Glomerulonephritis Flashcards
What is glomerulonephritis?
Inflammatory diseases involving the glomerulus and tubules of the kidney
May be primary or secondary
What are the mesangial cells of the kidney?
Modified smooth muscle cells.
Capable of contraction to regulate the blood flow and decrease the surface area of the basement membrane (decrease GFR)
Produce the mesangial matrix for structural support of the capillaries in the glomerulus
Describe what structures filtrate have to pass through to get from the blood into the tubules.
Fenestrated capillary membrane (endothelium)
Glomerular basement membrane
Podocyte (epithelial cell)
What are the two categories of pathological mechanisms that can cause glomerulonephritis?
Extrinsic mechanisms
Intrinsic mechanisms
By what extrinsic mechanisms can glomerulonephritis be caused?
Antibodies - bind to mesangial cells and cause them to release cytokines and GFs Immune complexes Complement Cytokines Lymphocytes Other infiltrating cells
By which intrinsic mechanisms can glomerulonephritis be caused?
Cytokines Growth Factors e.g. TGF-beta, PDGF, interferon-gamma Vasoactive factors Proteinuria
What part of the kidney can be a possible target for injury?
Mesangial cells Basement membrane Epithelial cells Endothelial cells Vasculature Tubular structures Integrity of glomerulus and tubules
Why can end-stage kidney failure happen even when the primary insult is removed?
Hyperfiltration theory
- some of the kidney is destroyed
- parts of the kidney that are left are overworked to try and take over the work of the dead cells
- eventually are exhausted and die as well
- end-stage kidney failure
Name some predictors of whether an acute insult may lead to ESKF.
Hypertension - glomerular and systemic Baseline GFR, serum creatinine Biopsy - extent of glomerulosclerosis Biopsy - extent of tubular loss/interstitial fibrosis (relates to glomerular damage) Age Primary disease
How is glomerulonephritis treated?
Control the precipitating factor Remove Ab/IC and block Abs Suppress the response to injury - steroids - cytotoxics (cyclophosphamide) - block matrix - anti-hypertensives Manage ESRF - treatment to slow fibrosis - dialysis - transplant - slow progression
Name some of the clinical syndromes/presentations of glomerulonephritis.
Proteinuria Hypertension Haematuria Renal impairment - reduced GFR (increased serum creatinine) Nephrotic syndrome - proteinuria - decreased serum albumin - oedema - hyperlipidaemia ( as liver trues to correct the albumin) Nephritic syndrome - hypertension - haematuria - oligouria Rapidly progressing glomerulonephritis - due to vasculitis - normal to end stage within 6 weeks
Name some histological features of ESKF.
Rapid proliferation
- lots of cells
- increased mitotic index
Glomerulosclerosis
What are crenated RBCs?
RBCs that have become crenated by hyper-concentrated urine (glomerular destruction)
Look like WBCs on microscopy
What is a RBC cast?
A tube shaped aggregation of RBCs
- a sign of bleeding in the kidney
- a sign of aggressive glomerulonephritis
(Renal tubular epithelial casts indicate severe renal tubular necrosis)
What are the main types of glomerulonephritis that you need to know?
Post-infectious GN IgA nephropathy (most common) Membranous GB change disease (most common cause of nephrotic syndrome in children) RPGN/Crescentic GN/Vasculitis Diabetic nephropathy
