Glomerular Disease Flashcards
Glomerular damage can be described in 4 ways:
1) focal (only some glomeruli)
2) diffuse (all glomeruli)
3) segmental (part of glomerulus)
4) global damage (all of glomerulus)
Minimal change
Most common nephrotic in children (and gen pop), commonly occurs in <10 years. Has heavy proteinuria, primary nephrotic. No change on LM, but EM shows podocyte effacement.
Generally idiopathic, but can be secondary to cancer, ifnection,NSAIDs, lymphoma. Responds well to steroids.
FSGS
Focal, so only some glomeruli, and segmental, so only part.
Primary nephrotic. on EM, podocyte effacement, but circulating factor also found. Sclerosis occurs (increased collagen deposit in mesangial matrix). More common in African pop. Less responsive to steroids. Affects children and adults. Can be secondary to HIV, sickle cell, heroin use and hypoxia inducing diseases. \
50% progress to RF
Membranous glomerulonephritis
Nephrotic. Most common cause of adult nephrotic. Has IgG and C3 involvement (deposits in subepithelial space (below podocytes) cause membrane thickening). Immune response against PLA2-R and antibodies collect in subepithelial space. May be secondary and associated with lymphoma, HIV and NSAIDs
Prognosis is 1/3 rules: 1/3 spontaenous remission, 1/3 persistent proteinuria (but stable), 1/3 progressive GFR loss and ESRF
Diabetes Melitus
Systemic nephortic. Microvascular disease, involves mesangial sclerosis (nodules) and BM thickening. Glycosylated proteins get stuck. EM shows thickened BM. IF shows linear IgG and glycosylated protein deposits. Leads to progressive proteinuria and progressive RF
IgA nephropathy
Most common nephritic. Idiopathic. Visible (sometimes invisible) haematuria - sometimes proteinuria but less than nephrotic. Association with mucosal infections. Mesangial expansion alters glomerulus shape (squashes capillary loops and reduces filtering area). IF shows IgA immunocomplexes in mesangium.Many patients progress to RF - no effective treatment
Acute Postinfectious Glomerulonephritis.
Uncommon. Post infection (1-4 weeks) IgG and C3 complexes form and deposit in mesangium and BM (subepithelial space)
Endothelial cell/mesangial cell proliferation/swelling - occludes lumen and allows RBC entry into filtrate. Monocytes and neutrophils enter filtrate.
Can occur post strep or mumps etc.
Symptoms include haematuria (cola colour), mild hypertension, oligouria and may have slight proteinuria.
More common in children, good prognosis, treat with Abx
Anti-glomerular BM disease
Damage to capillaries, targeted to BM of kidney (but can affect lung - goodpastures).
Autoantibodies recruit complement +lymphocytes, damaging capillaries. Proliferation+ accumulation in Bowman’s space (parietal epithelium)
- crescent accumulation. See antiGMB in GMB of capillaries on IF
Causes haematuria (and haemoptysis if lung too)
ANCA
Group of systemic disorders with nephortic presentation (Rapidly progressing glomerulonephritis - RPGN). HAs rapid GFR loss over 3 months, and often glomerular crescent formation.
Associated with anti-neutrophil cytoplasmic antibody (ANCA) - cytoplasmic so wont see on IF.
Treatable if caught earlySubtypes include Wagener’s disease (aka GPA -granulomatosis with polyangiitis)
Which glomerular diseases are crescent forming?
ANCA and Anti GBM
What expands in crescent forming?
Bowman’s parietal epithelium
Which conditions have both IgG and C3
Post infectious glomerulonephritis, membranous glomerulonephritis
Which conditions have Ig deposits
IgA (Ig A), DM (IgG), membranous glomerulonephritis (IgG and C3), Post infectious glomerulonephritis (IgG, C3)
Which conditions are more common in children?
Post infectious glomerulonephritis, miminal change
Which conditions are common in adults
Membranous glomerulonephritis, IgA
