Glomerular endothelial cytotoxity and dysfunction in nephrosis with focal segmental glomerulosclerosis

Article type: Research Article

Authors: Futrakul, Narisa^; | Siriviriyakul, Prasong | Panichakul, Tasanee | Butthep, Punnee | Patumraj, Suthiluk | Futrakul, Prasit

Affiliations: Department of Physiology, King Chulalongkorn Memorial Hospital, Bangkok, Thailand | Department of Pediatrics, King Chulalongkorn Memorial Hospital, Bangkok, Thailand | Department of Immunology, Chulabhorn Research Institute, Bangkok, Thailand | Department of Immunocytology, Ramathibodi Hospital, Bangkok, Thailand

Note: [] Corresponding author. E‐mail: fmednft@md2.md.chula.ac.th.

Abstract: Glomerular endothelial cell dysfunction (GED) with defective release of vasodilator has been delineated in nephrosis (NS) in vivo and in vitro studies. In NS with focal segmental glomerulosclerosis (FSGS), an immunocirculatory balance may be impaired due to defective anti‐inflammatory cytokine. This study aimed at simultaneous determination of both proinflammatory cytokine (tumor necrosis factor alpha) and an anti‐inflammatory cytokine (interleukin‐10) in NS with FSGS. An endothelial cell cytotoxicity (ECC) was also examined using nephrotic serum. It was shown that (1) the initial endothelial cell cytotoxicity was significantly different from the control, (2) ratio between tumor necrosis alpha and interleukin‐10 was significantly elevated, and (3) intrarenal hemodynamics was changed significantly.

Keywords: Glomerular endothelial dysfunction, cytokine, endothelial cell cytotoxicity, nephrosis, focal segmental glomerulo‐ sclerosis

Journal: Clinical Hemorheology and Microcirculation, vol. 29, no. 3-4, pp. 469-473, 2003