Dietary sodium restriction prevents kidney damage in high fructose-fed rats

Oudot, Carole; Lajoix, Anne; Jover, Bernard; Rugale, C.

doi:10.1038/ki.2012.478

Cited by 55 publications

(35 citation statements)

References 58 publications

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“…Recently, Shao et al demonstrated that RAS activation due to a low-salt diet did not increase intratubular angiotensinogen and angiotensin II levels in rat kidneys [34]. Another study showed that restricting dietary salt could reduce kidney damage in rats fed a high-fructose diet [35]. This beneficial effect was accompanied by anti-inflammatory responses, although not by systemic hemodynamic improvements.…”

Section: Discussionmentioning

confidence: 98%

Effects of Dietary Salt Restriction on Renal Progression and Interstitial Fibrosis in Adriamycin Nephrosis

Park¹,

Kim²,

Jo³

et al. 2014

Kidney Blood Press Res

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Background/Aims: Although high salt intake is thought to accelerate renal progression in proteinuric kidney disease, it is not known whether strict dietary salt restriction could delay renal inflammation and interstitial fibrosis. Here, we sought to answer this question in a rat model of adriamycin-induced nephrotic syndrome. Methods: Adriamycin was administered via the femoral vein in a single bolus (7.5 mg/kg), and the rats were put on a sodium-deficient rodent diet. Rats with intact kidneys were studied for 5 weeks (experiment 1), and uninephrectomized rats were studied for 6 weeks (experiment 2). Results: In experiment 1, restricting salt intake improved renal tubulointerstitial histopathology in adriamycin-treated rats. Immunohistochemical and immunoblot results additionally showed that restricting dietary salt lowered adriamycin-induced expression of osteopontin, collagen III, and fibronectin. In experiment 2, salt restriction improved adriamycin-induced azotemia, although it did not affect proteinuria or blood pressure. Dietary salt restriction also reduced adriamycin-induced infiltration of ED1-positive cells and the upregulated expression of osteopontin and a-SMA. Masson's trichrome and Sirius red staining revealed that salt restriction slowed Adriamycin-induced progression of renal interstitial fibrosis. Finally, qPCR revealed that adriamycin-induced expression of TNF-a, IκB-a, gp91^phox, p47^phox, and p67^phox mRNA was blocked by salt restriction. Conclusion: Our findings demonstrate that strict dietary salt restriction delays the progress of renal inflammation and fibrosis in proteinuric kidney disease, most likely via relieving the reactive oxygen species-mediated NF-κB activation.

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Section: Discussionmentioning

confidence: 98%

Effects of Dietary Salt Restriction on Renal Progression and Interstitial Fibrosis in Adriamycin Nephrosis

Park¹,

Kim²,

Jo³

et al. 2014

Kidney Blood Press Res

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“…15,16 To our knowledge, few studies have evaluated the effects of dietary salt on neovascularization. Previous studies have largely focused on heart 4,39 and kidney 40,41 disease, where an LS diet, has in general, provided benefit. In our study, we administered an LS diet in the last few days of pregnancy and during preweaning to mimic, to some extent, the human situation where newborns often receive nutrition from their mothers.…”

Section: Discussionmentioning

confidence: 99%

Retinal Vasculopathy Is Reduced by Dietary Salt Restriction

Deliyanti

Armani

Casely

et al. 2014

ATVB

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Objective— Neovascularization and vaso-obliteration are vision-threatening events that develop by interactions between retinal vascular and glial cells. A high-salt diet is causal in cardiovascular and renal disease, which is linked to modulation of the renin–angiotensin–aldosterone system. However, it is not known whether dietary salt influences retinal vasculopathy and if the renin–angiotensin–aldosterone system is involved. We examined whether a low-salt (LS) diet influenced vascular and glial cell injury and the renin–angiotensin–aldosterone system in ischemic retinopathy. Approach and Results— Pregnant Sprague Dawley rats were fed LS (0.03% NaCl) or normal salt (0.3% NaCl) diets, and ischemic retinopathy was induced in the offspring. An LS diet reduced retinal neovascularization and vaso-obliteration, the mRNA and protein levels of the angiogenic factors, vascular endothelial growth factor, and erythropoietin. Microglia, which influence vascular remodeling in ischemic retinopathy, were reduced by LS as was tumor necrosis factor-α. Macroglial Müller cells maintain the integrity of the blood–retinal barrier, and in ischemic retinopathy, LS reduced their gliosis and also vascular leakage. In retina, LS reduced mineralocorticoid receptor, angiotensin type 1 receptor, and renin mRNA levels, whereas, as expected, plasma levels of aldosterone and renin were increased. The aldosterone/mineralocorticoid receptor–sensitive epithelial sodium channel alpha (ENaCα), which is expressed in Müller cells, was increased in ischemic retinopathy and reduced by LS. In cultured Müller cells, high salt increased ENaCα, which was prevented by mineralocorticoid receptor and angiotensin type 1 receptor blockade. Conversely, LS reduced ENaCα, angiotensin type 1 receptor, and mineralocorticoid receptor expression. Conclusions— An LS diet reduced retinal vasculopathy, by modulating glial cell function and the retinal renin–angiotensin–aldosterone system.

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“…[34][35][36][37] In each of these studies, the duration of dietary change in sodium intake was short, and longer term effects on these cardiovascular biomarkers are not known.…”

Section: Biomarkersmentioning

confidence: 99%

Sodium Intake and Cardiovascular Health

O’Donnell

Mente

Yusuf

2015

Circulation Research

173

109

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Sodium is an essential nutrient. Increasing sodium intake is associated with increasing blood pressure, whereas low sodium intake results in increased renin and aldosterone levels. Randomized controlled trials have reported reductions in blood pressure with reductions in sodium intake, to levels of sodium intake <1.5 g/d, and form the evidentiary basis for current population-wide guidelines recommending low sodium intake. Although low sodium intake (<2.0 g/d) has been achieved in short-term feeding clinical trials, sustained low sodium intake has not been achieved by any of the longer term clinical trials (>6-month duration). It is assumed that the blood pressure-lowering effects of reducing sodium intake to low levels will result in large reductions in cardiovascular disease globally. However, current evidence from prospective cohort studies suggests a J-shaped association between sodium intake and cardiovascular events, based on studies from >300 000 people, and suggests that the lowest risk of cardiovascular events and death occurs in populations consuming an average sodium intake range (3-5 g/d). The increased risk of cardiovascular events associated with higher sodium intake (>5 g/d) is most prominent in those with hypertension. A major deficit in the field is the absence of large randomized controlled trials to provide definitive evidence on optimal sodium intake for preventing cardiovascular events. Pending such trials, current evidence would suggest a recommendation for moderate sodium intake in the general population (3-5 g/d), with targeting the lower end of the moderate range among those with hypertension. (Circ Res.

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Dietary sodium restriction prevents kidney damage in high fructose-fed rats

Cited by 55 publications

References 58 publications

Effects of Dietary Salt Restriction on Renal Progression and Interstitial Fibrosis in Adriamycin Nephrosis

Effects of Dietary Salt Restriction on Renal Progression and Interstitial Fibrosis in Adriamycin Nephrosis

Retinal Vasculopathy Is Reduced by Dietary Salt Restriction

Sodium Intake and Cardiovascular Health

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