scholarly journals Salt Intake and All-Cause Mortality in Hemodialysis Patients

2018 ◽  
Vol 48 (2) ◽  
pp. 87-95
Author(s):  
Tatsuyoshi Ikenoue ◽  
Kiyomi Koike ◽  
Shingo Fukuma ◽  
Satoshi Ogata ◽  
Kunitoshi Iseki ◽  
...  
Keyword(s):  
Salt Intake ◽  
Cardiovascular Death ◽  
Hemodialysis Patients ◽  
High Salt ◽  
Salt Restriction ◽  
Data Registry ◽  
High Salt Intake ◽  
Low Salt ◽  
All Cause Mortality ◽  
Registry Database

Background: Although some clinical practice guidelines regarding hemodialysis recommend salt restriction, few studies have examined the association between salt intake and clinical outcomes in hemodialysis patients. This study aimed to clarify the association between salt intake and mortality in hemodialysis patients. Methods: This retrospective cohort study was based on the Japanese Society for Dialysis Therapy renal data registry database (2008) and included 88,115 adult patients who had received hemodialysis for at least 2 years. Estimated salt intake was the main predictor and was calculated from intra-dialytic weight loss and pre- and post-dialysis serum sodium levels. Nonlinear logistic regression was used to determine the association between salt intake and mortality, adjusting for potential confounders. The outcomes considered were all-cause mortality and cardiovascular death at 1 year. Results: The median (25–75th percentile) salt intake at baseline was 6.4 (4.6–8.3) g/day. At 1 year, all-cause mortality occurred in 1,845 (2.1%) patients, including 807 cardiovascular deaths. The low salt intake group (< 6 g/day) demonstrated the highest all-cause mortality and cardiovascular deaths. No association was observed between high salt intake, all-cause mortality and cardiovascular deaths. The lowest risk for all-cause mortality and cardiovascular death occurred among patients with an estimated salt intake of 9 g/day. Conclusion: Low salt intake, but not high salt intake, was associated with all-cause and cardiovascular mortality in Japanese hemodialysis patients. Further studies to justify including a lower limit of salt intake for hemodialysis patients are suggested.

scholarly journals Eplerenone inhibits aldosterone-induced renal expression of cyclooxygenase

2012 ◽  
Vol 13 (3) ◽  
pp. 353-359 ◽  
Author(s):  
MA Bayorh ◽  
A Rollins-Hairston ◽  
J Adiyiah ◽  
D Lyn ◽  
D Eatman
Keyword(s):  
Salt Intake ◽  
High Salt ◽  
Prostaglandin E ◽  
Renal Tubules ◽  
Protective Effects ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Salt Intake ◽  
Low Salt ◽  
Cox 2

Introduction: The upregulation of cyclooxygenase (COX) expression by aldosterone (ALDO) or high salt diet intake is very interesting and complex in the light of what is known about the role of COX in renal function. Thus, in this study, we hypothesize that apocynin (APC) and/or eplerenone (EPL) inhibit ALDO/salt-induced kidney damage by preventing the production of prostaglandin E2 (PGE2). Methods: Dahl salt-sensitive rats on either a low-salt or high-salt diet were treated with ALDO (0.2 mg pellet) in the presence of EPL (100 mg/kg/day) or APC (1.5 mM). Indirect blood pressure, prostaglandins and ALDO levels and histological changes were measured. Results: Cyclooxygenase-2 (COX-2) levels were upregulated in the renal tubules and peritubular vessels after high-salt intake, and APC attenuated renal tubular COX-2 protein expression induced by ALDO. Plasma PGE2 levels were significantly reduced by ALDO in the rats fed a low-salt diet when compared to rats fed a high-salt diet. PGE2 was blocked by EPL but increased in the presence of APC. Conclusions: The beneficial effects of EPL may be associated with an inhibition of PGE2. The mechanism underlying the protective effects of EPL is clearly distinct from that of APC and suggests that these agents can have differential roles in cardiovascular disease.

Factors affecting Potassium Balance During Frusemide Administration

1984 ◽  
Vol 67 (2) ◽  
pp. 195-203 ◽  
Author(s):  
Christopher S. Wilcox ◽  
William E. Mitch ◽  
Ralph A. Kelly ◽  
Paul A. Friedman ◽  
Paul F. Souney ◽  
...  
Keyword(s):  
Salt Intake ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
High Salt ◽  
Renin Angiotensin Aldosterone System ◽  
Plasma Aldosterone Concentration ◽  
Water Load ◽  
Renin Angiotensin ◽  
High Salt Intake ◽  
Low Salt

1. We investigated the effects of Na+ intake, the renin-angiotensin-aldosterone system and antidiuretic hormone (ADH) on K+ balance during 3 days of frusemide administration to six normal subjects. Subjects received 40 mg of frusemide for 3 days during three different protocols: Na+ intake 270 mmol/day (high salt); Na+ intake 20 mmol/day to stimulate the renin-angiotensin-aldosterone system (low salt); Na+ intake 270 mmol/day plus captopril (25 mg/6 h) to prevent activation of the renin-angiotensin-aldosterone system. In a fourth protocol, a water load was given during high salt intake to prevent ADH release and then frusemide was given. 2. During high salt intake, frusemide increased K+ excretion (UKV) over 3 h, but the loss was counterbalanced by subsequent renal K+ retention so that daily K+ balance was neutral. 3. During low salt intake, the magnitude of the acute kaliuresis following the first dose of frusemide and the slope of the linear relationship between UKV and the log of frusemide excretion were increased compared with that found during the high salt intake. In addition, low salt intake abolished the compensatory renal retention of K+ after frusemide and cumulative K+ balance over 3 days of diuretic administration was uniformly negative (−86 ± 7 mmol/3 days; P < 0.001). 4. Captopril abolished the rise in plasma aldosterone concentration induced by frusemide. The acute kaliuresis after frusemide was unchanged compared with that observed during high salt intake. The compensatory reduction in UKV occurring after the diuretic was slightly potentiated. In fact, captopril given without the diuretic induced a small positive K+ balance. 5. When a water load was given concurrently with frusemide, the acute kaliuresis was >30% lower compared with that seen with frusemide alone, even though the natriuretic response was unchanged. 6. We conclude that: (a) K+ balance is maintained when frusemide is given during liberal Na+ intake because acute K+ losses are offset by subsequent renal K+ retention; (b) this compensatory K+ retention can be inhibited by aldosterone release which could account for the negative K+ balance seen during salt restriction; (c) the short-term kaliuretic response to frusemide is augmented by release of both ADH and aldosterone whereas changes in K+ balance over 3 days of frusemide are dependent on plasma aldosterone concentration.

Postprandial natriuresis in humans: further evidence that urodilatin, not ANP, modulates sodium excretion

1996 ◽  
Vol 270 (2) ◽  
pp. F301-F310 ◽  
Author(s):  
C. Drummer ◽  
W. Franck ◽  
M. Heer ◽  
W. G. Forssmann ◽  
R. Gerzer ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Sodium Excretion ◽  
Salt Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
High Salt ◽  
Peak Rate ◽  
High Salt Intake ◽  
Low Salt ◽  
Chloride Excretion

We examined the effects of a high-salt (100 mmol NaCl) and a low-salt (5 mmol NaCl) meal on the renal excretion of sodium and chloride in 12 healthy male upright subjects. We also measured the urinary excretion of urodilatin [ANP-(95-126)], and the plasma or serum concentrations of atrial natriuretic peptide [ANP-(99-126)], aldosterone, and renin. The high-salt meal produced a postprandial natriuresis (urinary sodium excretion from 59.0 to a peak rate of 204.6 mumol/min in 3rd h after ingestion of meal) and chloride excretion. In parallel, the urinary excretion of urodilatin increased from 35.7 to a peak rate of 105 fmol/min. The effect of high-salt intake on urinary sodium, chloride, and urodilatin excretion was significant (analysis of variance, P < 0.01), and close significant correlations were observed between urodilatin and sodium excretion (mean R = 0.702) as well as between urodilatin and chloride excretion (mean R = 0.776). In contrast, plasma ANP, which was acutely elevated 15 min after high-salt intake, was already back to low-salt values 1 h later. It did not parallel the postprandial natriuretic profile, and no positive correlation between plasma ANP and sodium excretion was observed. These results provide further evidence that urodilatin, not ANP, is the member of this peptide family primarily involved in the regulation of the excretion of sodium and chloride.

scholarly journals High Salt Intake Increases Copeptin but Salt Sensitivity Is Associated with Fluid Induced Reduction of Copeptin in Women

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Irina Tasevska ◽  
Sofia Enhörning ◽  
Philippe Burri ◽  
Olle Melander
Keyword(s):  
Body Weight ◽  
Salt Intake ◽  
Salt Sensitivity ◽  
High Salt ◽  
Dietary Salt ◽  
Urinary Volume ◽  
Salt Consumption ◽  
High Salt Intake ◽  
Low Salt ◽  
Induced Changes

This study investigated if copeptin is affected by high salt intake and whether any salt-induced changes in copeptin are related to the degree of salt sensitivity. The study was performed on 20 men and 19 women. In addition to meals containing 50 mmol NaCl daily, capsules containing 100 mmol NaCl and corresponding placebo capsules were administered during 4 weeks each, in random order. Measurements of 24 h blood pressure, body weight, 24 h urinary volume, and fasting plasma copeptin were performed at high and low salt consumption. Copeptin increased after a high compared to low dietary salt consumption in all subjects 3,59 ± 2,28 versus 3,12 ± 1,95 (P= 0,02). Copeptin correlated inversely with urinary volume, at both low (r= −0,42;P= 0,001) and high (r= −0,60;P< 0,001) salt consumption, as well as with the change in body weight (r= −0,53;P< 0,001). Systolic salt sensitivity was inversely correlated with salt-induced changes of copeptin, only in females (r= −0,58;P= 0,017). As suppression of copeptin on high versus low salt intake was associated with systolic salt sensitivity in women, our data suggest that high fluid intake and fluid retention may contribute to salt sensitivity.

scholarly journals SUN-LB94 Impact of the Gut Microbiome and Renin-Angiotensin-Aldosterone System in Hypertensive Patients With Low-Salt Intake

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Kouki Taniguchi ◽  
Satoshi Nagase ◽  
Shigehiro Karashima ◽  
Mitsuhiro Kometani ◽  
Daisuke Aono ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Gut Microbiome ◽  
Salt Intake ◽  
High Salt ◽  
Renin Angiotensin Aldosterone System ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
High Salt Intake ◽  
Low Salt ◽  
The Impact

Abstract Salt intake is one of most important environmental factors responsible for triggering the onset of hypertension. Renin-angiotensin-aldosterone system (RAAS) plays a key role in adjusting sodium homeostasis and blood pressure. Recently, the potential role of the gut microbiome (GM) in altering the health of the host has drawn considerable attention. We investigated the impact of intestinal microflora and RAAS in hypertensive patients with low-salt or high-salt intake using an observational study. A total of 239 participants were enrolled and their GMs and clinical backgrounds examined, including the renin-angiotensin-aldosterone system and inflammatory cytokine levels. On the basis of enterotypes—determined by cluster analysis—and salt intake, the participants were classified into four groups, low salt/GM enterotype 1, low salt/GM enterotype 2, high salt/GM enterotype 1, and high salt/GM enterotype 2. The prevalence of hypertension was significantly lower in the low-salt intake (low salt/GM enterotype 1 = 47% vs low salt/GM enterotype 2 = 27%, p = 0.04) groups. No significant difference in the prevalence of hypertension was observed for the two GM enterotype groups with high-salt intake (GM enterotype 1 = 50%, GM enterotype 2 = 47%; p = 0.83). Plasma aldosterone concentration was significantly different among the four groups (p &lt; 0.01). Furthermore, the relative abundance of Blautia, Bifidobacterium, Escherichia-Shigella, Lachnoclostridium, and Clostridium sensu stricto was also significantly different among these enterotypes. This suggested in certain individuals (with specific gut bacteria composition) changing dietary habits—to low salt—would be ineffective for regulating hypertension through RAAS. Our findings provide a new strategy for controlling blood pressure and preventing the development of hypertension through restoring GM homeostasis.

Blood pressure and fluid-electrolyte balance in mice with reduced or absent ANP

1996 ◽  
Vol 271 (1) ◽  
pp. R109-R114 ◽  
Author(s):  
S. W. John ◽  
A. T. Veress ◽  
U. Honrath ◽  
C. K. Chong ◽  
L. Peng ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Volume ◽  
Volume Expansion ◽  
Salt Intake ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Blood Volume Expansion ◽  
High Salt Intake ◽  
Low Salt

Atrial natriuretic peptide (ANP)-gene knockout mice of three genotypes (+/+, +/-, and -/-) were maintained on a low-salt diet (0.008% NaCl). They were then fed either the same low-salt diet or a high-salt diet (8% NaCl) for 1 wk. No differences were found among genotypes in daily food and water intakes or in urinary volume and electrolyte excretions. Arterial blood pressures measured in anesthetized animals at the end of the dietary regimen were significantly and similarly increased in -/- compared with +/+ mice on each diet. Renal excretion of fluid and electrolytes was measured in anesthetized mice before and after acute blood volume expansion. No genotype differences were observed before volume expansion. After volume expansion the wild-type (+/+) mice had much greater saluretic responses than either the heterozygous (+/-) or the homozygous mutant (-/-) animals on the low-salt diet but not on the high-salt diet. We conclude that ANP lowers blood pressure in the absence of detected changes in renal function; ANP is not essential for normal salt balance, even on high-salt intake; and ANP is essential for the natriuretic response to acute blood volume expansion on a low-salt but not high-salt intake.

scholarly journals High Salt Diet Impacts the Risk of Sarcopenia Associated with Reduction of Skeletal Muscle Performance in the Japanese Population

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3474
Author(s):  
Yasuko Yoshida ◽  
Keisei Kosaki ◽  
Takehito Sugasawa ◽  
Masahiro Matsui ◽  
Masaki Yoshioka ◽  
...  
Keyword(s):  
Older People ◽  
Salt Intake ◽  
Handgrip Strength ◽  
High Salt ◽  
Muscle Performance ◽  
World Health ◽  
Fat Percentage ◽  
High Salt Intake ◽  
Significant Difference ◽  
Low Salt

The World Health Organization has recommended 5 g/day as dietary reference intakes for salt. In Japan, the averages for men and women were 11.0 g/day and 9.3 g/day, respectively. Recently, it was reported that amounts of sodium accumulation in skeletal muscles of older people were significantly higher than those in younger people. The purpose of this study was to investigate whether the risk of sarcopenia with decreased muscle mass and strength was related to the amount of salt intake. In addition, we investigated its involvement with renalase. Four groups based on age and salt intake (“younger low-salt,” “younger high-salt,” “older low-salt,” and “older high-salt”) were compared. Stratifying by age category, body fat percentage significantly increased in high-salt groups in both younger and older people. Handgrip strength/body weight and chair rise tests of the older high-salt group showed significant reduction compared to the older low-salt group. However, there was no significant difference in renalase concentrations in plasma. The results suggest that high-salt intake may lead to fat accumulation and muscle weakness associated with sarcopenia. Therefore, efforts to reduce salt intake may prevent sarcopenia.

Effect of dietary salt on arteriolar nitric oxide in striated muscle of normotensive rats

1993 ◽  
Vol 264 (6) ◽  
pp. H1810-H1816 ◽  
Author(s):  
M. A. Boegehold
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Striated Muscle ◽  
Salt Intake ◽  
High Salt ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
High Salt Intake ◽  
Low Salt ◽  
Induced Hypertension

This study evaluated the influence of high dietary salt intake on nitric oxide (NO) activity in the arteriolar network of rats resistant to salt-induced hypertension. The spinotrapezius muscle microvasculature was studied in inbred Dahl salt-resistant (SR/Jr) rats fed low (0.45%)- or high (7%)-salt diets for 4–5 wk. Arterial pressures were not different between groups at any time during the study. NO synthesis inhibition with NG-nitro-L-arginine-methyl ester (L-NAME) constricted arcade arterioles in low-salt SR/Jr and dilated arcade arterioles in high-salt SR/Jr. Arcade arteriole dilation to acetylcholine (ACh), but not sodium nitroprusside (SNP), was impaired in high-salt SR/Jr. In contrast, transverse and distal arteriole responses to L-NAME, ACh, and SNP were identical in high- and low-salt SR/Jr. These findings indicate that high salt intake, in the absence of increased arterial pressure, suppresses the influence of basal and evoked NO on vascular tone in arcading arterioles, but not in smaller transverse and distal arterioles. Unaltered SNP responses in high-salt SR/Jr suggest that this effect does not involve a change in arteriolar smooth muscle responsiveness to NO.

Effect of Dietary Salt Restriction on Renal Sensitivity to Vasopressin in Man

1995 ◽  
Vol 89 (1) ◽  
pp. 37-43 ◽  
Author(s):  
M. Sutters ◽  
R. Duncan ◽  
W. S. Peart
Keyword(s):  
Arginine Vasopressin ◽  
Low Dose ◽  
Salt Intake ◽  
Renal Plasma Flow ◽  
High Salt ◽  
Dietary Salt ◽  
Salt Restriction ◽  
Vasopressin Infusion ◽  
Antidiuretic Effect ◽  
Low Salt

1. We have previously described a progressive antidiuresis in response to low-dose vasopressin infusion during salt restriction in man, despite stable or even declining plasma vasopressin concentration. In the present study we examine the hypothesis that renal sensitivity to the antidiuretic effect of arginine vasopressin may be enhanced by salt restriction. 2. Extremely low-dose infusions of arginine vasopressin were given to normal subjects after equilibration to high (260 mmol/day) and low (20 mmol/day) sodium intakes. 3. Salt restriction increased the antidiuretic effect of arginine vasopressin (2 fmol min−1 kg−1 arginine vasopressin increased urine osmolality from 67.8 ± 2.6 to 196.3 ± 35.7 mosmol/l in the high-salt study and from 268.3 ± 49 mosmol/l in the low-salt study; P < 0.05 between sodium intakes). Glomerular filtration rate, estimated from inulin clearance, was unchanged during arginine vasopressin infusion irrespective of salt intake (high salt 116.5 ± 9.4 to 118.9 ± 6.4 ml/min; low salt, 135.1 ± 9.2 to 111.2 ± 12.4 ml/min). Renal plasma flow, estimated from para-aminohippurate clearance, fell further during infusion of 2 fmol min−1 kg−1 arginine vasopressin in the low-salt study than in the high-salt study (low salt, from 555.7 ± 22.7 to 298.3 ± 27.6 ml/min; high salt, from 544.5 ± 30.2 to 452.9 ± 28.9 ml/min; P < 0.05 between sodium intakes). 4. Plasma atrial natriuretic peptide concentration increased during infusion of 2 fmol min−1 kg−1 arginine vasopressin in the low-salt study (to 136.5% ± 19.9% of baseline, P < 0.05), if anything falling in the high-salt study (to 90.5% ± 13.6% of baseline). Packed cell volume fell during arginine vasopressin infusion in the low-salt study (high salt, to 98.2% ± 0.4% of baseline; low salt, to 95.7% ± 0.4% of baseline, P < 0.05 for the low-salt study only). 5. Plasma arginine vasopressin concentration was constant throughout each study (high salt 0.48 ± 0.12 to 0.48 ± 0.1 pmol/l; low salt, 0.38 ± 0.05 to 0.4 ± 0.04 pmol/l). 6. Our findings suggest that renal sensitivity to the hydro-osmotic and vascular effects of arginine vasopressin is enhanced by salt restriction.

Salt loading enhances rat renal TxA2/PGH2 receptor expression and TGF response to U-46,619

1997 ◽  
Vol 273 (6) ◽  
pp. F976-F983 ◽  
Author(s):  
William J. Welch ◽  
Bo Peng ◽  
Kazuhisa Takeuchi ◽  
Keishi Abe ◽  
Christopher S. Wilcox
Keyword(s):  
Salt Intake ◽  
Receptor Activation ◽  
High Salt ◽  
Receptor Expression ◽  
Tubuloglomerular Feedback ◽  
Kidney Cortex ◽  
Salt Loading ◽  
Receptor Mrna ◽  
High Salt Intake ◽  
Low Salt

The tubuloglomerular feedback (TGF) response is potentiated by thromboxane A2(TxA2) and/or prostaglandin endoperoxide (PGH2) acting on specific receptors. Infusion of the TxA2/PGH2mimetic, U-46,619, into conscious rats leads to hypertension that is potentiated by a high-salt intake. Therefore, we tested the hypothesis that a high-salt intake enhances the expression of transcripts for TxA2/PGH2receptors in the kidney and glomeruli and enhances the response of TGF to TxA2/PGH2receptor stimulation. Groups of rats were accommodated to a low-salt (LS), normal salt (NS), or high-salt (HS) diet for 8–10 days. TxA2/PGH2receptor mRNA was detected by reverse transcription-polymerase chain reaction in kidney cortex, isolated glomeruli, and abdominal aorta. TxA2/PGH2mRNA abundance was significantly ( P< 0.001) increased during intake of high-salt compared with low-salt diets in the kidney cortex (1.34 ± 0.10 vs. 0.84 ± 0.04 arbitrary units) and isolated outer cortical glomeruli (0.68 ± 0.04 vs. 0.32 ± 0.03 arbitrary units), but there was no effect of salt on TxA2/PGH2receptor mRNA expression in the aorta. Maximal TGF responses were assessed from the increase in proximal stop flow pressure (an index of glomerular capillary pressure) during increases in loop of Henle perfusion with artificial tubular fluid from 0 to 40 nl/min. Compared with vehicle, the enhancement of maximal TGF with U-46,619 (10−6 M) added to the perfusate was greater in rats adapted to high-salt than normal salt (HS: +9.6 ± 1.1 vs. NS: +5.1 ± 0.4 mmHg; P < 0.001) or low-salt (LS: +3.8 ± 1.3 mmHg; P < 0.001) intakes. Responses to U-46,619 at each level of salt intake were blocked by >70% by the TxA2/PGH2receptor antagonist ifetroban. In contrast, enhancement of TGF by peritubular capillary perfusion of arginine vasopressin (AVP; 10−7 M) was similar in high-salt and low-salt rats (HS: +1.5 ± 0.6 vs. LS: +1.6 ± 0.5 mmHg; not significant). We conclude that salt loading increases selectively the abundance of TxA2/PGH2receptor transcripts in the kidney cortex and glomerulus, relative to the aorta, and enhances selectively TGF responses to TxA2/PGH2receptor activation but not to AVP.

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