Ace inhibitors have a "love-hate" relationship with the kidney: In
diabetes, early treatment even in a non hypertensive has been shown to
decrease the progression to proteinuria and renal failure, but it does
decrease the creatinine clearance rate by dilatation of the efferent
renal arteriole (due to the blockage of formation of Angiotensin II)

Given that scleroderma is an autoimmune disease that affects the
capillaries -skin most obviously, but any and all tissues can be
affected, kidney perfusion can become very lopsided where the afferent
arteriole is unable to dilate (as is caused by steroids and NSAIDS)
and the kidney becomes no longer able to autoregulate.

The clobetasol counteracts the inflammatory response associated with
tissue destruction and inhibits T and B cell proliferation and the
production of prostaglandins as inflammatory mediators in the skin.
Prostaglandins in the renal parenchyma however promote blood flow, so
they are needed there

Interestingly enough, where I practice medicine, there is a large
tribe of Native Americans (Choctaw) who have a _Fifty-fold_ incidence
of scleroderma so I get to see it a lot.
One memorable case was of a woman who had "poison ivy" of the face for
2 years and ended up having CREST syndrome: Calcinosis of the skin,
Reynaud's phenomenon, Esophageal Stricture, Sclerodactyly and
Telangiectasias. Took me 30 seconds to diagnose because "we see what
we know" (Impressed my medical student at the time:-))

david