Pathology of the Kidney Flashcards
What are the spectrum causes of kidney disease?
- trauma
- swelling, mass, tumour (non-neoplastic/benign/malignant)
- chronic (chronic inflammatory)
- acute (infection/inflammation/immunological)
- stone (genetic/metabolic)
What are some congenital and genetic disorders of the kidney?
- renal hypoplasia (not fully formed)
- Potter syndrome (renal agenesis means no urine production - not enough amniotic fluid in utero)
- vesicoureteric reflux (bowel not formed properly to pressure from urine build up causes reflux back into ureters)
- renal artery stenosis
- polycystic kidney disease
What are the 2 types of polycystic kidney disease?
- autosomal dominant (more common)
- autosomal recessive (more common in children)
Describe glomerular disease
- primary disease tends to be immunological and MHC/HLA associated
- primary disease: glomerulonephritis or glomerulopathy
- secondary disease can occur and can be vascular or autoimmune
Describe the morphology of Goodpasture Syndrome and its consequences
- type II hypersensitivity
- antibodies bind to every capillary loop, in any of these places you can get a hole blown by complement
- capillary loop is shrunken and crushed
- Bowman’s space instead of being clear as it is full of urine it is just full of cells
- results in no blood flow through glomerulus
- no movement of filtrate
- can spread to more glomeruli
What are the clinical effects of Goodpasture’s Syndrome
- fast (due to complement activation)
- haematuria in beginning (due to holes blown in the capillary walls)
- proteinuria in beginning
- eventually oliguria
- can cross react with alveolar basement membranes and involve lungs (haemoptysis and consolidation)
Other than Goodpasture’s, what are some other causes of type II hypersensitivity antigen cross-reactions in the kidneys?
- vasculitis: ANCA
- SLE (lupus)
- organic solvents
Describe proliferative glomerular nephritis
- type III hypersensitivity
- cannot get rid of immune complexes
- get stuck on inside of basement membrane
- bit of activation of complement and local damage
- will eventually erode their way through capillary wall and become stuck on outer surface
- endothelial cells (mesangial cells) can scavenge complexes while they are still on inside
- results in the production of more cells
What are the clinical effects of proliferative glomerular nephritis?
- can be fast or slow
- some haematuria
- can get either more or less urine
- can have some proteinuria (due to holes)
- pain (from complement activation causing inflammatory response)
=NEPHRITIC SYNDROME
What are the causes of proliferative glomerulonephritis?
- post strep infection (common in children)
- vasculitis (SNCA)
- SLE (lupus)
What happens in membranous glomerulonephritis?
- no proliferative response as scavengers do not see small immune complexes
- erode through basement membrane and become stuck
- disrupts electrical charge of membrane
- causes leakage esp of protein
- affects all glomeruli
What are the causes of membranous glomerulonephritis?
- cancer (15% in over 70s)
- Hep B
- idiopathic
- pencillamine
- SLE (lupus)
What are the clinical effects of membranous glomerulonephritis?
- small immune complexes
- slow (takes time for erosion)
- not much haematuria
- lots of proteinuria
- no pain (not inflammatory)
- hypercholesterolaemia
- significant oedema
= NEPHROTIC SYNDROME
Describe minimal lesion glomerulonephritis?
- type IV hypersensitivity reaction
- nephrotic syndrome in children
- glomeruli lacking foot processes
- filter not working so protein leaks through
What is the clinical presentation and treatment of minimal lesion glomerulonephritis?
- marked proteinuria
- steroid treatment
