q

In AKI, in which two areas are cells particularly affected?

A

Proximal convoluted tubule - high metabolic rate due to ion transport

S3 segment of nephron in outer stripe of medulla

88
Q

Name 6 potential markers for tubular injury besides Cr in AKI.

A

Cystatin-C - made by all cells, 90% filtered by glomeruli then reabsorbed PCT; better than Cr for estimations in patients with low muscle mass

NGAL - gives early diagnosis and predicts sustained AKI

IL-18

KIM-1

TIMP-2

IGFBP7

Top 2 are the important ones

89
Q

What is used for prevention and treatment in hepatorenal syndrome?

A

Prevention - IV albumin

Treatment - terlipressin

However, definitive management is liver transplantation

90
Q

What are the chromosomes and proteins associated with autosomal dominant polycystic kidney disease 1 and 2 respectively?

A

ADPKD1 - chromosome 16, polycystin 1

ADPKD2 - chromosome 4, polycystin 2

ADPKD1 is associated with more rapid decline

91
Q

As well as the kidneys, in which 4 other organs can polycystin be found?

A

Liver

Heart

Brain

Lung

92
Q

If patients have a positive family history for ADPKD, what are the criteria on imaging required in order to make a diagnosis?

A

Aged 15-40 - 3 or more cysts unilaterally or bilaterally

Aged 40-59 - 2 or more cysts in each kidney

Aged 60 and above - 4 or more cysts in each kidney

93
Q

What type of antibiotics should be used in patients with ADPKD and UTIs?

A

Fluoroquinolones - good cystic penetrance

94
Q

Name 2 cardiac complications associated with ADPKD.

A

Mitral valve prolapse

Aortic incompetence

95
Q

When should patients with ADPKD be screened for cerebral aneurysms?

A

FHx of cerebral aneurysms

High risk professions

Headache

GCUH FRACP Writtens 2020 (14 decks)

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