Background/Purpose: Hypertension is highly prevalent in patients with rheumatoid arthritis (RA). High sodium and low potassium intake are both modifiable determinants of blood pressure in the general population and can be estimated by measuring urinary sodium and potassium excretion. Moreover, a high sodium:potassium  ratio is associated with increased risk of high blood pressure. However, little is known about the relationship between sodium and potassium intake and blood pressure in patients with RA. Thus, we examined the hypothesis that sodium and potassium excretion is related to blood pressure and markers of inflammation in patients with RA.

Methods: We studied 166 patients with RA and 92 control subjects frequency-matched for age, sex, and race. First morning urine samples were collected and the concentrations of urine sodium and potassium were measured by flame photometry and 24 hour sodium and potassium excretion were estimated with the Kawasaki formula, a validated method that incorporates age, sex, height, weight, and urine creatinine. Blood pressure was the average of two resting measurements. In patients with RA, sedimentation rate and concentrations of vascular cell adhesion molecule-1, C-reactive protein, interleukin-6 and tumor necrosis factor were measured. Fisher’s exact and Wilcoxon’s tests were used to compare categorical and continuous variables, respectively. The associations between systolic (SBP), diastolic blood pressures (DBP), and inflammatory markers with estimated 24 hour urinary sodium, potassium, and sodium:potassium intake ratio were tested using Spearman correlations. For the blood pressure analyses, linear regressions were modeled to adjust for age, sex, and race.

Results: Patients with RA and control subjects had a similar mean age (54.2±11.9 vs. 53.2±11.6, p=0.43), were predominantly female (69% vs. 63%, p=0.41) and Caucasian (89% vs. 85%, p=0.44). Patients with RA had higher rates of hypertension (54% vs. 39%, p = 0.03). The estimated 24 hour sodium [median (interquartile range) of 5.1 (3.9-6.6) and 4.9 (4.0-6.5) g/day, respectively, p=0.90] and potassium [2.5 (2.1-3.2) and 2.7 (2.2-3.8) g/day, p=0.08] intake were similar in patients with RA and control subjects. The  urinary sodium:potassium ratio was higher in patients with RA than in controls [2.0 (1.6-2.4) and 1.7 (1.5-2.1), p=0.02] but was not associated with blood pressure in either group.  Lower potassium (g/day) intake was associated with DBP in patients with RA [β coefficient (95% CI) =-1.79, p=0.04], but there was no significant association between the estimated sodium or potassium intake or their ratio with markers of inflammation (all p>0.05).  

Conclusion: Patients with RA had significantly lower estimated sodium:potassium intake ratio than control subjects. Higher 24 hour potassium intake was significantly associated with lower DBP in patients with RA. Further studies are needed to evaluate the impact of diets with low sodium and high potassium content on blood pressure in patients with RA.

Grants: P60AR056116, K23AR064768, KL2TR000446, GM5M01-RR00095, UL1 RR024975-01, and 2 UL1 TR000445-06 from the NIH, and a grant from Alpha Omicron Pi

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/relationship-between-estimated-sodium-and-potassium-intake-with-blood-pressure-and-inflammatory-markers-in-patients-with-rheumatoid-arthritis/