A relatively large body of evidence supports the notion that glomerular capillary wall and mesangial alterations in
diabetic nephropathy involve biochemical alterations of
glycoproteins in these structures. Evidence in experimental animals rendered diabetic reveals that the administration of
heparin and other anionic
glycoproteins can effectively prevent the biochemical alterations that promote
albuminuria. Moreover,
angiotensin II inhibits
heparan sulfate synthesis, while heparins modulate
angiotensin II signaling in glomerular cells, inhibiting
aldosterone synthesis and lowering
proteinuria in diabetes patients.
Sulodexide, a mixture of
heparin and
dermatan sulfate, appears to be a promising treatment for diabetic
proteinuria partially resistant to renin-angiotensin system blocking agents.
Sulodexide prevents
heparan sulfate degradation, thus allowing reconstruction of
heparan sulfate content and restoration of glomerular basement membrane ionic permselectivity. The antiproteinuric effect appears to be mainly related to the basal
proteinuria and consequently to the
duration of treatment in a relatively large number of small clinical trials. On the other hand, several
sulodexide pharmacodynamic properties could improve the prognosis of
chronic kidney disease patients, also independently from its antiproteinuric effect. However,
sulodexide development as an antiproteinuric
drug needs to be continued, in order to define which kind of patients could better respond to this treatment.