Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

year 2 renal > Glomerular Disease (Clinical) > Flashcards

Glomerular Disease (Clinical) Flashcards

1
Q

Glomerulonephritis:

  • Immune-mediated disorders that affect the ________
  • Responsible for around ___ of end-stage kidney disease
  • Classified based on kidney _____ findings
A

glomeruli

15%

biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are podocytes?

A

Podocytes are cells in the Bowman’s capsule in the kidneys that wrap around capillaries of the glomerulus. Podocyte cells make up the epithelial lining of Bowman’s capsule, the third layer through which filtration of blood takes place

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the features of glomerulonephritis?

A
  • Haematuria (non-visible or visible)
  • Proteinuria (low grade or nephrotic)
  • Hypertension
  • Renal impairment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 2 different kinds of glomerulonephritis?

A

Nephritic state

Nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Nephritic state?

A
  • Active urine sediment: haematuria, dysmorphic RBCs, cellular casts
  • Hypertension
  • Renal impairment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is nephrotic syndrome?

A
  • Oedema
  • Nephrotic range proteinuria: >3.5g/day or 350mg/mmol creatinine
  • Hypoalbuminemia: serum albumin <35g/L
  • Dyslipidemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

name A

A

Nephrotic state

podocytes not there and wide spaces and albumin come out and not as much RBC come out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name B

A

Nephritic state

an influx of white cells and it inflicts damage and destruction of endothelial membrane and this leads to leukocytes and a lot of RBCs to go out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is A?

A

Proliferative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is B?

A

Non-proliferative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the difference between a diffuse and focal pathology?

A
  • Diffuse: >50% of glomeruli affected
  • Focal: <50% of glomeruli affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the difference between global and segmental pathology?

A
  • Global: all the glomerulus affected
  • Segmental: part of the glomerulus affected

(global top picture and segmental bottom)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

name A

A

Nephrotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

name B

A

Nephritic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Is Nephrotic proliferative or non-proliferative?

A

Non-proliferative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Is Nephritic proliferative or non-proliferative?

A

Proliferative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are examples of non-proliferative glomerulonephritis?

A

Minimal change disease

Membranous nephropathy

FSGS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are examples of proliferative glomerulonephritis?

A

Mesangioproliferative GN

Membranoproliferative GN

Diffuse proliferative GN

Crescentic GN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Commonest cause of glomerulonephritis world-wide is what?

A

IgA nephropathy

Characterized by IgA deposition in the mesangium +mesangial proliferation

Most common in 2nd and 3rd decade of life with males more commonly affected

Up to 30% of cases can progress to end stage kidney disease or halving eGFR at 10 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the presentation of IgA nephropathy?

A
  • Microscopic haematuria
  • Micoscopic haematuria + proteinuria
  • Nephrotic syndrome
  • IgA crescentic glomerulonephritis

(top is most common and bottom is leasT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Case 1:

  • 30 male referred to the renal clinic by GP for incidental microscopic haematuria
  • BP 150/90 mmHg
  • Creatinine 80 µmol/L, eGFR>60 ml/min/1.73m2
  • Urine dip: RBC+++, Protein ++
  • Urine protein creatinine ratio=180mg/mmol creatinine
  • Renal US: normal kidney size with no structural abnormalities

What happens next?

A
  • You decide to start ACE-I
  • You also decide to perform a renal biopsy
  • Renal biopsy confirms IgA nephropathy

Reduce proteinuria and tightly control BP

  • At 5 years: serum creatinine 210 µmol/L and eGFR 32 ml/min/1.73m2
  • 10 years later, serum creatinine 480 µmol/L and eGFR 14 ml/min/1.73m2
  • Brother considered as kidney donor for living kidney transplantation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Post-streptococcal/Post Infectious glomerulonephritis

A

Follows 10-21 days after infection typically of throat or skin

Most commonly with Lancefield group A Streptococci

Genetic predisposition: HLA-DR, -DP, -DP

23
Q

Case 2:

  • Six-year-old boy brought to GP generally unwell, dark urine
  • Puffy face, no rashes no oedema, BP 135/86mmHg
  • Sore throat 2 weeks previously
  • Presumptive diagnosis _________________

What investigations owuld be done and what treatments would be carried out?

A

post-streptococcal nephritis

investigations

  • Hb 130g/L; WCC 11.3 x 109
  • Urea 11.2mmol/L, creatinine 160mmol/L
  • Urine microscopy RBC +++, casts +
  • Complement: low C3

Treatment:

  • Antibiotics for infection, debatable
  • Loop diuretics such as frusemide for oedema
  • Anti-hypertensives e.g. vasodilator drugs
24
Q

What is Crescentic glomerulonephritis?

A

Crescentic glomerulonephritis is characterized by the presence of extensive glomerular crescents (usually greater than 50%) as the principal histologic finding. Because it often clinically presents with a rapid decline in kidney function, it is also known as rapidly progressive glomerulonephritis

25
Q

What are the different types of crescentic glomerulonephritis?

A
26
Q

Case 3:

  • 60-year-old woman presents to GP with three-month history of increasing tiredness, anorexia and weight loss
  • Physical examination revealed a rash on both ankles and lower legs, and bilateral basal crepitations: BP 150/85 mmHg
  • Urine dipstick: protein+++ and blood++
  • Serum creatinine 640 µmol/L, eGFR 8 ml/min/1.73m2

What is this and what is the treatment?

A
  • Anti-neutrophil cytoplasmic antibodies positive with MPO-ANCA of >134 units/L
  • Renal biopsy - Focal necrotizing glomerulonephritis
  • Treatment:
  • High dose steroids
  • Cyclophosphamide
  • Plasma exchange
27
Q

What is Anti-GBM disease?

A
  • Rare disease caused by circulating anti-GBM
  • Around 10-20% of crescentic glomerulonephritis

Presents as:

  • Nephritis (anti-GBM glomerulonephritis)
  • Nephritis+ lung haemorrhage (Goodpasture’s syndrome)
  • Two peaks: 3rd decade and 6th/7th decade
28
Q

how doyu diagnose Anti-GBM disease?

A

Diagnosed by demonstrating anti-GBM antibodies in serum and kidney

29
Q

What si the treatment of Anti-GBM disease?

A

aggressive immunesuppression: steroid, plasma exchange, and cyclophosphamide

30
Q

Summary - Proliferative glomerulonephritides

  • Present with _______ state - Haematuria + variable proteinuria + hypertension +/- renal impairment
  • Can cause rapid decline in renal function leading to _______
  • Early diagnosis is necessary to save ________ - _______ _______+ __________ ______ + _____ _______
A

nephritic

dialysis

nephrons

Clinical suspicion + immunology screen + renal biopsy

31
Q

onto Non-proliferative

A
32
Q

what is seen in Non-proliferative Glomerulonephritis?

A
  • Minimal Change Disease
  • Focal and segmental glomerulonephritis
  • Membranous Nephropathy
33
Q

WHat are the 2 types of Nephrotic syndrome management?

A

general measrues

specific therpay

34
Q

What are some general measures for Nephrotic syndrome management?

A

Treat oedema: salt and fluid restriction and loop diuretics

Hypertension: use Renin-Angiotensin-Aldosterone-blockade

Reduce risk of thrombosis: Heparin or Warfarin

Reduce risk of infection e.g. pneumococcal vaccine

Treat dyslipidemia e.g. statins

35
Q

nephrotic syndrome management - Specific therapy towards cause of the ______________

A

non-proliferative glomerulonephritis

36
Q

What is Minimal Change Disease and what does it cause?

A
  • Commonest form in children
  • Sudden onset of oedema – days
  • Complete loss of proteinuria with steroids
  • Relapse occurs in two thirds of patients

a kidney disease in which large amounts of protein is lost in the urine. It is one of the most common causes of the Nephrotic Syndrome (see below) worldwide

37
Q

what is the treatment of minimal change disease?

A
  • Prednisolone – 1mg/kg for up to 16 weeks
  • Once remission achieved , slow taper over 6 months
  • Initial relapse treated with further steroid course
  • Subsequent relapses treated with:
  • Cyclophosphamide
  • Cyclosporin
  • Tacrolimus
  • Mycophenolate mofetil
  • Rituximab
38
Q

what is the prognosis of minimal change disease?

A

Despite relapsing behaviour, prognosis is favourable

Risk of end stage kidney disease is low

Steroids toxicity as multiple exposure

39
Q

Case 4:

  • 22-year-old woman presents with bilateral leg oedema which has developed suddenly over a week
  • She also describes breathless and chest pain
  • Urine dip ++++ protein

what investigations would be carried out?

A

Urine protein creatinine ration 400mg/mmol.

Creatinine 60 mmol/l and eGFR of >60 ml/min/1.73m2

Serum Albumin 15 g/L

Haemoglobin 154 g/L

Cholesterol 9.2 mmol/l

Pregnancy test negative

40
Q

What is the treamtent and prognosis of case 4?

A
  • Salt and fluid restrictions
  • Daily weights
  • Loop diuretic e.g. Furosemide
  • Thromboprophylaxis e.g. low molecular weight heparin
  • Prednisolone 60 mg per day
  • Achieved remission after 8 weeks of treatment
  • Diuretics and thromboprophylaxis stopped
  • Prednisolone dose tapered over 6 months
41
Q

What is Focal and segmental glomerulonephritis?

A

Is not a single disease, rather a syndrome with multiple causes

Presents with nephrotic syndrome

Pathology reveals focal and segmental sclerosis with distinctive patterns e.g.

tip lesion, collapsing, cellular, perihilar, and not otherwise specified

42
Q

FSGS can be caused by what 2 main ways?

A

Primary (idiopathic) or secondary

43
Q

FSGS is resistant to what type of treatment?

A

Generally steroid resistant

44
Q

FSGS has a high chance of progression to what?

A

High chance of progression to end stage kidney disease

45
Q

What is the treatment of FSGS?

A

General measures, as previously described

Trail of steroids, positive response , even partial remission, carries better prognosis

Alternative options: cyclosporin, cyclophosphamide, and Rituximab

46
Q

Case 5:

  • 34-year-old man presented with severe oedema which developed over 3 weeks
  • Investigations:
  • Urine PCR 560mg/mmol creatinine
  • Serum albumin 18 g/L
  • Serum creatinine 130 µmol/L, eGFR 56 ml/min/1.73m2

•Renal biopsy showed FSGS

What is the treatment and prognosis?

A
  • Diuretics helped to reduce oedema
  • Prednisolone - no response
  • Trial of cyclosporin – progressively rising serum creatinine
  • Serum creatinine at 280 µmol/L and eGFR 26 ml/min/1.73m2 at 8 months from presentation
  • At 18 months serum creatinine 540 µmol/l and eGFR 11 ml/min/1.73m2
  • Pre-emptive renal transplantation from brother, early recurrence post-transplant
  • Plasma exchange and Rituximab
  • Remission at 3 months post-transplant with serum creatinine 80µmol/L and normal serum albumin
47
Q

What is Membranous Nephropathy?

A

deposition of immune complexes on the glomerular basement membrane (GBM) with GBM thickening

Commonest cause of nephrotic syndrome in adults

48
Q

Membranous Nephropathy is mainly caused by what?

A

Majority of cases occur in isolation (idiopathic)

49
Q

What are serological markers for Membranous Nephropathy?

A
  • Anti-phospholipase A2 receptor (PLA2R) antibody positive in 70% of idiopathic cases
  • Thrombospondin type 1 domain containing 7A (THSD7A) in ~2%
50
Q

What are secondary causes of Membranous Nephropathy?

A

Secondary causes include:

  • Malignancies
  • SLE
  • Rheumatoid arthritis
  • Drugs: NSAIDs, gold, penicillamine
51
Q

WHat is Membranous nephropathy-treatment

A
  • General measures for at least 6 months
  • Immunesuppression if symptomatic nephrotic syndrome, rising proteinuria or deteriorating renal function
  • Cyclophosphamide and steroids (alternate months) for 6 months
  • Tacrolimus
  • Rituximab
52
Q

What is Membranous nephropathy
Prognosis?

A
  • Resolves spontaneously in a third.
  • Prognosis good in treated patients whose proteinuria resolves
  • About 25% are on dialysis at 10 years
  • Can recur in renal transplants
53
Q

Case 6:

  • 66-year old man presented with cough, breathlessness, and peripheral oedema
  • He smokes 20 cpd
  • Urine dip: Proteinuria ++++
  • Urine protein creatinine ration 580mg/mmol
  • Serum albumin 20 g/L
  • Serum creatinine 135mmol/l
  • Renal biopsy: confirms ____________________

what happens next?

A

confirms membranous nephropathy

  • CT chest/abdomen/pelvis: suggestive of lung cancer
  • Bronchoscopy and biopsy confirm squamous cell carcinoma
  • General measures for nephrotic syndrome
  • No immunesuppression
  • At 3 months: partial remission following radiotherapy
54
Q

Summary - Non-proliferative glomerulonephritis:

  • Present with ________ syndrome
  • Renal ______ is key investigation
  • Identify _____, if possible
  • _______ measures are important in all cases
  • ________ treatment as appropriate
A

nephrotic

biopsy

cause

General

Specific

year 2 renal (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions