Synaptopodin immunoexpression in steroid-responsive and steroid-resistant minimal change disease and focal segmental glomerulosclerosis.

BACKGROUND AND

OBJECTIVES

Synaptopodin is protein of podocytes, and a part of the actin-based contractile apparatus of foot-processes. Recently, proteins expressed by the podocyte were found to be important for the integrity of the glomerular filtration barrier. Podocytes are injured in many forms of glomerulopathies, including minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS). The study was undertaken to determinate if synaptopodin immunoexpression in renal tissue specimens differs between patients with steroid-responsive MCD, steroid-resistant MCD, and FSGS.

METHODS

Synaptopodin immunoexpression was evaluated by immunoperioxidase staining with a mouse anti-human monoclonal antibody in 12 renal biopsy specimens in patients with steroid-responsive MCD, 10 renal tissues in steroid-resistant MCD, and in 14 renal biopsy specimens in patients with FSGS. As a control 10 tissue specimens of the kidneys removed because of trauma were used. Synaptopodin expression was quantified as a percentage of glomerular tuft by computerized image analysis system.

RESULTS

In normal controls synaptopodin immunoexpression was seen in podocytes along the glomerular basement membrane in a finely linear pattern. No changes were found in synaptopodin immunoexpression in steroid-responsive MCD versus controls. In patients with steroid-resistant MCD and FSGS a granular pattern of synaptopodin immunoexpression was seen. Areas of sclerosis in patients with FSGS did not demonstrate synaptopodin expression. Statistical analysis showed significantly diminished synaptopodin immunoexpresion in glomeruli in patients with steroid-resistant MCD and FSGS as compared with steroid-responsive MCD group and controls. Moreover, in renal tissues in patients with FSGS the immunoexpression of synaptopodin was decreased in comparison with renal biopsies in patients with steroid-resistant MCD.

IN

CONCLUSIONS

our results suggest that abnormal distribution and reduced expression of synaptopodin may be associated with poor response to steroid therapy in MCD and FSGS.