Glomerular Injury (Nephritic And Nephrotic) Flashcards
What are 3 classes of Glomerular Disease?
- Hereditary
- Primary (most common), disease originates from glomerulus
- Secondary, due to systemic diseases (Diabetes, Bacterial Endocarditis)
What does Glomerular disease result in?
What If this goes on for a long time?
Glomerulonephritis, can progress to Chronic Kidney Disease
What 4 glomerular structures are prone to damage?
- Capillary endothelium
- Glomerular Basement Membrane
- Mesangial cells (supporting capillaries)
- Podocytes (on outer surface of capillary)
What 4 things is Nephrotic Syndrome characterised by?
This syndrome is a group of conditions
- Proteinuria
- Hypoalbuminaemia
- Oedema
- Hyperlipidaemia (Increased hepatic lipoprotein synthesis)
(Usually associated with high cholesterol)
What is the physiological basis for Nephrotic Syndrome?
Glomerular basement membrane damage and increased pore size, lead to increased permeability (of glomerular filter) to Albumin
What are 4 methods of management of Nephrotic Syndrome?
- Control BP (ACE Inhibitors)
- Control Hyperlipidaemia
- Antigoagulants (if patient is hypercoagulable)
- Treat underlying cause
(Risk of thrombosis increases if albumin decreases)
List 4 Nephrotic conditions
- Diabetic Nephropathy
- Minimial Change Disease
- Membranous Glomerulonephritis
- Focal Segmental Glomerulosclerosis (FSGS)
What happens in Diabetic Nephropathy
- Excess blood glucose binds to proteins, especially at efferent Arteriole, obstructing blood flow
- Initially, increased GFR
- Mesangial cells secrete more structural matrix, thickening the Basement Membrane of Glomerulus
- Reduced GFR
How do we treat Diabetic Nephropathy?
Leading abuse of end stage renal disease
- Control BP (ACE Inhibitors, Angiotensin receptor blockers)
- Control blood glucose
State 3 characteristics of Minimal Change Disease
- Most common in Children <6
- No changes under LM (Podocyte effacement under EM)
- Good prognosis in children, variable in adults
What happens in Membranous Glomerulonephritis?
What percentage of Adult Nephrotic Syndrome cases is due to this?
- Deposition of immune complexes in Sub-epithelial space (Between epithelia and Podocytes)
- Results In Basement Membrane thickening
40%
Outline the causes of Membranous Glomerulonephritis
- Idiopathic (85%)
- Can be Primary
- Can be Secondary (infections/ tumours/ drugs/ systemic illnesses)
How do we treat Membranous Glomerulonephritis?
- Immunosuppressants
- Treat underlying disease
What is Focal Segmental Glomerusclerosis (FSGS)?
How does this appear?
- Podocyte damage leads to protein build up in Glomerulus
- Leading to Sclerosis
- Glassy appearance (Hyalinosis)
Outline the causes of Focal Segmental Glomerusclerosis (FSGS)
- Primary: Idiopathic
- Secondary: Sickle cell, HIV, Heroin, Kidney hyperperfusion
Describe the affected structures in Focal Segmental Glomerusclerosis (FSGS)
- Only SOME Glomeruli are affected
- Only PART of the Glomerulus is affected
How do we treat Focal Segmental Glomerusclerosis (FSGS)?
What can it lead to if treatment fails?
- Steroids, however results are inconsistent
- Chronic Renal Failure
What are the main 3 signs and symptoms of Acute Nephritic Syndrome?
Name 6 others
How do we treat generally?
- Oliguria/ Anuria
- Hypertension
- Haematuria (micro or macroscopic)
- Fluid retention
- Uraemia
- Proteinuria
- Loin pain
- Headaches
- General malaise
Steroids
List 4 Nephritic Conditions
- IgA Nephropathy/ Berger’s Disease
- Rapidly Progressive Glomerulonephritis
- Post streptococcal Glomerulonephritis
- Goodpasture’s Syndrome
IgA Nephropathy/ Berger’s Disease is the most common Primary Glomerular Disease worldwide, causing recurrent haematuria
What happens in it?
- Raised Hypertension and IgA levels, deposited in Mesangium-> Sclerosis of damaged segment
How do we treat IgA Nephropathy?
What do 20% of patients go on to develop
- Control BP (anti hypertensives)
- Steroids
Advanced CKD (Chronic Kidney Disease)
What happens in Rapidly Progressive Glomerulonephritis?
- Severe glomerular injury, fibrin leaks out of BM-> Macrophage and epithelial cell proliferation
- Crescent shape masses form in Glomerulus , reducing glomerular blood supply
- Loss of renal function within days to weeks
How do we treat Rapidly Progressive Glomerulonephritis?
- High dose steroids
- Immunosuppressants
- Plasma exchange to remove immune complexes causing this
When does Post streptococcal Glomerulonephritis present?
How do we treat?
- 1 to 3 weeks after group A Beta-haemolytic Streptococcal infection of tonsils/ pharynx/ skin
Antibiotics to treat remaining infection
Describe the Prognosis of Post streptococcal Glomerulonephritis in children and adults
Children: Recover completely
Adults: 40% develop hypertension or renal impairment (60% recover completely)
What happens in Goodpasture’s Syndrome?
- Development of antibodies to Type 4 collagen in BM, causing inflammation
- Leads to rapidly progressive Glomerulonephritis, Acute Renal Failure and Lung Haemorrhage
How do we treat Goodpasture’s Syndrome?
Describe the prognosis without treatment
- Plasma exchange to remove antibodies
- Corticosteroids to remove inflammation
Poor
Of Nephrotic Syndrome and Acute Nephritic Syndrome, which can lead to CKD as as long term consequence
Both of them
