Nephro: Primary Glomerulonephritis

Question 1

why is treating glomerulonephritis important?

Answer 1

• common cause of CKD

- there is an increasing incidence, poor outcomes and high associated costs

Question 2

which aspects of GN vary among populations?

Answer 2

• aetiology of GN

- presentation of GN

Question 3

2 main types of GN

Answer 3

• proliferative

- non-proliferative

Question 4

types of non-proliferative GN

Answer 4

• minimal change GN
• focal segmental glomerulosclerosis
• membranous GN

Question 5

types of proliferative GN

Answer 5

• IgA nephropathy
• rapidly progressive glomerulonephritis (vasculitic disorders and goodpasture’s syndrome)
• membranoproliferative GN
• post-infectious GN

Question 6

what is minimal change disease

Answer 6

• disease which presents with very mild glomerular abnormalities
• aka lipoid nephrosis

Question 7

causes of minimal change disease

Answer 7

• NSAIDs use

- Hodgkin’s lymphoma

Question 8

management of minimal change disease (initial episode)

Answer 8

• high-dose corticosteroids (4-16 weeks max)
• after achieving remission, taper steroids over 24w
• if steroids are contraindicated, use cyclophosphamide or calcineurin inhibitors

Question 9

management of frequently-relapsing/steroid-dependent MCD?

Answer 9

• oral cyclophosphamide for 8-12w
• CsA
• if intolerant of cyclophosphamide, use MMF

Question 10

management of corticosteroid-resistant MCD

Answer 10

• re-evaluate patients for other causes of nephrotic syndrome
• consider a repeat renal biopsy. which can reveal FSGS pathology

Question 11

what is FSGS?

Answer 11

focal segmental glomerulosclerosis

Question 12

what happens in FSGS?

Answer 12

• sclerosis of portions of the glomeruli
• consolidation of the tuft
• increased matrix
• accumulation of plasma proteins
• podocyte foot process effacement
• possible podocyte detachment

Question 13

causes of FSGS?

Answer 13

• primary (idiopathic)
• secondary causes
• • familial
• • virus-associated (HIV1, parvovirus B19)
• • drug-induced
• • adaptive (either from a low renal mass or initially normal renal mass)

Question 14

conservative treatment for FSGS?

Answer 14

• blood pressure control
• RAAS inhibition
• sodium restriction
• diuretics
• CKD management
• monitor proteinuria

Question 15

what is IgA nephropathy?

Answer 15

mesangial deposition of IgA; there are codeposits of IgG and complement

• Berger’s disease
• serum IgA levels not diagnostic

Question 16

what is the pathogenesis of IgA nephropathy?

Answer 16

exaggerated mucosal IgA response w abnormal glycosylation of IgA –> abnormal circulating IgA complexes –> trapped in mesangium

Question 17

what is Henoch-Schonlein purpura?

Answer 17

• IgA mediated systemic disease/vasculitis

- skin, kidney, GI involvement (rash and belly pain, more nephritic syndrome or RPGN)

Question 18

antiproteinuric and antihypertensive therapy for IgA nephropathy

Answer 18

• ACEi/ARB treatment used in patients with proteinuria >0.5g/d/1.73m2
• target BP - 125/75 for >1g/d patients and 130/80 for <1g/d

Question 19

what therapy is used if antiproteinuric/antihypertensive therapy fails to control IgA nephropathy?

Answer 19

6-month course of corticosteroid therapy if 3-6 months of supportive care failed and the patient has a GFR >50mL/min

Question 20

what treatment can be given to all patients with GN?

Answer 20

• BP control
• ACEi/ARB
• statin
• tonsillectomy if recurrent tonsillitis
• fish oils

Question 21

what is membranous nephropathy?

Answer 21

• subepithelial immune deposits of IgG and complement
• can be idiopathic or secondary
• primary cause of nephrotic syndrome in adults

Question 22

what are the 2 main causes of secondary membranous nephropathy?

Answer 22

• autoimmune

- infection

Question 23

clinical picture in primary MN

Answer 23

• renal biopsy: epimembranous deposits, containing IgG
• no recognisable underlying disease (autoimmune, heavy metal exposure and neoplasia)
• normal serum C3-C4 concentration