renal disease classification Flashcards
most common cause of chronic Renal failure requiring dialysis/renal transplantation
- diabetes
- glomerulonephritis
- hypertension
clinical presentation of renal disease
- acute renal failure
- chronic renal failure
- nephritic syndrome - rapidly progressive glomerulonephritis
- nephrotic syndrome
acute renal failure presentation
- azotaemia/uraemia
- usually accompanied by oliguria/anuria
- may completely resolve or progress to chronic renal syndrome
azotaemia
rise in serum urea and creatinine
serum creatinine is a marker of
renal function
uraemia
azotaemia becoming symptomatic
oligourea
drop in urine volume
anuria
failure to urinate completely
chronic renal failure presentation
gradual rise in serum urea/creatinine
symptoms and signs of renal dysfunction
eventual progressioon to end stage renal failure eGFR <5%
requiring dialysis/transplantation
clinical manifestations of renal dysfunction
lethargy anorexia SOB peripheral neuropathy oedema
pre renal cause of renal failure
anything impairing renal perfusion
- drop n blood volume
- cardiac shock
renal causes of renal failure
disease intrinsic to the kidney
- glomerulonephritis
- acute tubular necrosis
- scute interstitial nephritis
- tumour lysis syndrome
- drug induced nephrotoxicity
- contrast-induced nephropathy
post renal causes of renal failure
anything obstructing urine outflow
- stones
- stricture due to radiotherapy or trauma
- due to aa tumour growing in the retroperitoneum
nephritic syndrome
- azotaemia/uraemia
- oliguria
- haematuria - often macroscopic - mild to moderate proteinuria
- hypertension
nephritic syndrome usually due to
glomerularnephritis
rapidly progressive glomerulonephritis
RPGN
- subset of nephritic syndrome
- rise in serum level creatinine/urea is rapid and severe
- usually due to crescentic glomerulonephritis
RPGN is a subset of
nephritic syndrome
nephrotic syndrome
- proteinuria
- hypoalbuminaemia
- peripheral oedema
- hyperlipidaemia
- lipduria
mechanisms of nephrotic syndrome
increased glomerular capillary permeability - leaky
low serum protein - leaks into urine
reduced serum oncotic pressure
increased hepatic lipid synthesis - liver attempts to compensate
oncotic pressure
the ability of the vascular system to maintain fluid within the vascular system
pitting oedema
pressing down on the skin leaves an imprint
Dendant oedema
accumulates in areas under gravitational force
pathogenesis of glomerular nephritis
2 main pathogeneses
- immune complexes
- structural abnormalities - usually in podocytes, podcytopathy
immune complex pathogenesis of glomerulonephritis
proteins become trapped
immune complexes in thee mesangium - masangial cells proliferate causing mesangial hypercellularity and mesangial matrix expansion
immune complexes in sub endothelial space - between the endothelium and glomerular basement membrane, glomerulus proliferates endothelial cells, endothelial proliferation
immune complexes in the epimembranous/subepithelial space - glomerulus produces new basement membrane called ‘spikes’
diagnostic core biopsy
- light microscopy
- electron microscopy
- immunoflourescence
immunofluorescence
manufactured antibodies with fluorescent signal attatched that are specific for components of immune complexes
primary glomerulonephritis
no identifiable cause
idiopathic
secondary glomerulonephritis
- drug
- infections
- autoimmune diseases
- malignancy
minimal change disease
- type of glomerulonephritis
- disease of children
- structural abnormality - podocytopathy
- normal glomeruli under light microscopy
- no immune complexes
electron microscopy findings for minimal change disease
normal podocyte findings:
- cytoplasmic extensions - foot processes
- spaces in between called slit diaphragms - have an electrical charge which repels electrical charge in protein keeping protein in the circulation
minimal change disease finings:
- foot processes are fused which means slit diaphragms are lost causing protein to leak into urine causing nephritic syndrome
secondary causes of minimal change disease
- drugs
- malignancy
- vaccinations
prognosis of minimal change disease
- good in children - highly responsive to steroids
- poorer response in adults
membranous nephropathy
- usually effects adults especially Middle Ages males
- immune complex mediates
- nephritic syndrome/nephritic range proteinuria
findings for membranous nephropathy
light microscopy
- circumferential thickening of glomerular capillary loops - thickening due to immune complexes
- glomerulus reacts by producing new basement membrane spikes alternating with subepithelial deposits
immune fluorescence
- immune complexes - IgG and C3 (evidence of complement cascade)
electron microscopy
- subepitheial deposits
- intervening basement membrane spikes
primary membranous nephropathy
now known to be due to autoantibodies - protein on the podocytes
prognosis of membranous nephropathy
generally indolent
may progress to chronic renal failure
focal or diffuse glomerular nephropathy
- focal affects <50% of glomeruli
- diffuse affects >50%
segmental and global glomerular nephropathy
segmental affects <50% of an individual glomerulus
global affects >50%
focal segmental glomerulosclerosis
- most common cause of nephrotic syndrome in adults
structural abnormality - nephrotic syndrome.nephritic range proteinuria
findings of focal segmental glomerulosclerosis
focal and segmental
collapse of the capillary loops with scarring and fibrous adhesions to the bowman’s capsule
immunofluorescence
- antibodies found but not immune complex mediated, antibodies just trapped
electron microscopy
- segmental scarring
- subtotal effacement of the podocytic foot processes
secondary causes of FSGS
- any cause of nephron loss
- HIV, sickle cell, herion abuse, obesity
- all other types of glomerulonephritis
prognosis of FSGS
some respond to steroids
remainder progress to chronic renal failure
post infectious glomerular nephritis
acute proliferative/post streptococcal glomerulonephritis
- usually children
- 1-4 weeks post cellulitis/pharyngitis
- immune complex mediated - planted streptococcal pyogenic exotoxin (protein on the streptococcal organism)
findings I posy infectious glomerulonephritis
diffuse proliferative mesangial hypercellularity endocapillary proliferation neutropenic inflammation immunoflourescens - granular, mesangial and capillary loop IgG and C3 electron microscopy - sup epithelial 'humps'
cause of post infectious G
- always secondary - post infectious
- usually S progenies
- non streptococcal causes include other bacteria, viral and parasitic organisms
prognosis of post infectious G
most children recover with conservative treatment
adults may progress to chronic renal failure
IgA nephropathy
- berger’s disease
most common cause of G
usually young adults
immune complex mediated
clinical presentation of IgA nephropathy
microscopic haematuria/nephritic syndrome
sometimes precipitated by URTI
findings of IgA nephropathy
light microscopy diffuse mesangiaal matrix expansion and hypercellularity immunoflurescence - granular mesangial IgA electron microscopy - mesangiaal immune complex deposits
causes of IgA nephropathy
- drugs
- infections
- hepatobillary, GI, rheumatological diseases and malignancy
prognosis of IgA nephropathy
- 1/3 resolve
- 1/3 stable disease
- 1/3 progress to secondary FSGS/CRF
crescentic glomerulonephritis
pathological correlate to clinical presentation of rapidly progressive glomerulonephritis
- nephritic syndrome with rapid and severe rise in serum urea/creatinine
medical emergency - chronic renal failure within weeks to months untreated
histological pattern - not a diagnosis
crescentic GN under the microscope
crescent
- filing and occlusion of the bowman’s space by proliferation of parietal epithelial cells
- due to rupture of capillary loops - sign of severe glomerular injury
types of crescentic GN
- type 1 - anti glomerular basement membrane disease
- type 2 - immune complex mediated - post infectious, IgAA, mesangiocapillary GN
- type 3 - pauci immune GN
anti-GBM disease
autoantibody to a3 chain of type 4 collagen of GBM
autoantibodies may cross react with basement membrane of pulmonary alveolar ca[illaries
findings in anti-GBM syndrome
crescents with necrosis
linear capillary loop IgG
angle antibodies - no immune complexes found
lupus nephritis
lupus can affect the glomeruli in many ways
pauci-immune GN
anti neutrophil cytoplasmic antibody associated glomerulonephritis and vasculitis
autoantibodies against cytoplasmic enzymes in neutrophils are released - toxic and damage endothelial cells
associated with systemic small vessel vasculitis
two syndromes associated with pauci-immune GN
wegener’s GN - necorising graanulomaatous inflammatioon of upper and lower respiratory tract and kidney
charge-strauss syndrome - similar to WG with asthma and peripheral eosinophilia
findings in pauci-immune GN
crescents and granulomatous inflammation in Wegener’s
eosinophil rich granuloma in charge- Strauss syndrome
no findings in immunoflourescence and no immune complexes in electron microscopy
