Dietary Salt Intake And Diabetic Nephropathy

Systemic blood pressure elevation accelerates the progression of diabetic nephropathy in both type 1 and type 2 diabetic patients [93], and effective antihypertensive treatment reduces albuminuria and the rate of decline in GFR in these patients. Extracellular fluid volume expansion due to impaired renal sodium excretion is the most clinically important mechanism that leads to the development of secondary hypertension in diabetic and non-diabetic patients with chronic renal disease [94;95]. Regardless of which specific antihypertensive agent is used, sodium restriction and treatment with loop diuretics is of major importance for the management of hypertension in these patients [95]. Recent short-term studies have demonstrated that the antiproteinuric effect of blockers of the renin-angiotensin-system [RAS] and nondihydropyridine calcium channel blockers is enhanced during dietary salt restriction [independently of the blood pressure reduction] in both diabetic and non-diabetic renal diseases [96;97]. This additive effect of dietary salt restriction may have important implications for the treatment of diabetic nephropathy since proteinuria per se may contribute to the deterioration of kidney function in chronic renal disease [98].

Only a few short-term intervention studies in man have investigated the impact of dietary salt restriction upon kidney function in patients with diabetic nephropathy [99;100].

Mühlhauser et al. [99] performed a 4 weeks double-blind, randomised and placebo-controlled trial in type 1 diabetic patients with elevated urinary albumin excretion rate [>60 mg/day] and untreated mild hypertension. The major objective was to assess the effect of moderate sodium restriction on blood pressure. Eight patients were assigned to a low sodium diet [achieved 92 mmol/day] and 8 patients were assigned to a high sodium diet [achieved 199 mmol/day]. During follow-up there was a significant decline in clinic diastolic blood pressure of 3.1 mm Hg in the low sodium diet group, while blood pressure remained unchanged in the high sodium diet group. However, there were no significant differences in blood pressure, proteinuria or GFR [clearance of inulin] between groups at follow-up.

Yoshioka et al. [100] performed a 1-week randomised, cross-over trial in 19 lean type 2 diabetic patients with normo-, micro- or macroalbuminuria. Medication other than insulin and hyperglycaemic agents was not administered. The major objective was to evaluate glomerular size and charge selectivity in these patients, by comparing the effect of two diets with different salt contents (85 and 255 mEq of sodium/day, respectively) on the fractional clearance of IgG and albumin. Compared to normoalbuminuric patients, charge selectivity was worse in patients with microalbuminuria, while charge and size selectivity were completely lacking in macroalbuminuric patients. Interestingly, GFR (creatinine clearance) was significantly lower during a low-salt diet as compared to a high-salt diet in all three groups of patients. Although not significant, blood pressure was correspondingly lower during the low-salt diet compared to the high-salt diet.

In conclusion, dietary salt restriction is of major importance for the management of hypertension in chronic renal disease. However, future long-term studies may clarify whether dietary salt restriction has a beneficial effect in addition to antihypertensive treatment on the progression of diabetic nephropathy.

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