Biomarkers for Chronic Kidney Disease Associated with High Salt Intake

Abstract

High salt intake has been related to the development to chronic kidney disease (CKD) as well as hypertension. In its early stages, symptoms of CKD are usually not apparent, especially those that are induced in a “silent” manner in normotensive individuals, thereby providing a need for some kind of urinary biomarker to detect injury at an early stage. Because traditional renal biomarkers such as serum creatinine are insensitive, it is difficult to detect kidney injury induced by a high-salt diet, especially in normotensive individuals. Recently, several new biomarkers for damage of renal tubular epithelia such as neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (Kim-1) have been identified. Previously, we found a novel renal biomarker, urinary vanin-1, in several animal models with renal tubular injury. However, there are few studies about early biomarkers of the progression to CKD associated with a high-salt diet. This review presents some new insights about these novel biomarkers for CKD in normotensives and hypertensives under a high salt intake. Interestingly, our recent reports using spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) fed a high-salt diet revealed that urinary vanin-1 and NGAL are earlier biomarkers of renal tubular damage in SHR and WKY, whereas urinary Kim-1 is only useful as a biomarker of salt-induced renal injury in SHR. Clinical studies will be needed to clarify these findings.

Redox system and phospholipid metabolism in the kidney of hypertensive rats after FAAH inhibitor URB597 administration

“…The endocannabinoids that level is enhanced during hypertension [40] through activation of cannabinoid receptor may modulate ROS generation [41] , [42] . However, enhanced ROS generation enhances the inflammatory response and endothelial dysfunction, which can trigger the development of hypertension [3] and lead to kidney metabolic disorders [43] , [44] . The analysis of the functional parameters shown in this and previous study [16] suggests that the chronic administration of URB597, a FAAH inhibitor, in contrast to acute administration, does not prevent hypertension, particularly in rats with spontaneous hypertension.…”

High-Salt Loading Downregulates Nrf2 Expression in a Sodium-Dependent Manner in Renal Collecting Duct Cells

“…A cross-sectional survey showed that the overall prevalence of CKD in China was 10.8% (Zhang et al, 2012). Inappropriate lifestyle habits, especially dietary habits such as excessive salt intake, accelerate CKD via blood pressure (BP)dependent and -independent mechanisms (Hosohata, 2017). A number of clinical studies demonstrated that high sodium intake was associated with CKD progression in patients in early stages of CKD (Nerbass et al, 2015;Leonberg-Yoo and Sarnak, 2017;Malta et al, 2018).…”

Salted and Unsalted Zhàcài (Brassica juncea var. tumida) Alleviated High‐Fat Diet‐Induced Dyslipidemia by Regulating Gut Microbiota: A Multiomics Study

“…[10][11][12] Generally, salted vegetables are considered detrimental to cardiovascular health because an excessive intake of salt can cause health problems, including hypertension, cardiovascular disease, and others. [13] However, the salted radish also presents a health effect in reducing the blood pressure of rats, which might be because it still contains polyphenols, arginine, -linolenic acid, and other unknown antihypertension substances. [10] Moreover, Lactobacillus fermentum CQPC05 in salted Sichuan pickles can decrease serum TC and TG in high-fat diet-fed mice.…”