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Glomerulonephritis

Anna Hogarth Met3B Inglés 38 fichas

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  1. 1What is nephrotic glomerulonephritis?Pathology which affects the glomerulus; proteinuria occuring due to podocyte damage
  2. 2What is nephritic glomerulonephritis?Pathology which affects the glomerulus; haematuria due to inflammation
  3. 3Can classically nephritic GN can result in severe proteinuria?If there is severe scarring
  4. 4What are the diagnostic criteria for nephrotic syndrome?Proteinuria and hypoalbuminemia - podocyte disease allows proteins and albumin to leak into the urine
    1) Proteinuria >3g/24h
    2) Hypoalbuminaemia <30g/L
    3) Oedema
  5. 5What are the clinical consequences of nephrotic syndrome?Oedema (due to hypoalbuminemia) and hyperlipidaemia (compensatory increase in hepatic function)
  6. 6What are the main causes of nephrotic syndrome? (4)Minimal change disease (25%) (DOES NOT LEAD TO CKD)
    Focal segmental glomerulosclerosis (most common)
    Membranous nephropathy (25%)
    Membranoproliferative glomerulonephritis (10%)
  7. 7What causes minimal change disease?1) Idiopathic
    2) Drugs (e.g. lithium, NSAIDs)
    3) Paraneoplastic (haematological malignancy, usually Hodgkin's)
  8. 8How is minimal change diagnosed on biopsy? How is it managed?1) Appears normal on light microscopy, electron microscopy reveals podocyte effacement
    2) Managed by prednisolone 1mg/kg for 4-16 weeks (75% of adults respond; if frequent relapses then manage with longer-term immunosuppression e.g. cyclophosphamide, calcineurin inhibitors)
  9. 9What causes focal segmental glomerulosclerosis?Either idiopathic (primary) or HIV/heroin/lithium/lymphoma/decrease in kidney mass or nephrons/scarring from another glomerulonephritis
  10. 10How is FSGS diagnosed? How is it managed?1) Scarring of certain segments on biopsy
    2) ACE-i/ARB in all. Corticosteroids only in those with primary FSGS
  11. 11What causes membranous nephropathy?1) Primary
    or secondary to:
    2) Malignancy (breast, lung, GI, prostate or haematological)
    3) Drugs (gold, penicillamine)
    4) Infection (hepatitis B/C, streptococcus, malaria, schistosomiasis)
    5) Immunological disease: SLE, rheumatoid, sarcoidosis, Sjogren's
  12. 12How is membranous nephropathy diagnosed?1) Diffuse thickening of GBM (due to subepithelial deposits) and anti-phospholipase A2 antibodies in 70-80% of idiopathic cases. 'Spikes' on silver stain
  13. 13How is membranous nephropathy managed?ACE-i/ARB for all (to lower BP). 'Ponticelli' regimen for those at high risk of progression - proteinuria > 4g without response to ACE-i/ARB after 6 month, or a 30% increase in creatinine over 6-12 months; corticosteroids + cyclophosphamide/chlorambucil
    May remit in secondary if underlying cause is managed.
  14. 14What are the two forms of membranoproliferative glomerulonephritis?1) Immune-complex associated - driven by depositions of immune complexes which lead to activation of the complement system. An underlying cause may be infection, autoimmune, cryoglobulinemia, monoclonal gammopathy.
    2) C3 - genetic/acquired defect in the alternative complement system e.g. C3 nephritic factor
  15. 15How is membranoproliferative glomerulonephritis managed?ACE-i/ARB for everyone to manage BP. Can treat underlying cause in immune-complex associated.
  16. 16What are the diagnostic criteria for nephritic glomerulonephritis?1) Haematuria (micro- or macroscopic)
    2) Red cell casts (form in nephrons and indicate glomerular damage)
    3) Proteinuria (less so than in nephrotic)
    4) Mild hypertension
    5) Low urine volume (<300ml/day)
  17. 17What are the five underlying conditions which cause nephritic glomerulonephritis?1) IgA nephropathy
    2) Henoch-Schonlein purpura (HSP)
    3) Post-streptococcal GN
    4) Anti-glomerular basement membrane (anti-GBM) disease
    5) Rapidly progressive GN
  18. 18How does IgA nephropathy present?Most common primary GN in developed countries
    1) Present with NV-haematuria or episodic V-haematuria which may be synpharyngitic. Occurs within 12-72 hours of infection. Raised BP; proteinuria <1g, slow progression; 20-50% progress to renal failure over 30 years.
  19. 19How is IgA nephropathy diagnosed? How is it managed?1) IgA deposition in mesangium
    2) ACE-i/ARB to reduce proteinuria and protect kidney function. Corticosteroids and fish oil if proteinuria of >1g persists over 3-6 months of ACE-i/ARB and GFR > 50.
  20. 20What is Henoch-Schonlein purpura?Small vessel vasculitis and systemic variant of IgA nephropathy with IgA deposition in the skin/gut/joints in addition to the kidney.
  21. 21How does Henoch-Schonlein purpura present? How is it diagnosed? How is it managed?1) Nephritis, purpura rash on extensor surfaces (usually legs), flitting polyarthritis and abdominal pain (GI bleeding)
    2) Usually clinical. Confirmed with positive IF for IgA and C3 in skin. Renal biopsy is the same as with IgA nephropathy.
    3) Manage as with IgA nephropathy, steroids if there is gut involvement
  22. 22How does post-streptococcal GN occur? How does it present?1) Deposition of streptococcal antigen in the glomerulus leading to immune complex deposition after a throat (2 weeks) or skin (3-6 weeks) infection. Immune complex formation leads to inflammation
    2) Varies from haematuria to acute nephritis (haematuria, oedema, raised BP and oliguria)
  23. 23How is post-streptococcal GN diagnosed? How is it managed?1) Evidence of streptococcal infection; high ASOT, high anti-DNAse B, low C3.
    2) Supportive, antibiotics to clear the nephritogenic bacteria.
  24. 24What causes anti-GBM disease?Auto-antibodies to type IV collagen, found in the glomerular and alveolar basement membranes.
  25. 25How does anti-GBM present?Renal disease (oliguria/anuria, haematuria, AKI, renal failure) and lung disease (pulmonary haemorrhage in 50-90%: SOB, haemoptysis).
  26. 26How is anti-GBM diagnosed? How is it managed?1) Anti-GBM in circulation/kidney
    2) Plasma exchange, corticosteroids, and cyclophosphamide
    Poor prognosis is predicted by requirement for dialysis at presentation and high crescents on biopsy
  27. 27What is rapidly progressive GN?Any form of GN which rapidly progresses to renal failure over days to weeks (small vessel/ANCA vasculitis, lupus nephritis, anti-GBM disease) - other GNs can 'transform' to become rapidly progressive.
  28. 28How is rapidly progressive GN diagnosed? Treated?1) Breaks in GBM allow entry of inflammatory cells so that crescents are seen on biopsy.
    2) Treatment - corticosteroids and cyclophosphamide, other treatments depend on aetiology
  29. 29What are the secondary causes of nephrotic syndrome?SLE, DM, myeloma, amyloid and pre-eclampsia
  30. 30How is nephrotic syndrome managed in general?1) Reduce oedema - fluid (1L/day) and salt restriction. Diuresis with loop diuretics, eg furosemide. Aim for 0.5-1kg weight loss per day to avoid intravascular volume depletion and secondary AKI. Thiazide diuretics in resistant to high-dose loop diuretics.
    2) Treat underlying cause (i.e. in children is almost always Minimal Change Disease, do not need to biopsy if clinical suspicion is high)
    3) Reduce proteinuria - ACE-i/ARB (may not be needed in minimal change)
  31. 31What are the complications of nephrotic syndrome?1) Thromboembolism - hypercoagulable state due to high clotting factors, low anti-thrombin III, and platelet abnormalties. At risk of VTE/PE and renal vein thrombosis (loin pain, haematuria, raised LDH, AKI if bilateral)
    2) Infection - urine losses of immunoglobulins and immune mediators (high risk of urinary, respiratory and CNS infection). Infection also seen in areas of fluid accumulation (cellulitis, peritonitis, empyema). Risk of varicella with steroid treatment
    3) Hyperlipidaemia - high cholesterol, high LDL, high triglycerides and low HDL - thought to be due to hepatic synthesis in response to low oncotic pressure and defective lipid breakdown.
  32. 32In nephrotic/nephritic glomerulonephritis, what is the function of the following blood tests? Immunoglobulins, electrophoresis, complement (C3/C4), autoantibodies (ANA, ANCA, anti-dsDNA, anti-GBM, blood-culture and ASOT)?1) Immunoglobulins - IgA nephropathy, immune-complex associated membranoproliferative glomerulonephritis, Henoch-Schonlein
    2) Electrophoresis - to look at protein?
    3) Complement - membranoproliferative glomerulonephritis
    4) Auto-antibodies - anti-gbm, lupus, small vessel vasculitis, ASOT = anti-streptolysin O test (antibody to immunogenic streptococcal antigen)
    5) Blood culture - look for infection
  33. 33What is the function of the Bence-Jones protein urine test?Monoclonal globulin protein, suggestive of myeloma.
  34. 34What imaging and further investigations are done in glomerulonephritis?CXR (pulmonary haemorrhage - anti-GBM) and renal ultrasound (size and anatomy for biopsy).
    Renal biopsy is required for diagnosis
  35. 35What are the BP, FBC, and clotting requirements for a renal biopsy? What other blood test must be done?BP <160/95
    FBC: Hb>9; plt>100
    Clotting: PT and APTT >1.2
    Group and Save
  36. 36What are the complications of renal biopsy? What type of consent must be gained?Written consent
    Mild back/loin pain; visible haematuria (5%); bleeding requiring transfusion (1%); angiographic intervention (0.5%)
  37. 37What has to happen to aspirin, warfarin and heparin use before a renal biopsy?Stop aspirin a week before
    Get INR to 1.2
    Stop heparin 24hr beforehand
  38. 38After a renal biopsy, how long must the patient stay in hospital?Minimum 4 hours - monitor pulse, BP, symptoms and urine colour. Cannot be discharged until any visible haematuria has settled.

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(Renal Medicine) Met3B Fichas sobre Glomerulonephritis , creado por Anna Hogarth el 03/03/2020.
Creado por
Anna Hogarth · mar 2020
Actualizado
4 mar 2020
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