Glomerulonephritis Flashcards
What is Glomerulonephritis
Inflammation of Glomerulus
Glomerulonephritis is responsible for how much end stage kidney disease
15%
Glomerulonephritis classified based on
kidney biopsy findings
Glomerulonephritis features
Haematuria
Proteinuria
Hypertension
Renal Impairment
Nephritic State
Active Urine Sediment: Haematuria, Dysmorphic RBCS, Cellular Casts
Hypertension
Renal Impairment
Nephrotic Syndrome Features (4)
Oedema
Nephrotic Range Proteinuria >3.5g/day or 350mg/mmol creatinine
Hypoalbuminaemia: Serum Albumin <35g/L
Dyslipidaemia
What is nephrotic range of proteinuria
> 3.5g/day or 350mg/mmol creatinine
Hypoalbuminemia is classified as
Serum Albumin <35g/L
Proliferative Glomerulonephritis classified as
Excessive numbers of cells in glomeruli. These include infiltrating leucocytes
Non Proliferative Glomerulonephritis classified as
Glomeruli look normal or have areas of scarring. They have normal numbers of cells
Which diseases classified as Non Proliferative Nephrotic Glomerulonephritis
Minimal Change Disease
Membranous Neuropathy
FSGS
Which diseases classified as Proliferative Nephrotic Glomerulonephritis
IgA Nephropathy
Lupus Neuprhtis
Which diseases classified as Proliferative Nephritic Glomerulonephritis
Post Infectious GN
ANCA Associated GN
Commonest cause of Glomerulonephritis
IgA Nephropathy
IgA Nephropathy characterised by
IgA deposition in the mesangium and mesangial proliferation.
IgA Nephropathy most common in
2nd and 3rd decade of life with males more commonly affected.
IgA Nephropathy can progress to
end stage kidney disease or halving eGFR at 10 years
Presentation of IgA Nephropathy
Microscopic haematuria.
Micoscopic haematuria + proteinuria
Nephrotic syndrome
IgA crescentic glomerulonephritis
Post Streptoccal Glomerulonephritis follows
10-21 days after throat or skin infection
Post Streptoccal Glomerulonephritis commonly associated with
Lancefield Group A Streptocci
Post Streptoccal Glomerulonephritis genetic predisposition
HLA-DR, -DP, -DP.
Anti GBM Disease characterised by
Circulating Anti GBM
Related to Crescentic Glomerulonephritis
Anti GBM Disease Presentation
Nephritis (anti-GBM glomerulonephritis)
Nephritis+ lung haemorrhage (Goodpasture’s syndrome).
Anti GBM Disease Peaks
Two peaks: 3rd decade and 6th/7th decade.
Anti GBM Disease Diagnosis
demonstrating anti-GBM antibodies in serum and kidney
Anti GBM Disease Treatment
aggressive immunesuppression: steroid, plasma exchange, and cyclophosphamide.
How does Proliferative Glomerulonephritis present
with nephritic state
Haematuria + variable proteinuria + hypertension +/- renal impairment
Proliferative Glomerulonephritis can cause
rapid decline needing dialysis
To save nephrons in Proliferative Glomerulonephritis diagnosis
Clinical suspicion + immunology screen + renal biopsy
Nephrotic Syndrome Management
Treat oedema: salt and fluid restriction and loop diuretics.
Hypertension: use Renin-Angiotensin-Aldosterone-blockade.
Reduce risk of thrombosis: Heparin or Warfarin.
Reduce risk of infection e.g. pneumococcal vaccine.
Treat dyslipidemia e.g. statins.
Minimal Change Disease features
Commonest form in children.
Sudden onset of oedema – days.
Remission with steroids (often).
Relapse occurs in two thirds of patients.
Minimal Change Disease Treatment
Prednisolone – 1mg/kg for up to 16 weeks.
Once remission achieved , slow taper over 6 months.
Initial relapse treated with further steroid course.
Subsequent relapses treated with Cyclophosphamide Cyclosporin Tacrolimus Mycophenolate mofetil Rituximab
How to treat relapses of minimal change disease
Cyclophosphamide Cyclosporin Tacrolimus Mycophenolate mofetil Rituximab
How does Focal and Segmental Glomerulonephritis present
Nephrotic Syndrome
Pathology of Focal and Segmental Glomerulonephritis
tip lesion, collapsing, cellular, perihilar, and not otherwise specified.
Focal and Segmental Glomerulonephritis has high chance of
end stage kidney disease
Focal and Segmental Glomerulonephritis treatment
Cyclosporin or Cyclophosphamide or Rituximab
Commonest cause of Nephrotic Syndrome in Adults
Membranous Nephropathy
Serology Markers in Nephrotic Syndrome
Anti-phospholipase A2 receptor (PLA2R) antibody
Thrombospondin type 1 domain containing 7A
Secondary causes of Nephrotic Syndrome
Malignancies
SLE
Rheumatoid arthritis.
Drugs: NSAIDs, gold, penicillamine.
Membranous Nephropathy Treatment
General measures for at least 6 months.
Immunesuppression if symptomatic nephrotic syndrome, rising proteinuria or deteriorating renal function.
Cyclophosphamide and steroids (alternate months) for 6 months.
Tacrolimus.
Rituximab.
Prognosis for Membranous Nephropathy good for patients whose
proteinuria resolves
Membranous Nephropathy can recur in
Renal Transplant
Non Proliferative Glomeuleonphritis presents with
Nephrotic Syndrome
Key diagnosis in Non Proliferative Glomeuleonphritis
Renal Biopsy
What tubule comes off glomerulus
proximal
Blood enters glomerulus via
afferent arteriole
All proteins equal to or larger than albumin including immunoglobulins where will they go in glomerulus
stay in plasma
will not be filtered
Filter barrier in glomerulus contains what 3 things
Endothelial cell cytoplasm
basal lamina
podocyte
basal lamina is what type of tissue
connective
filtrate goes into where before proximal tubule
bowmen space
blood cells and unfiltered proteins exit glomerulus via
efferent arteriole
Diabetic Glomerulus disease has no what deposition
immunoglobulin
Glomerulonephtis common presentation
Haematuria
Heavy Proteinuria (Nephrotic Syndrome)
Slowly increasing Proteinuria
Acute Renal Failure
Haematuria main causes
UTI
Urinary Tract Stone
Urinary Tract Tumour
Glomerulonephritis
IgA in Iga Nephropathy stains
green
Which Immunoglobin and Complement component are in all mesangial area of al glomeruli
IgA and C3
Does IgA get filtered into urine in IgA Nephropathy
No it gets stuck in mesangium
What gets clogged with antibody in glomerulonephritis
Mesangium and not filter membrane
what happens to glomerulus basement membrane in membranous glomerulonephritis
it gets thickened
What immunoglobulin is deposited in membranous glomerulonephritis
IgG it gets stuck between basal lamina and podocyte and not filtered into urine
In normal glomerulular basement membrane what happens to antibody and albumin
stay in plasma and not filtered
What happens when IgG activates complement C3
it punches holes in filter allowing albumin to be filtered into urine causing nephrotic syndrome
which immunoglobulin is too big to be filtered into urine
IgG
what percentage of those with membranous glomerulonephritis get chronic renal failure within 10 years
1/4
What are the adhesions to bowmen capsules in diabetic nephropathy
glomerulus attempt to stop leak of albumin into urine
what is the thickened capillary wall leaking in diabetic nephropathy
albumin
what compresses capillaries in diabetic neprhopathy
increased mesangial matrix
what reduces blood flow to glomerulus in diabetic nephropathy
arterioles being thick and narrow
what are the nodules of mesangial matrix called in diabetic nephropathy
Kimmelsteil Wilson Lesion
Causes of Crescentic Glomerulonephritis
Granulomatosis with Polyangitis (Wegener)
Microscopic Polyarteritis
Antiglomerular Basement Membrane Disease
Granulomatosis with Polyangitis affects
Vasculitis which affects kidneys, nose and lungs
Serum tests in wegerers shows
presence of anti neutrophil cytoplasmic antibodies (ANCA)
ANCA are not deposited where
in kidney
ANCA are directed against what in glomerular disease
proteinase 3 and myeloperoxidase
If Wegener’s (Granulomatosis with Polyangitis) is left untreated what happens
Fatal
By giving Cyclophosphamide for Wegener Granulomatosis with Polyangitis) what happens?
75% complete remission
