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Nephrol Dial Transplant (2001) 16: 882-885
© 2001 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Permeability plasma factors in nephrotic syndrome: more than one factor, more than one inhibitor

Gian Marco Ghiggeri1,, Mary Artero2, Michele Carraro2 and Francesco Perfumo1

1 Unit and Laboratory of Nephrology, G. Gaslini Children Hospital, Genoa and 2 Istituto di Medicina Clinica, University of Trieste, Trieste, Italy

Idiopathic FSGS: definition and classification

Idiopathic focal segmental glomerulosclerosis (FSGS) is a common clinical entity characterized by the nephrotic syndrome, unresponsiveness to steroids and frequent progression to end-stage renal failure.

The basic pathological lesion of FSGS involves focal accumulation of extracellular matrix and lipids within glomeruli that is present also in other glomerular diseases leading to sclerosis. However, owing to the characteristic focal and segmental nature of the process, FSGS emerges as a well-defined clinical entity in which local, mechanical or other undefined mechanisms may play a pathogenetic role. Most cases of FSGS are sporadic, but a few family pedigrees have been reported in which the disease is inherited in dominant or recessive forms. Recent advances in molecular genetics of familial forms indicate that FSGS results from mutations in podocyte cytoskeleton components such as podocin [1] and {alpha}-actinin 4 [2] or structural proteins of the slit diaphragm [3] such . . . [Full Text of this Article]

The role of humoral factors in glomerular albumin permeability in idiopathic FSGS

Cellular origin of permeability factors

Physiologic inhibitors of increased glomerular permeability

Loss of inhibitors and specificity of permeability activity: the case of molecular FSGS

Future aspects and conclusions

Towards a new classification and selective therapeutic approaches
Note added in proof

Acknowledgments

Notes

References


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