11.2 Glomerulonephritis Flashcards
What is glomerulonephritis (and the more appropriate term)? Is it acute or chronic?
- Glomerulonephritis is usually regarded as inflammation of the glomeruli in the kidneys
- However, not all GN are inflammatory in histological nature - “glomerulopathy” may be more appropriate
- It can be either acute or chronic
Describe the clinical features of glomerulonephritis
- Haematuria
- Proteinuria
- Oedema
- Nausea/vomiting
- Oliguria
- Fatigue
- Decreased GFR
Describe some causes (and corresponding treatments) for glomerulonephritis
- Infection (give antibiotics)
- Autoimmune disease (such as lupus nephritis or goodpasture’s disease)
- Generalised vasculitis
Is proteinuria worse in nephritic or nephrotic syndromes? What is the threshold of the answer to the previous question in terms of daily protein loss?
Nephrotic (remember Matt Arnold)
Nephrotic threshold is 3.5g/day
Why might there be high levels of triglycerides and cholesterol in the blood during nephrotic syndrome?
Because the liver tries to compensate for massive proteinuria, but if it can’t make enough replacement albumin (despite hypoalbuminaemia), it spits out TAGs instead.
Nephritic vs nephrotic syndrome
Nephritic: haematuria, proteinuria (less than nephrotic), hypertension
Nephrotic: massive proteinuria (>=3.5g/day), oedema, hypoalbuminaemia, hypercoagulability
What is the relationship between glomerulonephritis and nephrotic/nephritic syndrome? Are they categories of one another? The same thing? Explain.
- Glomerulonephritis refers to inflammation of the glomerulus within the kidney
- Nephrotic/nephritic syndromes are exactly that; syndromes. They refer to specific collections of symptoms. Glomerulonephritis can cause these syndromes, but the syndromes themselves are not comparable to GN. They are in different categories.
What symptoms make up nephritic syndrome
- Haematuria
- Mild proteinuria
- Oliguria
- Oedema
- Hypertension
What symptoms make up nephrotic syndrome
- Heavy proteinuria
- Subsequent hypoalbuminuria
- Heavy oedema (since there is nothing holding the fluid in)
- Hyperlipidaemia (why?)
What is rapidly progressive GN?
Acute severe drop in GFR associated with glomerulonephritis.
Macro vs microscopic haematuria
Macroscopic: visible to the naked eye
Microscopic: visible only on dipstick/microscopy
How do we detect glomerulonephritis?
- Not difficult: do a urine dipstick test
- Looking for blood and protein in urine, both of which are leaked into urine following inflammation of the glomerulus
- Also, urine microscopy shows dysmorphic RBCs with cytoplasmic blebs (acanthocytes; acanthos = thorny flower)
Why is it a bad idea to use creatinine to detect glomerulonephritis?
- Inversely exponential relationship
- By the time creatinine is above normal range, over half of GFR is lost
How do we diagnose the cause of glomerulonephritis?
- Renal biopsy (we have no blood test at the moment)
- Some aetiologies have diagnostic blood tests
What are glomerular crescents? What do they indicate on histology?
- They are proliferation of bowmans capsule endothelium, forming an abnormal crescent-like structure alongside the glomerulus
- They indicate severe glomerulonephritis
The world’s most common primary glomerulonephritis is…
IgA glomerulonephritis
What is synpharyngitic haematuria? What condition is it known to occur in?
- Haematuria close in time to the development of URTI or GI infection
- Thought to occur in IgA nephropathy
Explain the pathophysiological mechanism of IgA nephropathy
- Abnormal IgA produced, which the body attacks with other Abs, forming immune complexes
- These immune complexes deposit in the mesangial cells of the glomerulus, causing localised inflammation and permanent kidney damage
Clinical features of IgA nephropathy
- Synpharyngitic haematuria
- Proteinuria
- Oedema (typically in face and legs)
- Hypertension
- Decreased GFR
Pathological findings of IgA nephropathy
Mesangial proliferation and signs of IgA deposition in mesangial areas (such as on immunofluorescense staining)
Anti-GBM glomerulonephritis/goodpastures pathophys and clinical features
- Loss of tolerance of type IV collagen, which is found in GBM and lungs, leading to autoantibody mediated attack
- Often leads to haemoptysis from lungs
- In terms of kidneys, patients always present with rapidly progressing glomerulonephritis, loss of GFR, proteinuria, and haematuria
Pathological findings in goodpasture’s
- IgG autoantibody deposition in GBM
(G for Goodpasture’s)
Clinical features of post-strep glomerulonephritis
- Smoky-dark urine (strep = s = smoky)
- Haematuria
- Mild peripheral oedema
- Hypertension
- Hypocomplementaemia
- Varying ARF
Pathologgical findings of post-strep glomerulonephritis
Positive antibodies for DNAaseB, streptolysin-O, and hylauronidase