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Nephrology & Urology > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What does GN present with?

A
  • HTN
  • Haematuria
  • Renal impairment
  • Nephrotic syndrome
  • Nephritic syndrome
  • Rapidly progressing glomerular nephritis
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2
Q

What is nephrotic syndrome?

A
  • Proteinuria (>3.5g/m2/day)
  • Reduced serum albumin (less than 25g/L)
  • Oedema
  • Hyperlipidaemia
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3
Q

What is nephritic syndrome?

A
  • Haematuria
  • Oliguria (<300mls per day)
  • Proteinuria (<3g/m2/day)
  • Fluid retention
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4
Q

What is rapidly progressive glomerular nephritis (RPGN)?

A
  • Normal renal function to ESRF over a period of weeks
  • Includes diseases like Wegener granulomatosis and polyarteritis
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5
Q

What are the pathophysiology of post infectious GN?

A
  • Infection (streptococci production of Ab/IC - usually type 12, group A strep)
  • Deposition of Ab/IC in mesangium etc, complement activation and infiltration of leukocytes
  • Destruction of glomerular cells, proliferation of epithelial cells and crescent formation
  • Glomerulosclerosis, tubular loss and hypertensive damage
  • Histology shows crescentic GN
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6
Q

What are the clinical and histological features of post infectious GN?

A
  • Patients typically presnet 1-3 weeks after a streptococcal infection (i.e. tonsilitis, impetigo)
  • Symptoms and investigation results include:
    • Haematuria
    • Proteinuria
    • HTN
    • Renal impairment
    • Urinary red cell casts
    • Proliferation of all glomerular cells, crescents
    • Infiltrating cells
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7
Q

What is the pathophysiology of IgA nephropathy?

A
  • Infection or HSP, cirrhosis, coeliac disease? Production if IgA
  • Mesangial deposition of IgA
  • Lysis of mesangium, proliferation of MC, matrix production and healing or scarring
  • Glomerulosclerosis, tubular loss and hypertensive damage
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8
Q

What are the clinical and histological features of IgA nephropathy?

A
  • Most common cause of primary GN
  • Peak age at presentation in 20s
  • Haematuria
  • Proteinuria
  • HTN
  • Renal impairment
  • ESFR-Upro
  • HBP
  • Histology shows IgA deposits and glomerular mesangial proliferation
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9
Q

What is the pathophysiology of membranous GN?

A
  • Tumour? Drugs? Infection? CTD? Production of IC and Ab
  • Deposition or formation of IC in the GBM and mesangium
  • Altered GBM charge, permeability, selectivity and thickening
  • Glomerulosclerosis, tubular loss and hypertensive damage
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10
Q

What are the clinical features of membranous GN?

A
  • Most common type of GN overall
  • Bimodal peak in age at presentation in 20s and 60s
  • Proteinuria
  • Nephrotic syndrome
  • HTN
  • Renal impairment
  • Histology shows IgA and complement deposits on the basement membrane
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11
Q

What are the causes of crescentic GN/RPGN?

A
  • Goodpastures syndrome
  • Polyarteritis nodosa
  • Wegeners granulomatosis
  • Post infectious/bacterial endocarditis
  • Lupus
  • Idiopathic
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12
Q

What is the pathophysiology of systemic vasculitis?

A
  • Necrotising granulomas of midline structures
  • Necrotising vasculitis
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13
Q

What are the clinical and histological features of systemic vasculitis?

A
  • Bleeding
  • Stiffness
  • Deafness
  • Pulmonary symptoms include opacities and haemorrhage
  • Urinary red cell casts
  • ANCA
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14
Q

What is the pathophysiology of minimal change disease?

A
  • T cell and cytokine mediated
  • Target epithelial cells causing GBM change
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15
Q

What are the clinical and histological features of minimal change disease?

A
  • Most common cause of nephrotic syndrome in children
  • Nephrotic syndrome
  • May follow UTI
  • Light microscopy normal
  • EM (foot process fusion)
  • IF (CT, IgM deposition)
  • eGFR normal or reduced due to intravascular depletion
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16
Q

How is GN treated?

A
  • Post infectious (antibiotics)
  • IgA nephropathy (no specific, antihypertensive)
  • Membranous (non specific; antihypertensive therapy, NSAIDs, statins, specific therapy; steroids, chlorambucil, cyclophosphamide/azathioprine, rituximab, treat underlying disease)
  • Systemic vasculitis (steroids, cytotoxics, septrin)
  • Minimal change disease (steroids, cyclophosphamide, cyclosporine)

Nephrology & Urology (17 decks)

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