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My MRCP > Nephrotic vs nephritic syndrome > Flashcards

Nephrotic vs nephritic syndrome Flashcards

1
Q

Nephrotic syndrome [3]

A

Failure of glomerular filtration barrier, injury to podocytes or slit diaphragm.
Reduced GFR with microscopic haematuria or red cell casts.
Increased risk of venous thrombosis, loss of anticoagulant factors

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2
Q

Nephrotic syndrome - why is there the increased risk of venous thrombosis

A

Loss of anticoagulant factors like antithrombin II in urine, increased platelet aggregation and endothelial dysfunction

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3
Q

Causes of nephrotic syndrome [9]

A
  • Minimal change disease.
  • FSGS.
  • Membranous nephropathy.
  • Mesangiocapillary GN (mixed)

Secondary
* HIV-associated nephropathy.
* Renal amyloidosis.
* Light chain deposition disease.
* SLE with type 5 lupus nephritis.
* Diabetic glomerulosclerosis.

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4
Q

Diagnosis of nephrotic syndrome [4]

A

Nephrotic syndrome is defined by:
1. Proteinuria >3.5 g/24 hours (equivalent to urine protein/creatinine ratio >350 mg/mmol).
2. Hypoalbuminaemia (<35 g/L).
3. Oedema.
4. Hyperlipidaemia/hypercholesterolaemia.

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5
Q

Management of nephrotic syndrome [4]

A
  • Salt and fluid restriction.
  • Loop diuretics.
  • Anti-proteinuric drugs: ACE inhibitors/angiotensin receptor blockers.
  • Anticoagulation in selected patients.
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6
Q

Acute nephrotic syndrome - minimal change disease
Management
Relapse

A

90% of children below 6
Normal glomerular appearance on light microscopy
Diffuse effacement of podocytte foot processes on electron microscopy

Management
- Steroid treatment is responsive in up to 90% of adults within 12 weeks
- Rate of relapse 50-75%

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7
Q

FSGS
Presentation
Name some mutations which are associated with steroid resistant nephrotic syndrome

A

Primary FSGS commonly presents with nephrotic syndrome, nephrotic- or sub-nephrotic-range *protein- uria.
Renal impairment and progression to ESRD are common.

Mutations in some podocyte proteins are associated with steroid-resistant nephrotic syndrome and childhood-onset FSGS, including NPHS1 (nephrin), NPHS2 (podocin), ACTN4 (alpha-actinin 4) and TRPC6. Afro-Caribbean people also have increased susceptibility to FSGS, either alone or in association with hypertension or HIV infection.

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8
Q

Describe causes of secondary FSGS

A

Secondary FSGS results from various kidney insults leading to a common pattern of glomerular injury related to haemodynamic stress and glomerular hyperfiltration.
Infections: HIV, malaria, parvovirus, schistosomiasis
Drugs: adriamycin, heroin, interferon alpha, lithium, pamidronate
Malignancies: HL and NHL
Npehron loss from surgical ablation, reflux nephropathy

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9
Q

Treatment approaches of secondary FSGS [2]

A

General management of nephrotic syndrome
Try to induce remission and reduce proteinuria initally with course of steroids
Usually relapse on steroids so need additional agent, cyclosporin.

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10
Q

Membranous nephropathy (MN)

A

Idiopathic MN - autoantibody against antigen M-type phospholipase A2 receptor
Secondary MN
- Autoimmune causes
- Infectious diseases
- Drugs
- Malignancy

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11
Q

Secondary membranous nephropathy

A
  • Autoimmune causes
    SLE
    RA
    Sarcoidosis
    Crohns disease
  • Infectious diseases
    Hepatitis B and C
    Syphilis
    Fliariasis, hydatid cysts, schistosomiasis
  • Drugs
    Gold, penicillamine
    NSAIDs
    Captopril
  • Malignancy
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12
Q

How is MN diagnosed on histology, light microscopy and electron microscopy?

A

Histologically immunoglobulin (usually IgG) and C3 deposition along the capillary walls or outer aspect of the GBM is evident.
Light microscopic features include thickening of the basement membrane and ‘spikes’ on silver staining
Sub-epithelial deposits are seen on electron microscopy.

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13
Q

Management of MN
Remission
Progression
Poor prognosticators
Management

A

Remission 30%
Progression 30%
Abnormal kidney function and heavy proteinuria (>10 g/ 24 hours), or persistent proteinuria >1 year after presentation

Treatment
- Immunosuppressive therapy - alternate steroids monthly and cyclophosphamide or chlorambucil

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14
Q

Mesangiocapillary GN or membranoproliferative GN

A

Conditions associated with a mesangiocapillary pattern of injury
1. Immune complex-mediated diseases
2. Complement mediated diseases
3. Conditions without immunoglobulin or complement deposition

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15
Q

Give 4 immune complex mediated diseases associated with mesangiocapillary pattern of injury

A

Chronic infections
Autoimmune diseases
Idiopathic
Paraprotein deposition diseases like light chain deposition or cryoglobulinemia

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16
Q

Give 4 complement mediated diseases associated with mesangiocapillary pattern of injury

A
  • Dense deposit disease (MCGN type II).
  • C3 glomerulopathy - partial lipodystrophy
  • Atypical haemolytic uraemic syndrome (HUS).
17
Q

Give 3 conditions without immunoglobulin or complement deposition that are associated with mesangiocapillary pattern of injury

A
  • Chronic and healed thrombotic microangiopathies.
  • Antiphospholipid syndrome.
  • Radiation nephritis.
18
Q

IgA nephropathy

A

IgA nephropathy is the commonest primary glomerulonephritis in the world. Peak incidence is in the sec- ond and third decades of life.
Tissue injury is caused by deposition of ab- normally glycosylated IgA immune complexes in the mesangium, subsequent mesangial cell activation, and cytokine and growth factor production.
Associations: liver cirrhosis, coeliac disease, IBD, rheumatic conditions, HSP

19
Q

IgA nephropathy
Presentation [4]

A
  • Asymptomatic microscopic haematuria ± mild proteinuria.
  • Recurrent macroscopic haematuria, typically within 1–3 days of an upper respiratory tract infection (‘sympharyngitic haematuria’).
  • CKD from longstanding undiagnosed disease.
  • Rarely, AKI with oliguria, which may be associated with a crescentic pattern of injury on biopsy.
20
Q

IgA nephropathy
Prognosis - risk of progression, predictors of esrd
Management [2]

A

Prognosis
* Most patients with isolated haematuria and no proteinuria have low risk of progression, while those with renal impairment at presentation, heavy proteinuria, or tubulo-interstitial fibrosis or glomerulosclerosis on biopsy are at risk of progressive renal impairment.
* Persistent proteinuria of >1 g/24 hours and/or hypertension carries a 50% risk of ESRD at 10 years.
Management
Supportive measures for all patients: * BP management.
* Renin-angiotensin system blockade with ACE-I or ARBs.

21
Q

Tubulo-interstitial kidney disease
Acute interstitial nephritis
Chronic tubule-interstitial kidney disease

A

Common causes of AIN [4]
- Drugs: antibiotics, NSAIDs, PPI, allopurinol, anti-retroviral
- Infections: asending pyelonephritis, TB, leptospirosis, Hanta virus
- Autoimmune disease
- Idiopathic

22
Q

In AIN, what is TINU syndrome

A

Tubulointerstitial nephritis + Uveitis

23
Q

AIN presentation
Biopsy in AIN will show
Treatment

A

AIN- fever, arthralgia, rash, eosinophilia, hypertension.
Investigations
sterile pyuria
white cell casts
If biopsied, characteristic features include an inflammatory cell infiltrate in the interstitium, which may be eosinophil-rich and include granulomata.

Treatment of drug-induced AIN is withdrawal of the likely agent, plus corticosteroid therapy if the AIN is severe (dialysis-dependent AKI) or if no improvement is seen 10 days after withdrawal of the inciting agent.

24
Q

Chronic tubule-interstitial kidney disease- how does it develop?

A

Untreated AIN, or prolonged exposure to the causative agent, can progress to chronic tubulo-interstitial disease. Histologically this is characterised by varying tubular atrophy, interstitial fibrosis and inflammation.

25
Q

Renovascular disease
Aetiology [2]
Presentation [4]
Ix [4]

A

50% of those atherosclerosis have renal artery stenosis
5% - caused by fibromuscular dysplasia
Hypokalaemia
Resistant to tx HTN
Progressive CKD - ischaemic nephropathy
Recurrent flash pulmonary oedema
Ix
Doppler
MAG3 (nuclear imaging) with captopril
CT/MR angio
Gold standard - DSA

26
Q

Management of renal artery stenosis

A

Management of cardiovascular risk factors
Definitive - angioplasty
Stenting may not improve BP control or preserve kidney function because atherosclerosis is a systemic process
Endovascular intervention is indicated in those with refractory HTN or rapidly declining kidney function

27
Q

Nephritic syndrome

Rapidly progressive glomerulonephritis - name 3 types

Also known as crescentic GN

A
  1. Type 1 linear
  2. Type 2 granular - immune complex mediated
  3. Type 3 pauci immune
28
Q

Name Type 1 RPGN

A
  • Goodpasture- Anti-GBM disease
29
Q

Name Type 2 Immune complex mediated RGPN

A
  • Post-streptococcal
  • Lupus class V
  • IgA nephropathy
  • Henoch schonlein purpura
30
Q

Name Type 3 RGPN (pauci-immune)

A
  • ANCA positive usually but non immune complex mediated, non anti-GBM
  • cANCA - Wegener
  • pANCA - eGPA
31
Q

Distinguish between Post-streptococcal and IgA nephropathy

A
32
Q

SLE nephritis
Describe 6 stages

A

WHO classification
class I: normal kidney
class II: mesangial glomerulonephritis
class III: focal (and segmental) proliferative glomerulonephritis
class IV: diffuse proliferative glomerulonephritis
class V: diffuse membranous glomerulonephritis
class VI: sclerosing glomerulonephritis

33
Q

Summary

A
34
Q

Describe the 6 stages of lupus nephritis

Which one is the most common form?

A

WHO classification
class I: normal kidney
class II: mesangial glomerulonephritis
class III: focal (and segmental) proliferative glomerulonephritis
**class IV: diffuse proliferative glomerulonephritis - most common!
**class V: diffuse membranous glomerulonephritis
class VI: sclerosing glomerulonephritis

35
Q

Lupus nephritis

Describe diffuse proliferative glomerulonephritis biopsy

A

Renal biopsy characteristically shows the following findings:
glomeruli shows endothelial and mesangial proliferation, ‘wire-loop’ appearance
if severe, the capillary wall may be thickened secondary to immune complex deposition
electron microscopy shows subendothelial immune complex deposits
granular appearance on immunofluorescence

36
Q

Pulmonary stenosis vs aortic stenosis murmur

A

Pulmonary stenosis
* ejection systolic murmur, loudest in inspiration

Aortic stenosis
* same murmur but louder on expiration

My MRCP (43 decks)

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