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      An In-Depth Review of the Evidence Linking Dietary Salt Intake and Progression of Chronic Kidney Disease

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          Background: Dietary salt has been debated for decades as having a potentially deleterious influence on human health. Objectives: To determine the quality of research and the relationship between dietary salt and markers for progression of kidney disease. Methods: Data sources included 7 electronic databases comprehensively searched for literature published between January 1, 1966, and August 31, 2004, and a manual search of bibliographies of relevant papers, and consultation with experts in the field. Differences between the paired reviewers were reconciled through consensus or by a content expert. Results: Sixteen studies met the inclusion-exclusion criteria and were identified for review; however, the study methodologies were extremely heterogeneous. Conclusions commonly cited in the studies include: variations in salt consumption are directly correlated with albuminuria, and an increase in salt consumption is associated with an acute increase in glomerular filtration rate, while a reduction in salt consumption may slow the rate of renal function loss. Conclusions: The available published information, while highly variable in methods and quality, suggests that variations in dietary salt consumption directly influence albuminuria, with increasing salt intake associated with worsening albuminuria; however, results are inadequate and conflicting on the effects of dietary salt consumption on renal function, especially over a prolonged time. There was no evidence of a detrimental effect of reduced salt intake. On the other hand, there is consistent experimental evidence to link increased salt exposure with kidney tissue injury. On the basis of these data, we believe that dietary salt restriction should be considered in patients with chronic kidney disease.

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          Most cited references 16

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          The hazards of scoring the quality of clinical trials for meta-analysis.

           Peter Jüni (1999)
          Although it is widely recommended that clinical trials undergo some type of quality review, the number and variety of quality assessment scales that exist make it unclear how to achieve the best assessment. To determine whether the type of quality assessment scale used affects the conclusions of meta-analytic studies. Meta-analysis of 17 trials comparing low-molecular-weight heparin (LMWH) with standard heparin for prevention of postoperative thrombosis using 25 different scales to identify high-quality trials. The association between treatment effect and summary scores and the association with 3 key domains (concealment of treatment allocation, blinding of outcome assessment, and handling of withdrawals) were examined in regression models. Pooled relative risks of deep vein thrombosis with LMWH vs standard heparin in high-quality vs low-quality trials as determined by 25 quality scales. Pooled relative risks from high-quality trials ranged from 0.63 (95% confidence interval [CI], 0.44-0.90) to 0.90 (95% CI, 0.67-1.21) vs 0.52 (95% CI, 0.24-1.09) to 1.13 (95% CI, 0.70-1.82) for low-quality trials. For 6 scales, relative risks of high-quality trials were close to unity, indicating that LMWH was not significantly superior to standard heparin, whereas low-quality trials showed better protection with LMWH (P<.05). Seven scales showed the opposite: high quality trials showed an effect whereas low quality trials did not. For the remaining 12 scales, effect estimates were similar in the 2 quality strata. In regression analysis, summary quality scores were not significantly associated with treatment effects. There was no significant association of treatment effects with allocation concealment and handling of withdrawals. Open outcome assessment, however, influenced effect size with the effect of LMWH, on average, being exaggerated by 35% (95% CI, 1%-57%; P= .046). Our data indicate that the use of summary scores to identify trials of high quality is problematic. Relevant methodological aspects should be assessed individually and their influence on effect sizes explored.
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            Modest salt reduction reduces blood pressure and urine protein excretion in black hypertensives: a randomized control trial.

            High blood pressure and proteinuria are the major risk factors for cardiovascular and renal disease. In black individuals, there is an increased risk of hypertension, stroke, heart failure, and kidney disease. There are no controlled studies of the effects of reducing salt intake on blood pressure and urine protein excretion in black individuals. Therefore, the aim of our study was to determine the effects of modest salt restriction on blood pressure and urine protein excretion in nondiabetic black hypertensive subjects. The study was randomized, double blind, and placebo controlled. After run-in periods on their usual diet and on reduced salt, participants continued to restrict their salt intake and then received either slow sodium tablets, designed to bring their salt intake back to normal, or placebo tablets for 4 weeks in a randomized, double-blind, crossover study. In the 40 who completed the study, urinary sodium excretion fell on slow sodium to placebo from 169+/-73 to 89+/-52 mmol per 24 hours (P<0.001; approximately 10 to 5 g salt per day). Blood pressure fell from 159/101+/-13/8 to 151/98+/-13/8 mm Hg (P<0.01). Protein excretion fell from 93+/-48 mg to 75+/-30 mg per 24 hours (P<0.008). Thus, reducing salt intake from approximately 10 to 5 g per day reduced blood pressure and urine protein excretion in black hypertensives. In light of these findings, we would recommend that all black individuals with raised blood pressure reduce their salt intake to < or =5 g per day.
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              L-arginine abrogates salt-sensitive hypertension in Dahl/Rapp rats.

              This study examined the contribution of nitric oxide (NO) to the susceptibility or resistance to the hypertensive effects of high sodium chloride (8.0% NaCl) intake in young Dahl/Rapp salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) rats. Using NG-monomethyl-L-arginine (L-NMMA) as a probe for NO production in vivo, we found that increasing dietary sodium chloride increased NO activity in salt-resistant rats, but not in salt-sensitive rats. Exogenous L-arginine, the substrate for NO synthesis, decreased blood pressure to normotensive levels in salt-sensitive rats made hypertensive for 2 wk from 8.0% NaCl chow. D-arginine had no effect on blood pressure of these rats and L-arginine did not change blood pressure of salt-resistant rats. Intraperitoneal injections of L-arginine and its precursor, L-citrulline, and oral L-arginine, but not D-arginine, prevented the increase in blood pressure in salt-sensitive rats on the high salt chow over 2 wk of observation. In contrast, L-arginine did not alter the development of hypertension in spontaneously hypertensive rats. Mean urinary cGMP levels were higher in salt-sensitive rats on oral L-arginine than salt-sensitive rats on D-arginine. Infusion of L-NMMA acutely decreased, whereas intravenous L-arginine rapidly increased, urinary cGMP in both groups. L-arginine and L-citrulline increased production of NO and prevented salt-sensitive hypertension in Dahl/Rapp rats.

                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                July 2006
                19 July 2006
                : 26
                : 3
                : 268-275
                aDepartment of Medicine, Division of Nephrology, and bDepartment of Epidemiology and Preventive Medicine, and Office of Policy and Planning, University of Maryland School of Medicine, Baltimore, Md., and cDepartment of Preventive Medicine, Hypertension/Clinical Research Center, Rush University Medical Center, Chicago, Ill., USA
                93833 Am J Nephrol 2006;26:268–275
                © 2006 S. Karger AG, Basel

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                Page count
                Tables: 1, References: 39, Pages: 8
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/93833
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