Biomarkers of high salt intake.

Abstract

High salt intake is associated with hypertension, which is a leading modifiable risk factor for cardiovascular disease (CVD) and chronic kidney disease (CKD). International Guidelines recommend a large reduction in the consumption of sodium to reduce blood pressure, organ damage, and mortality. In its early stages, the symptoms of CKD are generally not apparent. CKD proceeds in a "silent" manner, necessitating the need for urinary biomarkers to detect kidney damage at an early stage. Since traditional renal biomarkers, such as serum creatinine, are not sufficiently sensitive, difficulties are associated with detecting kidney damage induced by a high salt intake, particularly in normotensive individuals. Several new biomarkers for renal tubular damage, such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), vanin-1, liver-type fatty acid-binding protein (L-FABP), and monocyte chemotactic protein-1 (MCP-1), have recently been identified. However, few studies have investigated early biomarkers for CKD progression associated with a high salt diet. This chapter provides insights into novel biomarkers for CKD in normo- and hypertensive individuals with a high salt intake. Recent studies using spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) fed a high salt diet identified urinary vanin-1 and NGAL as early biomarkers for renal tubular damage in SHR and WKY, whereas urinary KIM-1 was a useful biomarker for salt-induced renal injury in SHR only. Clinical studies are needed to confirm these findings.