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Perit Dial Int 29(Supplement_2): 45-48
2009
© 2009 International Society for Peritoneal Dialysis
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Part 2: Cellular and Molecular Biology of the Peritoneum and Peritoneal Dialysis

TAMING APOPTOSIS IN PERITONEAL DIALYSIS

Beatriz Santamaria1, Alvaro Conrado Ucero1, Alberto Benito–Martin1, Rafael Selgas2, Marta Ruiz–Ortega3, Ana B. Sanz1, Jesús Egido1 and Alberto Ortiz1,a

Dialysis Unit,1 Fundación Jiménez Díaz, Universidad Autónoma de Madrid, Instituto Reina Sofía de Investigación Nefrológica; Servicio de Nefrología,2 Hospital Universitario La Paz; Laboratory of Cellular Biology in Renal Diseases,3 Universidad Autónoma de Madrid, Madrid, Spain

a All authors (except JE) belong to REDinREN (Red de Investigación Renal Española del Instituto de Salud Carlos III, RETICS 06/0016).

Correspondence to: A. Ortiz, Unidad de Diálisis, Fundación Jiménez Díaz, Av Reyes Católicos 2, 28040 Madrid, Spain. aortiz{at}fjd.es

Excessive, insufficient, or untimely apoptosis may result in disorders of cell numbers. Peritoneal demesothelization is an example of disease by decreased cell number; untimely leukocyte apoptosis impairs peritoneal defense. Conventional peritoneal dialysis solutions accelerate neutrophil apoptosis. Glucose degradation products such as 3,4-dideoxyglucosone-3-ene (3,4-DGE) decisively contribute to apoptosis induced by these solutions, in both leukocytes and mesothelial cells and in both culture and peritoneal dialysis patients. Pan-caspase inhibition retards neutrophil apoptosis and improves peritoneal clearance of Staphylococcus aureus in animal models. However, regulation of apoptosis in mesothelial cells is more complex than in leukocytes, and caspase inhibitors may not be the optimal drugs to modulate apoptosis in these cells. In this regard, Bax antagonistic peptides protect mesothelial cells from 3,4-DGE. In addition, novel molecular targets have been identified. Short-term modulation of apoptosis may be useful to accelerate recovery and to prevent irreversible peritoneal injury following peritonitis.

KEY WORDS: Apoptosis; caspases; Bax; Bcl-xL; mesothelial; peritonitis.






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