Introduction: Adherence to a low salt diet has been shown to improve long term outcomes in kidney transplant recipients (KTRs), but the mechanism of this effect is unknown. Salt is now recognized as having a direct effect on multiple immune cells, including Th17 and Tc17 cells, which are implicated in acute and chronic allograft rejection. We investigated how salt may affect in vitro IL-17 responses in KTRs.

Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from KTRs (>3 months post transplantation) and healthy controls, and cultured for 7 days under Th17 polarising conditions in standard media (Na concentration 133mmol/l) and in media supplemented with 40mM NaCl (‘high salt media’). Th17 and Tc17 cells were analysed with fluorescence-activated cell sorting, and supernatant IL-17 concentrations were measured via an enzyme-linked immunosorbent assay. Cell populations and IL-17 concentrations were compared between standard and high salt media, and KTRs and controls.

Results: 14 KTRs (age 53 ± 14 years; median creatinine 108μmol/l) and 10 controls were included. All KTRs were on immunosuppression (13 maintenance calcineurin inhibitor with/without antiproliferative; 1 sirolimus monotherapy). Th17 cells accounted for 9.9 ± 8.5% of CD4+ cells in standard media and 15.5 ± 7.9% in high salt media (p=0.0134; Figure). Tc17 cells accounted 4.0 ± 2.6% of CD8+ cells in standard media and 11.6 ± 6.3% in high salt media (p=0.0017; Figure). Supernatant IL-17 concentrations were 3.3 ± 3.9ng/ml and 6.3 ± 7.6ng/ml in standard and high salt media respectively (p=0.0046). Th17 and Tc17 polarisation were greater in KTRs than controls in high salt conditions, whereas IL-17 production was greater in controls.

Discussion: Salt increases pro-inflammatory IL-17 responses in KTRs, despite in vivo immunosuppression. Whether salt restriction may be used to reduce immune mediated allograft injury in KTRs is to be investigated.

[MP04] Salt augments in vitro IL-17 responses in kidney transplant recipients