Specific Renal Pathologies Flashcards by Clara Sage

Difference between primary and secondary glomerular disease

Primary - only the kidney is affected

Secondary - other organs are also affected

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4 ways that glomerular disease can affect the glomerulus

Focal - only some glomeruli
Diffuse - all glomeruli are affected
Segmental - only part of glomerulus
Global - affects all of the glomerulus

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5 pathologies of glomerular disease

Proliferative - abnormal proliferation of cells - can form a cresent appearance if severe proliferation of macrophages

Mesangial - excess production of mesangial matrix

Membranous disease - basement membrane is damaged and thickened

Membranoproliferative - thickening of glomerular basement membrane and cellular proliferation - usually of mesangial cells

Vasculitis - inflammation of blood vessels

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Signs of mild glomerular damage

Asymptomatic proteinuria or haematuria

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Signs of acute nephritic syndrome

Hematuria, acute fall in GFR, sodium and water retention and hypertension

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Signs of chronic glomerulonephritis

Slow progressive glomerular damage

Proteinuria, haematuria and hypertension

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Signs of rapidly progressive glomerulonephritis

Rapid renal failure

Oliguria, haematuria and proteinuria

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Signs of nephrotic syndrome

Heavy proteinuria, hypoalbuminemia and oedema

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Effects of glomerulonephritis

Inflammation of glomerulus and nephrons

1) Restricts blood flow - compensatory rise in BP
2) Damage to filtration system - protein and blood leak into urine
3) Loss of usual filtration capacity = acute kidney injury

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Types of glomerulonephritis x6

1) IgA nephropathy
2) Henoch-Schonlein purpura (HSP)
3) SLE
4) Goodpastures
5) Post-streptococcal
6) Rapidly progressive GN

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What is IgA nephropathy

- typical presentation

Commonest GN in developed world
Macroscopic haematuria 1-2 days after URTI
Young male, intermittent episodic macroscopic haematuria
IgA raised (post-infection)
deposits in mesangial cells

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Treatment of IgA nephropathy and HSP

BP control with ACE-i

If nephritic presentation - immunosuppression

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Prognosis of IgA nephropaty

20% develop ESRF in 20years

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What is HSP

Systemic variant of IgA nephropathy - small vessel vasculitis
Mainly affects children under 10

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Features of HSP

Purpuric rash on extensor surfaces - ankles, elbows, buttocks
Flitting polyarthritis
Abdominal pain (GI bleeding)
Nephritis

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DX of IgA nephropathy and HSP

IgA in biopsy and C3 - complement

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Prognosis of HSP

15% nephritic patients - ESRF

If nephritic and nephrotic - 50% - ESRF

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What is Goodpastures disease

Autoantibodies to G BM - type 4 collagen

Also affects the lungs - haemoptysis from haemorrhage - especially if they smoke

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Presentation of Goodpastures disease

Haematuria/nephritic syndrome

AKI may occur within hours of onset

Treatment of Goodpastures syndrome

Plasma exchange, steroids

Cytotoxics - cyclophosphomide may be needed

Prognosis of Goodpastures syndrome

If treatment started early then prognosis is good and relapses are unlikely
If renal damage (diffuse therefore likely) then good for renal transplant

What happens in post-streptococcal GN

Diffuse GN occurs 1-2 weeks after sore throat or skin infection
Antigen deposited on glomerulus - host reaction and immune complex formation
- presents with nephritic syndrome

Treatment of post-streptococcal GN

Supportive and 95% recover renal function

What is rapidly progressive GN?

Most aggressive GN - can cause ESRF in days

All have cresents in glomerulus with biopsy

Causes of RPGN

Immune complex (post-infectious, SLE) Pauci-immune disease Anti-GBM disease

Triad of nephrotic syndrome

Proteinuria, hypoalbuminaemia, oedema

Secondary causes of nephrotic syndrome

SLE, Hep B/C, Diabetic nephropathy, para-neoplastic, amyloidosis, drug related

Drug related nephrotic syndrome

NSAIDs, penicillamine, Anti-TNF, gold

Investigations in nephrotic syndrome

Majority of children its minimal change - therefore no biopsy done All adults should be biopsied - difficult because hypercoagulable state and oedema

Complications of nephrotic syndrome - x3

Susceptibility to infection - decreased serum IgG, decreased compliment activity and decreased T cell function - also because of immunosuppressive treatment Thromboembolism - hypercoagulable state because increased clotting factors and platelet abnormalities - loss of antithrombin III Hyperlipidaemia - increased cholesterol and triglycerides - thought to be due to increased hepatic lipoprotein synthesis due to low oncotic pressure

General treatment of nephrotic syndrome

1) Reduce oedema - loop diuretics eg. furosemide 0 fluid and salt restrict 2) ARB or ACEi - reduce proteinuria 3) Anti-coagulate and give statin for cholesterol 4) Vaccinate and treat infections rapidly 5) Treat underlying cause

What is minimal change nephropathy?

Commonest cause of nephrotic syndrome in children and 20% of adults Light microscope shows no change - hence name Electron microscopy shows fusion of podocyte foot processes

Presentation of minimal change in children

Association with atopy - eczema, asthma and hayfever | Often follows URTI

Treatment of minimal change

Steroids If relapses - ciclosporin 1% get ESRF - renal impairment does not occur

What is membranous nephropathy

Commonest cause of nephrotic syndrome in older patients | Thickening of GBM and subepithelial deposits

Causes of membranous nephropathy

Usually idiopathic Secondary to malignancy, Hep B, SLE Gold or penicillamine

Treatment of membranous nephropathy

Treat underlying cause If idiopathic or autoimmune Steroids and chorambucil or cyclophosphamide

Prognosis of membranous nephropathy

Minority develop ESRF

What is mesangiocapillary glomerulonephritis?

Also known as membranoproliferative | Uncommon - occurs mainly in young adults and children

Two types of mesangiocapillary glomerulonephritis

Immune complex-mediated (underlying cause can usually be found) and complement-mediated

Treatment of mesangiocapillary GN

Most develop ESRF and there is no treatment Treat underlying cause if one is found ACE/ARB for all Steroids + cyclophosphamide if rapidly progressive

What is focal segmental GN?

Accounts of 15% of adult nephrotic syndrome | IgM and C3 deposits in affected areas

Treatment of focal segmental GN

30% respond to steroids | If steroid resistant - try cyclophosphamide or ciclosporin

Prognosis of focal segmental GN

30-50% go on to develop end stage renal failure

Causes of chronic tubulointerstitial nephritis

Abnormal anatomy disorders eg. reflux nephropathy and PCKD | In normal anatomy much more rare - 3% and cause is normal analgesic nephropathy