TOPIC DISCUSSION: SECONDARY VS PRIMARY FSGS

FSGS can be broadly divided into genetic causes, primary or secondary causes. Leaving genetic aside, how does one differentiate between primary FSGS vs Secondary FSGS ( say from hyperfilatration, Obesity or Anabolic steroids use)?

Clinically and pathologically?
Some clues
1. Obviously, a good history might help you guide this differentiation.
2. Usually, its a slower increase in proteinuria in secondary cause usually Obesity or hyperfiltration related
3. The proteinuria amount is much much lower in a secondary cause. Someone with 30gm of proteinuria, think more primary
4. The progression to ESRD is also slower in the secondary cause unless probably a drug that is toxic like pamidronate induced collapsing FSGS
5. The pathology usually shows more glomerulomegaly in secondary causes.
6. The pathology usually shows more spotty and irregular foot process effacement in secondary cause and more diffuse in primary cause.
7. Absence of hypoalbumenemia might suggest a secondary cause as well
8. Normal blood pressure and no edema on exam might also suggest a secondary cause( classically seen in HIVAN)
9. Foot process width over 1500nm usually more points towards idiopathic form of FSGS.

Some interesting references:
http://www.ncbi.nlm.nih.gov/pubmed/17059996
http://www.ncbi.nlm.nih.gov/pubmed/18813290
http://www.ncbi.nlm.nih.gov/pubmed/11260414