Increased salt consumption is related to blood pressure rise, while glucose metabolism deterioration increases cardiovascular risk. Their interplay and their relation to target organ damage are explored in the present study.Design and method:
We studied 11820 never treated patients with uncomplicated essential hypertension, 6733 with normal glucose metabolism (N), 2216 with impaired fasting glucose (IFG), 1731 with impaired glucose tolerance (IGT) and 1090 with type 2 diabetes mellitus (T2DM). From 24 h urinary collection Na+ and K+ excretion was measured and their ratio (Na/K) was calculated, as was the 24 h albumin to creatinine ratio (ACR). 24 h systolic blood pressure (SBP) was obtained from simultaneous ambulatory blood pressure measurements and left ventricular mass index (LVMI) was derived from echo tracings.Results:
24 h SBP increased from N to IFG to IGT to T2DM (135 to 137 to 139 to 142 mmHg, p < 0.0001), as did LVMI (116 to 122 to 126 to 130 g/m2 p < 0.0001) and ACR (29 to 40 to 49 to 76 mg/g, p < 0.0001). 24 h Na+ increased and K+ decreased in parallel from N to IFG to IGT to T2DM (3715 to 4084 to 4359 to 4711 mg/24 h, p for trend 0.0014, and 1297 to 1245 to 1189 to 1142 mg/24, p for trend 0.0005), and the Na/K ratio (3.14 to 3.62 to 4.04 to 4.66, p for trend 0.004). SBP was strongly related to Na+ (r = 0.33), less so to K+ (r = −018) and best to Na/K (r = 0.40). LVMI was related to Na+ (r = 0.37), less so to K+ (r = −0.19) and best to Na/K (r = 0.48). The correlations of urine electrolytes with SBP, LVMI and ACR decreased with increasing glucose metabolism impairment (best these of Na/K to ACR, r = 0.56 to 0.39 to 0.35 to 0.19). Overall, Na/K was related to both Hba1c (r = 0.36) and HOMA-IR (r = 0.40).Conclusions:
It is concluded that in hypertensives urinary Na+ excretion increases and K+ decreases as glucose metabolism deteriorates, with inverse relations to SBP and target organ damage.