K/DOQI guidelines recommend that most patients limit daily sodium intake to less than 2.4 g.

Renal health professionals recognize the detrimental effects of high sodium intake on BP control, congestive heart failure, and fluid balance in CKD patients.

Cutting back on salt is a challenge for Americans because more than 75% of our sodium intake comes from processed and restaurant foods, with average consumption almost twice the recommended daily limit of 2,300 mg, according to the Center for Science in the Public Interest (CSPI). In response to a complaint filed by CSPI, the FDA recently initiated hearings to re-address the need for regulations to reduce salt in processed foods and include warnings regarding sodium on food labels.

Supporting the potential benefit of sodium reduction in CKD are results of a systematic review of salt intake and kidney disease by Jones-Burton et al (Am J Nephrol. 2006;26:268-275). Meeting the inclusion criteria were 16 studies published during 1966-2004.

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The authors acknowledge that although methodologic quality of studies varied, results suggest that “variations in dietary salt consumption directly influence albuminuria, with increasing salt intake associated with worsening albuminuria.” Highlighting the importance of reducing sodium consumption, the authors note that “given that there are few pharmacologic agents to control CKD progression, behavior modification can make an important contribution to CKD management, specifically dietary salt restriction.”

Individuals with metabolic syndrome—which is characterized by  problems such as central obesity, reduced high-density lipoprotein (HDL) cholesterol, increased triglycerides, high BP, and abnormal glucose metabolism—may be especially sensitive to the effects of sodium intake, as evidenced by results of a study by Hoffmann and Cubeddu (J Human Hypertension. 2007;21:438-444).

In examining the role of salt intake in increased BP for 109 patients with metabolic syndrome, the authors report that salt restriction reduced the percentage of hypertensive patients from 23.8% to 8.2%, suggesting that “dietary salt is a major determinant of the increased BP associated with the metabolic syndrome.”

Study results presented by Bellizzi et al (Kidney Int. 2007;71:245-251) also showed how reduced sodium intake can control BP. In a six-month prospective, controlled trial, 110 patients with stages 4 or 5 CKD followed either a low protein diet (LPD: 0.6 g/kg/day), very low protein diet supplemented with  of essential amino acids (VLPD: 0.35g/kg/day), or a free diet (FP).

All were counseled on a 2,300 mg/day sodium limit at baseline, though actual sodium intake of the VLPD group was significantly less by ~1000 mg/day due to the lower sodium content of low protein products. Results indicated improved BP control in the VLPD group correlating with decreased urinary sodium, with the authors noting that “in moderate to advanced CKD, VLPD has an antihypertensive effect likely due to reduction of salt intake, type of proteins, and ketoanalogs supplementation, independent of actual protein intake.”

The case for salt restriction in assessment and treatment of hypertension in dialysis patients is strengthened in a review by Paul W. Sanders, MD, of the University of Alabama, Birmingham (Seminars in Dialysis 2007;20:408-411).

The author emphasizes the importance of salt reduction in decreasing extracellular fluid volume (ECF), citing information that moderately cutting salt intake down to 80 mmol/day (2800 mg) from 160 mmol/day (3580 mg) reduces body weight and ECF volume by 1-1.5 L in otherwise normal subjects. Dr. Sanders concludes that “while the data are incomplete, careful attention to the dialytic management of ECF with lifelong adherence to dietary salt restriction will likely improve outcomes in ESRD.”