Salt Intake and Renal Outcome in Patients with Progressive Renal Disease

Abstract

Experimental studies suggest that salt intake plays a critical role in the progressive glomerular filtration rate (GFR) loss of established renal disease; however, this issue has never been addressed in humans. To this aim, we have retrospectively analyzed the clinical data of patients with chronic renal failure (CRF), in whom a low-protein diet was prescribed, over a period of about 3 years. On the basis of the daily urinary sodium output, the patients were divided into two groups: a group of patients constantly ingesting >200 mEq NaCl/day (high sodium intake, HSD, n = 30) and a group in which salt intake was <100 mEq/day (low sodium intake, LSD, n = 27). Patients taking diuretics or ACE inhibitors were excluded. At baseline, the LSD group, as compared to the HSD group, was characterized by significantly lower creatinine clearance (24 ± 2 vs. 28 ± 2 ml/min) and higher proteinuria (2.9 ± 0.3 vs. 1.5 ± 0.2 g/day). Despite the presence of these risk factors for progression, and a similar control of blood pressure (the average of the mean arterial pressure during follow-up was 111 ± 2 mm Hg in LSD and 107 ± 2 mm Hg in HSD), the LSD patients showed a better renal outcome: in this group, as compared to HSD, the GFR decline was lower (0.25 ± 0.07 vs. 0.51 ± 0.09 ml/min/month, p < 0.05), and proteinuria did not change while it markedly increased in HSD. During follow-up, LSD patients also ingested a significantly lower amount of protein. This study therefore suggests that efficacious salt restriction in CRF patients improves the outcome of renal disease independent from its antihypertensive effects.

Effect of weight loss using formula diet on renal function in obese patients with diabetic nephropathy

“…In the present study, dietary salt intake was low (2.70 or 4.90 g/day). Cianciaruso et al 15 observed improvements in renal function and proteinuria with low sodium intake compared to high sodium intake in patients with progressive renal disease. Allen et al 16 reported suppression of hyperfiltration, renal enlargement and albuminuria by salt restriction in diabetic rats.…”

Salt Intake, Oxidative Stress, and Renal Expression of NADPH Oxidase and Superoxide Dismutase

“…ROS activate mitogen-activated protein kinase in renal tubule cells (38), contribute to hypertrophic responses to Ang II (38) and to cellular injury (39), and increase fibrogenic matrix protein synthesis in mesangial cells (40). A high salt intake enhances oxidative stress in rat skeletal muscle arterioles and vessels (23) and increases BP, protein excretion, and renal fibrosis and worsens renal function in several models of chronic renal failure (7,38,(41)(42)(43) and accelerates the decline of renal function in patients with chronic renal failure (44). Conversely, salt restriction ameliorates renal disease progression in animal models (42) and is recommended for patients with chronic renal failure (45).…”

Sodium Intake, ACE Inhibition, and Progression to ESRD

“…17 Consistently, observational studies in humans showed that increased dietary sodium intake increases proteinuria and accelerates renal disease progression. 18 However, no study thus far has evaluated the associations between salt intake, proteinuria, and renal disease progression in patients receiving RAS-inhibiting treatment. Hence, in this study, we evaluated the association of sodium intake with proteinuria and progression to ESRD in 500 patients with CKD retrieved from the Ramipril Efficacy in Nephropathy (REIN) [1][2][3] and REIN-2 19 trials who were receiving stable ramipril therapy.…”