T-cell ageing in end-stage renal disease patients: Assessment and clinical relevance

Figure 1 Schematic overview of the effects on the T-cell compartment caused by the uremia-induced pro-inflammatory milieu in end-stage renal disease patients. Loss in renal function creates a pro-inflammatory milieu by the retention of uremic toxins and cytokines which increases oxidative stress and the production of inflammatory cytokines. This pro-inflammatory uremic milieu is associated with premature T-cell ageing, which results in defective T-cell immunity. End-stage renal disease (ESRD) patients have a lower thymic output of naïve T cells which can be measured by the TCR excision circles (TREC) content and the percentage of CD31-expressing naïve T cells. Furthermore, ESRD patients have an expanded population of highly differentiated T cells with a loss in CD28 expression and an increase in apoptotic markers. Moreover, these expanded T cells have a high proliferative history causing a decline in telomere length which can be measured by the relative telomere length analysis.