Does salt intake truly affect outcomes in HF patients?

Roshini Claire Anthony
18 Oct 2022
Does salt intake truly affect outcomes in HF patients?

A small, single-centre study has suggested that increasing sodium intake does not affect weight or kidney function in patients hospitalized for acute heart failure (HF) who are undergoing aggressive diuretic therapy.

“We encountered no difference in the primary endpoint or safety despite a median dose of 13 g of sodium chloride in the treatment group,” presented study author Dr Robert Montgomery from the Kaufman Center for Heart Failure Treatment and Recovery, Cleveland Clinic, Cleveland, Ohio, US, at HFSA 2022.

In the double-blind OSPREY-AHF* trial, 65 adults (mean age 70 years, 37 percent female) hospitalized (non-ICU) with acute HF were randomized 1:1 to receive oral sodium chloride (2 g) or placebo TID during intravenous diuretic therapy in addition to the sodium-restricted diet provided at the hospital. Patients needed to have NT-proBNP levels 1,000 ng/L and be treated with furosemide 10 mg/hour to be included. Patients with acute coronary syndrome, eGFR <15 mL/min/1.73 m2, malabsorptive gastrointestinal disorders, or hypernatremia (serum sodium >145 or <120 mEq/L) were among those excluded. 

Forty-nine percent of patients had HF with preserved ejection fraction. Mean eGFR at baseline was 39 mL/min/1.73 m2. The most common comorbidities were hypertension and atrial fibrillation (71 and 68 percent, respectively). Patients had a mean two hospitalizations for HF in the previous year. The most common medications used were beta-blockers, mineralocorticoid receptor antagonists, and hydralazine and/or isosorbide dinitrate (72, 52, and 52 percent, respectively). Baseline characteristics were generally well balanced between groups, though patients assigned to the sodium chloride group had higher serum creatinine levels compared with placebo (2.0 vs 1.6 mEq/L).

At 96 hours, change in creatinine levels and weight did not significantly differ between patients assigned to sodium chloride and placebo (p=0.33). This lack of difference applied to both change in creatinine levels (0.04 [sodium chloride] vs 0.15 [placebo] mg/dL; p=0.30) and change in weight (–4.0 vs –4.6 kg; p=0.57). [HFSA 2022, session: Late Breaking Clinical Trials 1]

Serum sodium levels decreased more in the placebo vs sodium chloride group (–2.6 vs –0.03 mEq/L; p<0.001). Blood urea nitrogen levels increased more with placebo vs sodium chloride (11 vs 3.1 mEq/L; p=0.02).

Other secondary outcomes such as changes in Thirst Distress-HF score (–1.2 [sodium chloride] vs 0.1 [placebo]; p=0.39), serum chloride levels (–1.0 vs –3.0 mEq/L; p=0.19), and eGFR levels (–2.3 vs –3.3 mL/min/1.73 m2; p=0.18) did not differ between groups. Total recorded urine output was also comparable between groups (10,000 vs 9,400 mL; p=0.61).

Time to discharge from hospital (from enrolment) was similar between patients in the sodium chloride and placebo groups (8 vs 7 days). Three and five patients, respectively, were admitted to the ICU during hospitalization. Two and one patients, respectively, required renal replacement therapy within 90 days of enrolment. Seven patients from each group were readmitted to hospital within 30 days. There were four and three deaths, respectively, within 90 days.

There was no significant difference between groups in terms of serious adverse events, though the trial was not powered to detect between-group differences. The apparent lack of harm points to the need for larger clinical trials to assess the effect of sodium chloride in this patient population, said Montgomery.


A change in mindset required?

“Since the 1940s, we’ve been taught that salt is the main reason why people become congested with fluid, which led to the idea that we need to keep people low on salt while in the hospital with fluid overload,” said senior author Dr Wilson Tang from the Heart, Vascular & Thoracic Institute at Cleveland Clinic, Cleveland, Ohio, US.

However, a low sodium intake is associated with complications such as decreased nutritional quality or caloric intake, decreased diuretic response, and increased renin-angiotensin-aldosterone system activation and renal sodium avidity, noted Montgomery.

“There have even been some reports of potential benefits of infusing salt to facilitate more urination with high-dose diuretic drugs in patients with congestive heart failure. However, our study did not show such benefits with raising oral salt supplementation and gave us an indication that keeping a low-salt diet during aggressive diuretic therapy may not be as effective as we thought,” added Tang.

“We believe that the null result of this study does challenge the routine practice of sodium chloride restriction in acute HF,” Montogomery pointed out.

“[Nonetheless,] our findings do not mean that patients with HF should start eating more salt, as we only studied the role of oral salt supplementation in those receiving high-dose diuretic drugs during their hospitalizations,” Tang said. “Patients with HF still need to be mindful that excessive salt intake may cause fluid congestion,” he concluded.



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