The association between urinary sodium-potassium ratio, kidney function, and blood pressure in a cohort from the general population.

Introduction Subclinical kidney dysfunction may contribute to salt sensitive hypertension. We assessed the association between the urinary sodium-potassium ratio (Na/K-ratio) and blood pressure (BP) in a general population cohort without diabetes, chronic kidney disease, cardiovascular disease or treated hypertension. We investigated whether any such association was mediated by the kidney function markers measured glomerular filtration rate (mGFR), urinary albumin creatinine ratio (ACR) and epidermal growth factor - creatinine ratio (EGF-Cr). Methods The Tromsø Study is a population-based study of inhabitants of the municipality of Tromsø, Northern Norway. Participants aged 50-62 years, without diabetes, chronic kidney disease or cardiovascular disease, were invited to the substudy Renal Iohexol Clearance Survey in Tromsø 6 (RENIS-T6; 2007-09). For the present study we excluded participants reporting the use of 1 or more antihypertensive agents, leaving 1311 RENIS-T6 participants for a cross-sectional analysis. We measured office BP, 24-hour ambulatory blood pressure (ABP) and mGFR using iohexol-clearance. Na/K-ratio, ACR, and EGF-Cr were measured in morning urine samples. Results Urinary Na/K-ratio was significantly associated with systolic office BP and ABP independently of cardiovascular risk factors and kidney function markers. A one standard deviation unit increase in the Na/K-ratio was associated with increased systolic ABP by 1.0 (0.3-1.6) mmHg. Urinary Na/K-ratio showed a stronger association with office BP than ABP. EGF-Cr, ACR and mGFR did not mediate the relationship between urinary Na/K-ratio and systolic BP. Conclusions In a representative sample of the middle-aged North-European population without diabetes, chronic kidney disease, cardiovascular disease or treated hypertension, there was a consistent association between urinary Na/K-ratio and BP. The association with BP was not mediated through kidney function measures, suggesting a relationship between a diet with high sodium and low potassium and higher BP regardless of kidney function.