Abstract
Chronic high-salt diet-associated renal injury is a key risk factor for the development of hypertension. However, the mechanism by which salt triggers kidney damage is poorly understood. Our study investigated how high salt (HS) intake triggers early renal injury by considering the ‘gut-kidney axis’. We fed mice 2% NaCl in drinking water continuously for 8 weeks to induce early renal injury. We found that the ‘quantitative’ and ‘qualitative’ levels of the intestinal microflora were significantly altered after chronic HS feeding, which indicated the occurrence of enteric dysbiosis. In addition, intestinal immunological gene expression was impaired in mice with HS intake. Gut permeability elevation and enteric bacterial translocation into the kidney were detected after chronic HS feeding. Gut bacteria depletion by non-absorbable antibiotic administration restored HS loading-induced gut leakiness, renal injury and systolic blood pressure elevation. The fecal microbiota from mice fed chronic HS could independently cause gut leakiness and renal injury. Our current work provides a novel insight into the mechanism of HS-induced renal injury by investigating the role of the intestine with enteric bacteria and gut permeability and clearly illustrates that chronic HS loading elicited renal injury and dysfunction that was dependent on the intestine.
Highlights
The prevalence of hypertension is continuously increasing and is becoming a major public health problem around the world.[1,2] The pathogenesis of hypertension is not fully understood
Chronic high salt intake led to enteric dysbiosis First, we examined whether HS intake could influence intestinal bacteria
Our results demonstrated that chronic HS feeding could result in enteric dysbiosis, as evidenced by the changes in bacterial count and microflora composition
Summary
The prevalence of hypertension is continuously increasing and is becoming a major public health problem around the world.[1,2] The pathogenesis of hypertension is not fully understood. Alcohol consumption can induce enteric dysbiosis and can disrupt gut barrier integrity, which allows pathogenassociated molecular patterns to penetrate the blood and translocate into the liver to result in hepatic steatosis and further alcoholic hepatitis.[8,9,10] This theory prompted us to investigate whether salt uptake is able to directly disrupt intestinal homeostasis and, in turn, trigger early renal injury. To test this hypothesis, we fed mice with HS water for 8 weeks and studied the resulting intestinal pathophysiological changes and their contributions to early renal abnormalities
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