Long‐term high salt diet delays development of renal injury and inflammation in murine systemic lupus erythematosus (860.12)

Systemic lupus erythematosus (SLE) is an autoimmune disorder with prevalent renal disease, for reasons that continue to be elucidated. Recent evidence suggests that dietary salt may be an important environmental factor that promotes some autoimmune diseases. Therefore, we hypothesized that a long‐term high salt diet would accelerate the progression of renal disease during SLE. In order to test this, an established experimental model of SLE (female NZBWF1 mice) was fed a standard (0.4% NaCl) or high salt (4% NaCl) diet starting at 10 weeks of age. Sodium intake (in meq/day) was measured three times throughout the study and was significantly greater in high salt fed animals at 16 weeks of age (2.9±0.6 vs. 0.5±0.06 , p=0.01), 23 weeks (4.8±0.8 vs. 0.6±0.06, p=0.004) and 29 weeks (5.7±0.6 vs. 0.6±0.05, p=0.0007). Urinary albumin was monitored monthly until 30 weeks then weekly by dipstick assay as a marker of renal injury until 34 weeks of age at which time the mice were euthanized and the kidneys were harvested. Renal cortex enriched mRNA was analyzed by qRT‐PCR for inflammatory markers. 80% of animals (n=5) on a normal diet developed albuminuria (蠅 100 mg/dL), whereas none (0%, n=5) of the high salt fed animals developed albuminuria. Renal cortical interleukin‐2 (IL‐2), a cytokine important for T cell differentiation, expression was significantly lower in high salt fed animals (0.26±0.14 relative to normal chow fed mice, p=0.03). These data suggest that, contrary to the original hypothesis, a long‐term high salt diet may protect against the renal injury associated with SLE, possibly through alterations in IL‐2 mediated T cell differentiation. Furthermore, the data advance our overall understanding of how dietary salt may impact different autoimmune disorders. Grant Funding Source : Supported by T32HL105324, 12GRNT12060203, HL085907, and HL051971