Glomerulonephritis Flashcards

(42 cards)

1
Q

what makes up the renal parenchyma

A

tubules, interstitium, glomeruli

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2
Q

what type of disease is glomerulonephritis

A

glomerular disease

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3
Q

what are the two types of glomerulonephritis

A

chronic- 2nd commonest cause of end stage renal failure

acute- important treatable cause of acute renal failure

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4
Q

what is glomerulonephritis

A

range of immune mediated diseases of the kidneys affecting the glomeruli (with secondary tubulointerstitial damage)

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5
Q

what is the difference between primary and secondary glomerulonephritis

A
primary= no associated disease (majority idiopathic)
secondary= glomerular involvement is part of systemic disease (e.g. SLE, infections, drugs, malignancies, ANCA, goodpastures, HSP)
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6
Q

what does damage to endothelial or mesangial cells cause

A

a proliferative lesion

  • red cells in urine
  • aggressive nephritic picture
  • influx of inflammatory cells
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7
Q

what does damage to podocytes cause

A

a non proliferative lesion

  • protein in urine
  • dont get dramatic inflammatory response
  • loose ability to retain albumin
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8
Q

what happens when there is podocyte damage

A

it atrophies
loss of specific barrier function
proteinuria

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9
Q

what happens when there is mesangium damage

A

proliferative response
release of Ang.2, chemokines
attract inflammatory cells

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10
Q

what causes damage to the glomerular endothelium

A

vasculitis

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11
Q

what tests to diagnose GN

A
blood tests 
urinalysis 
urine microscopy- RBC (dysmorphic), 		RBC  & granular casts, lipiduria
urine protein: creatinine ratio 
kidney biopsy
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12
Q

what types of haematuria will renal presentation cause

A

asymptomatic microscopic

episodes of painless haematuria (wont produce painful haematuria)

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13
Q

what are the parameters of proteinuria

A
Microalbuminuria (30-300mg albuminuria/day)
Asymptomatic proteinuria (< 1 g/day)
Heavy proteinuria (1-3 g/day)
Nephrotic syndrome (> 3 g/day))
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14
Q

do you do a kidney biopsy for everyone

A

no as risk of bleeding

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15
Q

what are red cell casts Pathognomonic of

A

GN with injury to mesangium

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16
Q

what are the clinical presentations of GN

A

impaired renal fucntion (AKI, CKD/ ESRD)
hypertension
nephritic/nephrotic syndrome
nephritic-nephrotic syndrome

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17
Q

what is nephritic syndrome

A
  • acute renal failure
  • oliguria
  • oedema/ fluid retention (caused by reduce urine output)
  • hypertension
  • active urinary sediment (RBC’s, granular casts)
18
Q

what is nephritic syndrome indicative of

A

proliferative process

affecting endothelial cells

19
Q

what is nephrotic syndrome

A
  • proteinuria >3g/day
  • hypoalbuminaemia
  • oedema
  • hypercholesterolaemia (live working overtime)
  • usually normal renal function (normal creatinine and BP)
20
Q

what is nephrotic syndrome indicative of

A

a non proliferative process affecting podocytes

21
Q

what are the possible complications of nephrotic syndrome

A

infection (loss of opsonising antibodies)
renal vein thrombosis
PE (increased DVT risk)
volume depletion (overaggressive use of diuretics may lead to ARF)
vit d def
subclinical hypothyroidism

22
Q

How does the presentation of GN differ from a non glomerular disease like Interstitial Nephritis?

A

In glomerular disease can have blood or protein in urine

In a interstitial nephritis- should not have blood or protein or urine

23
Q

how do you classify GN

A

aetiology (primary or secondary)

histology (renal biopsy, light microscopy, immunofluorescence, EM)

24
Q

what are the histological classifications of GN

A

proliferative vs non proliferative (proliferation of mesangial cells)

focal/ diffuse (< or > 50% glomeruli affected)

global/ segmental (all or part of glomerulus affected)

crescentic (presence of cresents- epithelial cell extracapillary proliferation- e.g. RPGN in vasculitis)

25
what are the principles of GN treatment
reduce degree of proteinuria induce remission of nephrotic syndrome preserve longterm renal function
26
what are the non immunosuppressive treatments for GN
``` Anti-hypertensives (target BP <130/80 - <120/75 if proteinuria) ACE inhibitors/ ARBs Diuretics Statins (hypercholesterolaemia) ? Anticoagulants/ Aspirin/ Antiplatelets ? Omega 3 fatty acids/ Fish oil ```
27
what are the immunosuppression therapies for GN
Drugs Corticosteroids (Prednisolone po/MethylPred IV) Azathioprine Alkylating agents (Cyclophosphamide/ Chlorambucil) Calcineurin inhibitors (Cyclosporin/Tacrolimus) Mycophenolate Mofetil (MMF) Plasmapharesis (TPE-therapeutic plasma exchange) Antibodies:IV Immunoglobulin Monoclonal T or B cell Antibodies
28
what is the general treatment for nephrotic patients
``` Fluid restriction Salt restriction Diuretics ACE Inhibitors/ ARBs ? Anticoagulation IV Albumin (only if volume deplete) ``` IMMUNOSUPPRESSION
29
what is the aim of treatment for nephrotic patients
``` to induce sustained remission: complete remission (proteinuria < 300 mg/day) partial remission (proteinuria < 3g/day) ```
30
what are the types of non proliferative GN
minimal change GN focal segmental glomerulosclerosis membrane GN
31
describe minimal change GN
damage to podocytes commonest cause of nephrotic syndrome in children seen on EM 94% complete remission with oral steroids doesnt cause progressive renal failure
32
describe focal segmental glomerulosclerosis
commonest cause of nephrotic syndrome in adults primary/ secondary to HIV/herion/obesity/reflux/ nephropathy segements of glomeruli develop sclerosis 60% response to steroids 50% progress to ESRF
33
describe membranous nephropathy
2nd commonest cause of nephrotic syndrome in adults primary/ secondary (hep b, parasites, CTD- lupus, malignancies, drugs (gold, pencillamine)) renal biopsy- immune complex deposition in BM thickened glomerular BM steroids/ alkylating agents/ B cell monoclonal Ab 1/3rd progress to ESRD 1/3rd go into remission anti PLA2r antibody
34
what are the types of proliferative GN
IgA nephropathy rapdily progressive GN membranoproliferative GN post infectious GN
35
describe IgA nephropathy
most common GN in adults proliferative macroscopic haematuria after resp/GI infection AKI/CKD associated with HSP (arthritis, colitis, purpuris skin rash) renal biopsy- IgA deposits, proliferation 5% ESRF in 10 years BP control, ACRi, ARBs, fish oil
36
describe rapidly progressing GN
cresenteric (glomerular cresents on biopsy) either ANCA positive or ANCA negative treatable cause of AKF rapid deterioration in renal function over weeks/ days RBCs and granular casts in urine
37
what are the ANCA positive RPGN
GPA (vasculitis affecting lungs, kidneys, ect. c-ANCA positive, treat with steroids + cyclophosphamide) MPA (small vessel vasculitis, p-ANCA +ve, tx with long term steroids)
38
what are the ANCA negative RPGN
Goodpasture’s disease-Anti-GBM Henoch Scholein Purpura HSP/IgA Systemic Lupus Erythematosus SLE
39
what is the tx for RPGN
AIM IS TO CONTROL THE SYSTEMIC AS WELL AS RENAL DISEASE Immunosuppression Steroids (IV Methylprednisolone / Oral Prednisolone) Cytotoxics (Cyclophosphamide/ Mycophenolate/ Azathioprine Plasmapharesis
40
what is membraneprolifrative GN
primary/ secondary (SLE, hep) | usually progresses to ESRF
41
describe post infectious GN
occurs weeks after URTI (usually strep pyogenes) supportive Tx resolves in 2-4 weeks
42
describe IgA nephropathy
most common GN in adults proliferative macroscopic haematuria after resp/GI infection AKI/CKD associated with HSP (arthritis, colitis, purpuris skin rash) renal biopsy- IgA deposits, proliferation 5% ESRF in 10 years BP control, ACRi, ARBs, fish oil