GN Flashcards
Where does HSP appear?
Extensor surfaces, buttocks
Nephrotic syndrome
Hypoalbuminaemia
Proteinuria >3g/day
Oedema (peripheral, facial)
Hypercholesterolaemia
Nephritic syndrome
Oedema (pulmonary) AKI Oliguria HT Active urinary sediment (RBCs, granular casts, proteinuria) - Post strep GN
GN can present in 2 ways:
Chronic GN - most common cause of ESRF after diabetes
Acute GN - treatable cause of AKI
How is the glomerulus damaged?
Immune mediated with secondary tubulointerstitial damage
Humoral mediated - antibodies
Cell mediated - T cells, inflamm cells, complement
Damage to endothelial or mesangial cells leads to:
Proliferative lesion
Haematuria
Damage to epithelial or podocytes leads to:
Non-proliferative lesion
Proteinuria
Diagnosis of GN
Clinical Bloods Urinalysis Urine microscopy - casts, RBCs Urine protein:creatinine ratio Biopsy
Microalbuminuria
30-300mg/day
Asymptomatic proteinuria
Less than 1g/day
Heavy proteinuria
1-3g/day
Nephrotic proteinuria
More than 3g/day
Dysmorphic RBCs
From UUT
Red cells escaping GBM = squished
Isomorphic RBCs
From LUT
Round
Red cell casts
Always pathological
Nephritic syndrome
Is nephrotic syndrome proliferative or non-proliferative?
Non-proliferative = proteinuria
Damage to podocytes/epithelium
Complications of nephrotic syndrome
Infection Renal vein thrombosis PE Volume depletion Vit D deficiency Sub-clinical hypothyroid
Is nephritic syndrome proliferative or non-proliferative?
Proliferative = haematuria
Damage to endothelium/mesangial cells
Focal GN
less than 50% affected
Diffuse GN
> 50% affected
Global GN
All of glomerulus affected
Segmental GN
Part of glomerulus affected
Crescents
Extra-capillary proliferation of inflammatory cells in Bowman’s space, e.g. RPGN in vasculitis, due to break in GBM from ANCA = compression and ischaemia
Non immunosuppressive treatment of GN
Anti-HT (aim for 130/80 or 120-75 for proteinuria) ACEI/ARB Diuretic Statin Anticoag/aspirin Omega 3/fish
Immunosuppressive treatment of GN
Steroids
Azathioprine
Alkylating agents (cylcophosphamide/chlorambucil)
Calcineurin inhibitors (tacrolimus/cyclosporin)
Mycophenolate
Plasmapheresis
IV IG, MABs
Treatment of nephrotic syndrome
Fluid and salt restriction Diuretic ACEI/ARB Anticoagulant IV albumin (if low volume) Steroids + another immsup agent
Types of primary idiopathic GN
Minimal change GN FSGS Membranous GN Membranoproliferative GN IgA nephropathy RPGN
Minimal change GN
Commonest cause of nephrotic syndrome in kids
Non-proliferative - podocyte side
Does NOT cause progressive renal failure
IL-13
Biopsy of minimal change GN
Normal on LM and IF
Foot process fusion on EM
Treatment of minimal change GN
Steroids
Cyclophosphamide/MAB
FSGS
Commonest cause of nephrotic syndrome in adults
Primary (most common) or secondary to HIV/heroin/obesity/reflux
Non-proliferative - podocyte side
50% progress to ESRF after 10 years
suPAR
Biopsy of FSGS
FSGS on LM
Ig/Complement deposition on IF
Podocyte effacement
Treatment of FSGS
Steroids
LT calcineurin inhibitors
Membranous GN
2nd commonest cause of nephrotic syndrome in adults
Primary or secondary to Hep B/carcinoma/lymphoma/SLE/CTD
30% progress to ESRF after 10 years
Anti-PLA2r Ab
Non-proliferative = podocytes
Biopsy of Membranous GN
Immune complex deposition in basement membrane on LM
Thickened BM
Treatment of Membranous GN
Steroids
Alkylating agents (cyclophosphamide)
MABs
IgA nephropathy
Commonest GN in the world Broad spec (microhaematuria and
What is IgA nephropathy associated with?
Colitis, arhtritis, HSP
Biopsy of IgA nephropathy
Mesangial cell proliferation and expansion on LM
IgA deposits in meseangium on IF
Increased inflammatory cells
Treatment of IgA nephropathy
BP control
ACEI/ARB
Fish oil
RPGN
Treatable cause of AKI
Rapid deterioration over days/weeks
Urinary sediment (RBCs, casts) and crescents
ANCA positive RPGN
Vasculitis
GPA
MPA
ANCA negative RPGN
Goodpasture’s
HSP
SLE
Treatment of RPGN
Prompt immunosuppression: steroids, aza/cyclophosphamide/mycophenolate, MAB
Plasmapheresis
Supportive dialysis
