MO506RELATIONSHIP BETWEEN SODIUM CONSUMPTION, PRO-INFLAMMATORY PARAMETERS AND KIDNEY DISEASE IN THE JACKSON HEART STUDY

Abstract

Abstract Background and Aims Kidney disease is thought to be linked to inflammation. Pro-inflammatory parameters like C-reactive protein (CRP), endothelin-1, and TNF-a inversely associate with kidney function cross-sectionally and some have predictive value for longer-term kidney outcomes. Given the recently argued pro-inflammatory effect of sodium, we questioned whether sodium consumption has a role in the relationship between pro-inflammatory parameters and renal outcomes. Method Our research question was investigated using the Jackson Heart Study, which is a large prospective cohort study involving n=5301 Afro-Americans residing in Jackson, Mississippi, US. Spot urine sodium was used to estimate 24-hour sodium excretion with the Kawasaki formula, serving as a proxy for sodium consumption, and was available for n=1831 participants (depicting a random sample of the total population) that had a median follow-up of 8 years. Multiple linear regression was used to assess the relationship between sodium consumption and pro-inflammatory parameters. The parameters available for this cohort involved endothelin-1, high-sensitivity CRP, and leukocyte subsets (monocytes, neutrophils, and lymphocytes). Models were adjusted for potential confounders, involving sex, age, body mass index, estimated potassium intake, smoking status, and presence of diabetes. Subsequently, linear regression analyses between pro-inflammatory parameters and baseline estimated glomerular filtration rate (eGFR CKD-EPI) and change during follow-up were carried out with and without adjustment for sodium consumption as a confounder, to explore the possibility of a causal mediating pathway. Results Increased sodium consumption significantly associates with increased serum endothelin-1 levels in both unadjusted and adjusted models (Table 1). There was no association between sodium consumption and leukocyte subsets. There was a negative association between sodium consumption and CRP (Table 2). CRP was not associated with eGFR at baseline (p=0.20) or eGFR change from baseline (p=0.20). Endothelin-1 was inversely associated with eGFR at baseline (beta -0.06, p<0.001) and with eGFR change from baseline (beta 2.3 p=0.03). However, when these models were corrected for sodium consumption, endothelin-1 was no longer a significant predictor (beta -0.01 p=0.4 for eGFR at baseline) or was inversed (beta -0.1; p=0.001 eGFR during follow-up). Conclusion In this prospective cohort of Afro-Americans, increased sodium consumption is associated with increased circulating endothelin-1 levels. If this relationship proves to be causal (as suggested by animal sodium loading studies), this implies that sodium consumption may (at least partly) be underlying the relationship between endothelin-1 and worse renal outcomes.