Furthermore, high dietary sodium intake is associated with a high incidence of cardiovascular disease in T2DM patients 14. Some previous studies have also demonstrated that many Japanese patients with DKD have salt-sensitive hypertension 13. High sodium intake also causes resistant hypertension 12. High sodium intake is associated with high blood pressure (BP), a risk factor for cardiovascular and renal diseases 8, and the restriction of sodium intake lowers BP 9, 10, 11. Furthermore, aberrant proximal tubular handling of sodium plays an important role in the pathogenesis of glomerular hyperfiltration 6, which contributes to the increase in urinary albumin excretion and the progressive decline in renal function 7. High dietary sodium intake and volume expansion are risk factors for hypertension, which promotes the progression of DKD 3, 5. From a renal mechanistic perspective, sodium plays an important role in the pathogenesis of DKD. DKD is conventionally thought to predominantly affect the glomerulus, through intraglomerular hypertension, which promotes glomerulosclerosis and inflammation especially in the context of systemic hypertension 3, 4. The home BP-lowering effects of dapagliflozin are larger in HS than LS, concomitant with a larger reduction in eGFR, suggesting a dapagliflozin-induced improvement in glomerular relative hyperfiltration in HS.ĭiabetic kidney disease (DKD) is a common comorbidity in patients with type 2 diabetes mellitus (T2DM), which is the leading cause of end-stage renal disease (ESRD) 1, 2. In contrast, the reductions in evening home systolic BP and eGFR from baseline were larger in HS than in LS (BP: − 13 ± 2.08 vs. − 6 ± 1.88, P = 0.020 eGFR: − 3.33 ± 1.32 vs. After 24 weeks, the reductions from baseline in ln-UACR were comparable in the two groups.
At baseline, clinic-/home-measured BPs, UACR, and eGFR, were comparable in the two groups. The effects on UACR, home-measured BP, and eGFR were compared between high- and low-sodium intake groups (HS and LS groups), which were created using baseline urinary sodium-to-creatinine ratio of 84 participants with available basal sodium-to-creatinine ratios. We investigated the impact of basal dietary sodium intake on the dapagliflozin-induced changes in albuminuria and blood pressure (BP) measured at home in patients with diabetic kidney disease (DKD).This was a secondary analysis of the Y-AIDA Study, in which DKD patients with estimated glomerular filtration rate (eGFR) ≥ 45 ml/min/1.73 m 2 and urinary albumin-to-creatinine ratio (UACR) ≥ 30 mg/g creatinine were administered dapagliflozin for 24 weeks, and dapagliflozin significantly improved albuminuria levels and home BP profiles.
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