11.3 Nephrotic Syndrome Flashcards
How might functional proteinuria come about?
- increased blood flow to nephron causes increased protein filtration
- Can occur in conditions such as heart failure, exercise, and fever
Diagnostic triad of nephrotic syndrome (incl. numbers). Also mention others
- Hypoalbuminaemia (<30mg/L)
- Proteinuria (> 3.5g/day)
- Oedema
Others:
- Hypercoagulability
- Hyperlipidaemia
- Low nitrogen balance
Describe the two hypothesised mechanisms of oedema formation in nephrotic syndrome
- Underfill: low oncotic means lkow blood volume, which means RAAS activation
- Overfill: starts with increased retention of sodium and water, leading to transudation
Nephrotic syndrome can cause hyperlipidaemia due to increased hepatic lipoprotein synthesis. Give two examples of clinical signs that can indicate this
- Xanthelasma
- Lipiduria (frothy)
How does nephrotic syndrome affect coagulability and nitrogen balance?
- Hypercoagulable (inc synthesis thrombotic, dec synthesis antithrombotic)
- Negative nitrogen balance (can cause loss of function)
How is nephrotic syndrome diagnosed
- Can be detected w/ clinical presentation and lab features
- With kids, give steroids for “exquisite” effect; most have minimal change disease
- In adults, give biopsy to determine underlying cause
In which demographic is minimal change disease more common?
Children and young adults
Pathogenesis of minimal change disease
- Effacement of podocytes; glomerulus is minimally changed
- Mechanism not exactly clear, postulated that T cell autoreaction is involved
Clinical features of minimal change disease and membranous nephropathy
Same as nephrotic syndrome (what are they?)
Management of nephrotic syndrome
- Oedema: diuretics + reduced sodium intake (careful to avoid hypovolaemia)
- Anticaogulation may be indicated
- Statin to reduce hyperlipidaemia
- ACEi/ARB to reduce hypertension (CKD) and anti-proteinuric due tor lower filtration pressure
Management of minimal change disease?
Corticosteroids (reduce swelling)
Management of membranous nephropathy
- Corticosteroids
- Rituximab (targets B cells)
- Calcineurin inhibitors
Pathogenesis of membranous nephropathy. What are some proposed secondary causes
- Autoimmune condition involving phospholipid A2 receptor autoantibodies (receptor found on podocytes)
- Characterised by subepithelial deposits and GBM thickening
- 2° causes incl. Lupus and malignancy
What is the histopathological basis for nephrotic syndrome?
- Increased GBM permeability and decreasd effectivenes of podocyte layer barrier
- Causes proteinuria and thus oedema etc.
Does/how does nephrotic syndrome influence coagulation?
Nephrotic syndrome causes HYPERcoagulability.