• DOI:10.1186/s13075-021-02571-2
• Corpus ID: 235763061

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

@article{Rastmanesh2021IsUN,
  title={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},
  author={Reza Rastmanesh},
  journal={Arthritis Research \& Therapy},
  year={2021},
  volume={23}
}

• R. Rastmanesh
• Published 8 July 2021
• Medicine
• Arthritis Research & Therapy

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. Authors have concluded that urinary Na/K ratio is an independent indicator associated with current RA disease activity. First, physiologically, with regard to dietary sodium intake, it is worth to remind that some people are more sodium-responsive [2]. 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. With regard to hypertension, it is known that in sodium-responsive individuals, KCl prevents the rise in blood pressure induced by dietary salt; however, with a low sodium intake, no significant effect on blood pressure is seen. It is also known that potassium itself reduces the rise in blood pressure caused by sodium chloride intake and reduces the increased sympathetic postural response which is seen in people on lowsodium diets [3]. 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. Urinary potassium was initially suggested to be reliable for use as a recovery biomarker in dietary studies [5]; however, precautions should be taken into account, as these findings are not replicated in an outpatient setting. Furthermore, in subsequent replication study [6], researchers concluded that due to measurement error in one or both estimates from dietary and urine measures, correlations between dietary and urinary sodium or potassium is very low [6]. In Japanese population, this may be even more pronounced because of significant difference in terms of dietary sodium and potassium intake among people [7]. This raises another issue since relation between blood pressure and dietary salt can be modulated by other dietary factors, such as potassium, where potassium intake can blunt the sodium-blood pressure relationship [8]. 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