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