Glomerular diseases Flashcards
Clinical presentation of glomerulonephritis
- Asymptomatic proteinuria and/or non visible haematuria
- Progressive CKD
- Acute nephritic syndrome
- Rapidly progressive glomerulonephritis
- Nephrotic syndrome
Symptoms of nephrotic syndrome
Proteinurea Low albumin Oedema High cholesterol
Difference between nephrological and urological haematuria
Microscopy shows dysmorphic
RBCs in glomerular disease
Presentation of acute nephrotic syndrome
Haematuria (Non visible/ may be visible)
Proteinuria
Oliguria
Salt and water retention ( oedema, hypertension)
Uraemia
Common causes of glomerular nephritis
IgA nephropathy
Membrane proliferative nephropathy
Focal segmental sclerosis
Membranous
Difference between urological and nephrological haematuria
Haematuria can result from bleeding into the urinary tract or from the glomerulus into the urethra
UTIs are the most common cause of haematura. Assocaited with LUTS (dysuria, frequency)
Urological causes of haematuria include stones, renal cell carcinoma, transitional cell carcinoma
Glomerular causes are due to inflammation and bleeding
Features which suggest a nephrological cause of haematuria
abnormal renal function
proteinuria
oedema (salt and water retention)
hypertension
young age
Presentation of glomerulonephritis
Can present as:
Asymptomatic haematuria and proteinuria
Acute nephritic syndrome (haematuria, hypertension, oedema)
nephrotic syndrome (heavy proteinuria, hypoalbuminaemia and peripheral oedema)
Chronic kidney disease
Presentation can be acute or chronic, rapidly or slowly progressive.
Structures within the glomerulus prone to damage
Capillary endothelial lining
Glomerular basement membrane
Mesangium
Podocytes
When damage occurs to the glomerulus, it results in painless haematuria and proteinuria
Mechanisms of glomerular injury
Circulating immune complexes: Immune complexes from outside the kidney become trapped in the glomerulus and activate the complement pathway, leading to acute inflammation. This increases vascular permeability
Complex deposition: Ag-ab complexes form within the kidney and are deposited in the glomerulus. e.g. Goodpasture’s syndrome - antibodies form against teh basment membrane causing haemorrhage. Damage leads to progressive renal failure.
Cell mediated immunity: sensitised T cells mediates progression from acute to chornic damage.
Nephrotic syndrome
Proteinuria >3.5g in 2hrs
Hyperalbuminaemia
Oedema
Hyperlipidaema
Increased permeability of the glomerular filtration barrier as a result of damage to the basement membrane. Heavy proteinuria causes low plasma albumin and therefore tissue oedema.
Decreased circulating volume stimulates RAAS which increases Na+ and H2O retention, leading to further oedema
Management: blood pressure control, ACEi to reduce proteinuria, anticoagulants (low albumin increases risk of coagulation).
Acute Nephritic syndome
Haematuria
Hypertension
Oliguria
Proteinuria
Fluid retention (facial oedema)
Primary glomerular causes of nephrotic syndrome
Minimal change disease
Membranous glomerulonephropathy
Membranoproliferative glomerulonephritis
Focal segmental glomerulosclerosis
Minimal change disease
Most common cause of heavy proteinuria and nephrotic syndrome in children.
No changes seen on light microscope and immunofluorescence. EM shows damge to epithelial food processes
Treatment includes corticosteroids and ciclosporin.
Most common form of nephrotic syndrome in older patients
Membranous glomerulonephropathy
Chronic disease characterised by subepithelial depositions of immune complexes and thickening of the basement membrane.
Secondary causes: infection, melanoma, heroin, SLE