Eric R. Schroeder1, Soolim Jeong1, Matthew C. Babcock2, Joseph C. Watso3, Austin T. Robinson1. 1Auburn University, Auburn, AL. 2University Of Colorado, Aurora, CO. 3Florida State University, Tallahassee, FL.

BACKGROUND: Chronic high salt diet (HSD) increases the risk of cardiovascular disease and kidney disease. In rodents, HSD causes tubular injury despite no changes in blood pressure and glomerular injury. Recently, our group and others demonstrated that short-term HSD increases tubular injury in humans; however, it is unclear whether HSD causes glomerular injury in humans. Therefore, we sought to examine whether a short-term HSD increases urinary nephrin excretion, a biomarker for glomerular injury, in healthy young adults. METHODS: We analyzed data from 13 participants (7 Males/6 Females; age: 24 ± 4 years; BMI: 23.8 ± 2.9 kg/m2; BP: 112 ± 11/66 ± 10 mmHg, mean ± SD) recruited from a larger randomized, crossover, double-blind study (NCT03565653). Participants consumed HSD (3.9 grams of sodium) or placebo (PLA; dextrose) capsules for 10 days each separated by ≥ two weeks. Participants collected a 24-hr urine sample in a light-protected container from which mixed aliquots were used to measure urine flow rate, sodium excretion, and biomarkers of glomerular injury (nephrin) and filtration (Cystatin C excretion and creatinine clearance). We measured urine nephrin and Cystatin C concentration using enzyme-linked immunosorbent assays. We measured urine and serum creatinine using the Jaffe reaction to subsequently calculate creatinine clearance. Statistical analysis included paired t-tests and Wilcoxon signed rank tests with α set at < 0.05. RESULTS: There were no significant differences for urine nephrin concentration in HSD versus PLA (0.82 ± 0.66 vs 0.69 ± 0.62 μg/ml, p = 0.38), nephrin indexed to flow rate (1.04 ± 0.67 vs 0.89 ± 0.97 μg/min, p = 0.22), or nephrin indexed to creatinine (9.72 ± 6.56 vs 9.81 ± 8.79 ng/ml÷mg/dL, p = 0.89). Similar to our previous findings, there was an increase in urinary Cystatin C excretion (0.13 ± 0.04 vs 0.10 ± 0.04 mg/day, p = 0.04) and a trend for elevated creatinine clearance (143 ± 26 vs 125 ± 58 mL/min/1.73m2 p = 0.08) after HSD. CONCLUSION: These preliminary findings suggest that a short-term high salt diet does not elicit glomerular injury in a small cohort of healthy young adults, but does increase glomerular filtration. Further research on high salt and glomerular injury is warranted in larger, diverse cohorts.

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