Glomerulonephritis Flashcards
what are the consequences of inflammation of the glomeruli and nephrons
damage to glomerulus- restricts blood flow leading to incr BP. damage to filtration mechanism- blood and protein to enter urine,. loss of usual filtration capacity- AKI
what do patients present with
specific syndromes- nephrotic and nephritic syndromes
what happens to the bp in nephrotic
mild incr
what happens to the urine in nephrotic
proteinuria >3.5g/day
what happens to the GFR in nephrotic
mild decr
what happens to the bp in nephritic
severe incr
what happens to the urine in nephritic
haematuria (mild-macro)
what happens to the GFR in nephritic
moderate to severe decr
what bloods need to be done
FBC, U&E, LFT, ESR, CRP, immunoglobulins, electrophoresis, complement, autoantibodies, blood culture, ASOT, HBsAg, anti HCV
what autoantibodies are checked for
ANA, ANCA, anti-dsDNA, anti-GBM
what is tested in the urine
RBC casts, MC&S, Bence Jones protein, ACR
what imaging is performed
CXR, renal ultrasound
what type of test will give the most information
renal biopsy
what are the specific types of GN
IgA nephropathy, Henoch-Schlonlein purpura, SLE, anti-glomerular basement membrane disease, post-streptococcal GN, rapidly progressive GN
what is the commonest GN in developed world
IgA nephropathy
IgA nephropathy- presentation
macro or microscopic haematuria, occasionally nephritic syndrome. typical patient- young male, recovery rapid between attacks
what is increased in IgA nephropathy
IgA- forms immune complexes and deposits in mesangial cells
IgA nephropathy- treat
bp control with ACEi. with nephritic presentation- immunosuppression
prognosis IgA nephropathy
worse if incr bp, male, proteinuria, renal failure at presentation
what is Henoch-Schlonlein purpura
a systemic variant of IgA nephropathy causing small vessel vasculitis
features of Henoch-Schlonlein purpura
purpuric rash on extensor surfaces typically legs, polyarthritis, abdo pain, nephritis
treatment Henoch-Schlonlein purpura
bp control ACEi
what fraction of SLE patients will have renal disease
1/3 with vascular, glomerular and tubulointerstitial damage
what are the classes split into in SLE
I-iv: increasing in severity. v- membranous
what is Anti-glomerular basement membrane disease also known as
Goodpastures disease
Anti-glomerular basement membrane disease- what is it caused by
auto antibodies to type IV collagen which is an essential component of the GBM
where else is type IV collagen found and thus is also affected in Anti-glomerular basement membrane disease
in the lung so pulmonary haemorrhage can occur
Anti-glomerular basement membrane disease presentation
haematuria/ nephritic syndrome, AKI may occur within days
Anti-glomerular basement membrane disease treatment
plasma exchange, steroids, cytotoxics. prognosis poor if dialysis dependent
Post streptococcal GN
after sore throat or skin infection.
what happens in Post streptococcal GN
strep antigen deposited on glomerulus causes host reaction and immune complex formation
Post streptococcal GN presentation
usually nephritic syndrome
Post streptococcal GN treatment
supportive
what is the most aggressive GN
rapidly progressive GN
rapidly progressive GN what can these be classified into
immune complex disease- post infectious; Pauci- immune disease- granulomatosis with polyangiitis; anti-GBM disease
rapidly progressive GN clinical presentation
AKI +- systemic features. commonest cause of death in ANCA +ve patients- pulmonary hemorrhage
treatment rapidly progressive GN
immunosuppression with high dose steroids IV, cyclophosphamide and plasma exchange.
rapidly progressive GN prognosis
5 year survival 80%
