Early urinary biomarkers for renal tubular damage in spontaneously hypertensive rats on a high salt intake

• DOI: 10.1038/hr.2015.103
• Publication Date: 2015-09-17T06:01:12Z
• Authors: Keiko Hosohata; Daisuke Yoshioka; Akira Tanaka; Hitoshi Ando; Akio Fujimura
• Keywords: Male; Blood Pressure; GPI-Linked Proteins; Lipocalins; Amidohydrolases; Rats; 03 medical and health sciences; Kidney Tubules; 0302 clinical medicine; Lipocalin-2; Creatinine; Proto-Oncogene Proteins; Rats, Inbred SHR; Hypertension; Albuminuria; Animals; Sodium Chloride, Dietary; Cell Adhesion Molecules; Biomarkers; Acute-Phase Proteins

A high salt intake exacerbates hypertension and accelerates renal tubular damage in hypertensive patients. However, data concerning early biomarkers for renal tubular change induced by a high salt intake are limited. The objective of this study was to clarify the time course of new biomarkers for renal tubular damage during high salt intake in spontaneously hypertensive rats (SHR). Male SHR received a regular or high-salt diet from 9 to 17 weeks of age. At 10 weeks of age, a high salt intake caused renal tubular damage, which was further exacerbated at 17 weeks of age. Although albuminuria was detected in salt-loaded SHR at 14 weeks of age, urinary excretion of vanin-1 and neutrophil gelatinase-associated lipocalin (NGAL) was elevated in these animals from 10-17 weeks of age. However, kidney injury molecule-1 (Kim-1) was elevated at 15 weeks of age in salt-loaded SHR. These results suggest that urinary vanin-1 and NGAL are potentially early biomarkers for renal tubular damage in SHR under a high salt intake.