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Blood pressure and albuminuria in a female mouse model of systemic lupus erythematosus: Impact of long-term high salt consumption.

Sodium intake is linked to hypertension in both human and animal studies. Dietary salt may be an important environmental factor that promotes autoimmunity. We hypothesized that a long-term high salt diet would accelerate the progression of autoimmunity, hypertension, and albuminuria during systemic lupus erythematosus (SLE), a chronic autoimmune disorder associated with prevalent hypertension and renal disease. To test this, an experimental model of SLE (female NZBWF1 mice) with hypertension and renal disease was used. SLE mice were fed a high salt (4% NaCl) or normal (0.4% NaCl) diet for 24 weeks from 10 weeks to 34 weeks of age, a time by which female NZBWF1 mice typically have hypertension and renal disease. Plasma anti-dsDNA autoantibodies were measured as an indicator of active SLE disease, and urinary albumin was monitored as a marker of renal disease. Arterial pressure was measured in conscious mice at 34 weeks of age. Urinary endothelin-1 (ET-1) excretion, renal endothelin A and B receptor protein expression, and renal mRNA expression of NOS1, NOS2, NOX2, MCP-1, TNF-a, SGK1, and IL-2 were assessed to determine the impact on transcripts commonly altered by high salt diet. SLE mice fed a high salt diet had increased circulating autoantibodies, but high salt diet did not significantly affect albuminuria or arterial pressure. Urinary ET-1 excretion was increased, whereas renal endothelin A receptor and IL-2 expression were decreased in response to a high salt diet. These data suggest that chronic high salt diet may not accelerate cardiovascular and renal consequences commonly associated with SLE.