Reference
Nouvenne A, Meschi T, Prati B, et al. Effects of a low-salt diet on idiopathic hypercalciuria in calcium-oxalate stone formers: a 3-mo randomized controlled trial. Am J Clin Nutr. 2010;91(3):565-570.
Design
Randomized, controlled clinical trial
Participants
A total of 210 patients affected by idiopathic calcium stone disease and hypercalciuria (.300 mg Ca/d in men and .250 mg Ca/d in women) were randomly assigned to receive either water therapy alone (control diet) or water therapy and a low-salt diet (low-sodium diet) for 3 months.
Key Findings
24-hour urine samples were obtained twice from all patients: one sample at baseline on a free diet and one sample after 3 months of treatment. At the follow-up visit, patients on the low-sodium diet had lower urinary sodium (68 mmol/d at 3 months compared with 228 mmol/d at baseline; P<0.001). Concomitant with this change, they showed lower urinary calcium (271 mg/d at 3 months compared with 361 mg/d on the control diet, P<0.001) and lower oxalate excretion (28 mg/d at 3 months compared with 32 mg/d on the control diet, P=0.001). Urinary calcium was within the normal range in 61.9% of the patients on the low-salt diet and in 34.0% of those on the control diet (difference:+27.9%; P<0.001).
Practice Implications
It is well-known that there is a direct relation between sodium and calcium excretion, but randomized studies evaluating the sustained effect of a low-salt diet on hypercalciuria were lacking until this study. And, though this study involved patients with a history of calcium-oxalate kidney stones, the findings have considerably deeper implications. Specifically, this study provides considerable evidence that salt restriction (i.e., restriction of sodium chloride) can lead to better retention of calcium and possibly other minerals within the body by reducing their excretion.
Possible mechanisms to explain the urinary calcium–reducing effect of the low-sodium diet include the well-known fact that in the distal segments of the renal tubule, sodium and calcium compete for reabsorption; therefore, as the quantity of sodium arriving at the distal tubule increases, the calcium excretion also increases. Another very important mechanism involves the acid–base balance. Other studies have shown an excess of sodium chloride intake promotes a chronic state of subclinical metabolic acidosis leading to a release of bone calcium.1 A low-sodium diet is a critical component of favorably modifying the acid-base imbalance, leading to a reduction of the urinary excretion of calcium.
A low-salt diet is especially important in older patients. With increasing age, the kidneys’ ability to excrete daily net acid loads declines. As a result, there is increased utilization of base stores from bone and skeletal muscle on a daily basis to deal with increased baseline metabolic acidosis, leading to increased calciuria and net losses of body calcium. Those effects of net acid production and its attendant increased body fluid acidity may contribute to development of osteoporosis and renal stones, loss of muscle mass, and age-related renal insufficiency.2
One of the interesting findings of this 3-month study was a slight decrease in body mass index (BMI) associated, indicating the low-sodium diet might have brought about wider, but subtle, dietary changes, such as a decrease in caloric intake.
One of the interesting findings of this 3-month study was a slight decrease in body mass index (BMI) associated, indicating the low-sodium diet might have brought about wider, but subtle, dietary changes, such as a decrease in caloric intake.
