SLE

Like Dr House said, it’s always LUPUS!

What is it?

  • Common (clinical disease >50%)
  • Black / hispanic / asian > white

Presentations:
–Isolated urinary abnormalities
–Nephrotic syndrome
–Progressive renal impairment
–RPGN
–Other (eg TMA)
– Joint pains
-Rash

6 Classes:

  1. Class I – Minimal mesangial
  2. Class II – Mesangial proliferation
  3. Class III – Focal proliferative
  4. Class IV – Diffuse proliferative
  5. Class V – Membranous nephropathy
  6. Class VI – Advanced glomerulosclerosis

and a final class that is coming :

Lupus podocytopathy

  • Indistinguishable from MCN
  • Serologic or clinical features of SLE
  • Normal or minimal mesangial
  • Mesangial deposits only
  • Typically steroid responsive
  • > common than chance

Lupus path copy

Treatment?

By no means 100% correct, but based on guidelines

Lupus treatment copyFor Class III – V :

  • EUROLUPUS : NIH recommends HIGH dose cyclophosphamide
  • ACCESS trial : abatacept; confirms comparable efficacy in black + hispanic patients, but no benefit as add on therapy
  • ALMS : MMF vs NIH Cyc – no difference in outcomes but possible MMF > Cyc benefit in black patients, but equivalent in all with GFR < 30

Relapse:

Mild : Increase steroids +/- aza / MMF
Moderate /  severe :  Repeat initial successful induction therapy. Can repeat CYC. Consider RTX

In pregnancy:

  • Wait until remission > 6/12
  • Continue HCQ
  • No – MMF / ACE / ARB / cyclophos
  • Yes – Aza / CNIs / labetalol / nifedipine/ steroids
  • KDIGO: do not taper steroids or Aza during pregnancy or for three months after
  • Aspirin

 

Bad prognostic factors:

  • Male
  • Younger age < 24 yrs
  • Low socioeconomic status
  • Black race
  • high Cr at presentation
  • HTN
  • Severe anaemia
  • Hypocomplementaemia
  • High proteinuria
  • Elevated dsDNA
  • Delay in starting treatment
  • Nephritic relapse
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