PMID: 11924754Apr 2, 2002Paper

Lymphopenia in dialysis patients: a preliminary study indicating a possible role of apoptosis

Clinical Nephrology
M BhaskaranP C Singhal

Abstract

Lymphopenia is a common finding in dialysis patients. Since infection rate and mortality associated with infection are high in dialysis patients, lymphopenia may be one of the contributing factors. In the present study, we evaluated the mechanism responsible for lymphopenia in these patients. Lymphocytes isolated from dialysis patients showed increased apoptosis (p < 0.001) when compared to lymphocytes isolated from healthy subjects (healthy subjects, 0.5 +/- 0.2% vs. dialysis patients, 8.8 +/- 0.7% apoptotic cells/field). Sera from dialysis patients promoted lymphocyte apoptosis in a time- and dose-dependent manner. These sera also enhanced lymphocyte DNA fragmentation into multiple integers of 180 base pairs in the form of a ladder pattern. Cellulose acetate membranes promoted T cell apoptosis when compared to polysulfone membranes and to control. Cellulose acetate dialysis membranes also appear to promote lymphocyte FasL expression. Similarly, dialysis sera enhanced T cell Fas as well as FasL expression. Neither the cellulose acetate nor polysulfone membranes could induce FasL expression on B cells. Similarly, dialysis sera failed to induce FasL expression on B cells. On the other hand, anti-FasL antibodies attenuated dialys...Continue Reading

Citations

Apr 6, 2005·Pediatric Nephrology : Journal of the International Pediatric Nephrology Association·Jacek ZachwiejaAldona Siwińska
Nov 17, 2006·Nephron. Experimental Nephrology·Madhu BhaskaranPravin C Singhal
Feb 1, 2008·Clinical Journal of the American Society of Nephrology : CJASN·Stéphanie BadiouAnne-Marie Dupuy
Jul 13, 2005·Mayo Clinic Proceedings·Ayalew TefferiDavid J Inwards
Jan 24, 2009·Biochemical and Biophysical Research Communications·Jinlei LvGuohua Ding
Mar 3, 2006·Clinical Chemistry·Johanna AtamaniukMathias M Mueller

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

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