Urinary sodium-to-potassium ratio associates with hypertension and current disease activity in patients with rheumatoid arthritis: a cross-sectional study

Abstract

Background Excessive salt intake is thought to exacerbate both development of hypertension and autoimmune diseases in animal models, but the clinical impact of excessive salt in rheumatoid arthritis (RA) patients is still unknown. We performed a cross-sectional study to clarify the associations between salt load index (urinary sodium-to-potassium ratio (Na/K ratio)), current disease activity, and hypertension in an RA population. Methods Three hundred thirty-six participants from our cohort database (KURAMA) were enrolled. We used the spot urine Na/K ratio as a simplified index of salt loading and used the 28-Joint RA Disease Activity Score (DAS28-ESR) as an indicator of current RA disease activity. Using these indicators, we evaluated statistical associations between urinary Na/K ratio, DAS28-ESR, and prevalence of hypertension. Results Urinary Na/K ratio was positively associated with measured systolic and diastolic blood pressure and also with prevalence of hypertension even after covariate adjustment (OR 1.34, p < 0.001). In addition, increased urinary Na/K ratio was significantly and positively correlated with DAS28-ESR in multiple regression analysis (estimate 0.12, p < 0.001), as was also the case in gender-separated and prednisolone-separated sub-analyses. Conclusion Urinary Na/K ratio was independently associated with current disease activity as well as with prevalence of hypertension in RA patients. Thus, dietary modifications such as salt restriction and potassium supplementation should be investigated as a potential candidate for attenuating both disease activity and hypertension in RA patients.

Is urinary Na/K ratio an independent indicator associated with current hypertension and RA disease activity or just an artifact? Comment on article by Minamino H et al

“…I read with interest the article by Minamino et al [ 1 ]. I would like to clarify some of the significant findings and suggest re-analysis needed to validate their core conclusion.…”

“…In a recent study in Japanese evacuees after the Great East Japan Earthquake investigating salt intake and risk of disaster hypertension, “there was an interaction between estimated sodium intake and disaster hypertension according to the presence or absence of high risk of salt-sensitive hypertension in the group without prevalent hypertension (P=0.03)”. Considering that participants in the study of Minamino et al [ 1 ] were enrolled from a cohort database (KURAMA) in a non-random manner, this raises a concern whether subpopulations existed in their study population (e.g., sodium-responsive subjects) in which adaptation to sodium-induced hypercalciuria [ 3 ] or sodium-induced hypokalemia [ 4 ] could be compromised.…”

“…Minamino et al [ 1 ] have estimated daily salt intake using Tanaka’s formula; however, there was no report on dietary potassium intake or an estimation of K intake.…”

“…In support of this, it is worth to mention results of a recent international study (INTERMAP Research Group) carried out to determine dietary potassium intake in Japanese participants aged 40–59 years. Here, potassium intake per 1000 kcal of total energy intake, with participants stratified by urinary potassium excretion per unit of body weight (UK/BW) quartiles, was significantly different (P for trend < 0.001) [ 7 ], suggesting that due to the cross-sectional nature of the study by Minamino et al [ 1 ], and non-random enrollment of the participants in their cohort, it is quite rational to assume that dietary potassium intakes in RA outpatients in the study of Minamino et al to be different as well. This is especially important since daily dietary potassium intake can be as large as the extracellular potassium pool [ 9 ].…”

“…This is especially important since daily dietary potassium intake can be as large as the extracellular potassium pool [ 9 ]. This is again relevant because Minamino et al [ 1 ] have used spot urine samples to estimate salt intake using Tanaka formula [ 10 ], which has recently been questioned, mean differences for the Tanaka formula compared to the referred 24-h urinary sodium excretion was significantly different (difference (95% CI), 542 (261, 824); P < 0.001) [ 11 ].…”