Nutritional management of heart failure.

Nutrition in the cardiovascular field to date has focused on improving lifestyle-related diseases such as hypertension and diabetes from the viewpoint of secondary prevention. For these conditions, "nutrition for weight loss" is recommended, and nutritional guidance that restricts calories is provided. On the other hand, in symptomatic Stage C and D heart failure, it is known that underweight patients who manifest poor nutrition, sarcopenia, and cardiac cachexia have a poor prognosis. This is referred to as the "Obesity paradox". In order to "avoid weight loss" in patients with heart failure, a paradigm shift to nutritional management to prevent weight loss is needed. Rather than prescribing uniform recommendation for salt reduction of 6 g/day or less, awareness of the behavior change stage model is attracting attention. In this setting, the value of salt restriction will need to be determined to determine the priority level of intervention for undernutrition versus the need to prevent congestive signs and symptoms. In the Intensive Care Unit (ICU)/Cardiac Care Unit (CCU) for acute heart failure, nutritional intervention should be considered within 48 h of admission. Key points are selection of access route, timing of intervention, and monitoring of side effects. In nutritional management at home and in end-of-life care, food is a reflection of an individual's values, as well as a source of joy and encouragement. The importance of digestive tract should also be recognized in heart failure from oral flail to intestinal edema, constipation, and the intestinal bacteria called the heart-gut axis. Finally, we would like to propose a new term "heart nutrition" for nutritional management in patients with heart failure in this review. Compared to the evidence for exercise therapy in heart failure, studies assessing nutritional management remain scarce and there is a need for research in this area in the future.

Mendelian Randomization Analysis Reveals a Causal Effect of Urinary Sodium/Urinary Creatinine Ratio on Kidney Function in Europeans.

Salt restriction was recommended in clinical practice guideline for chronic kidney disease (CKD) treatment, but its effect on kidney outcomes remains conflicting. We aimed to test the causal effect of salt intake, using estimated 24-h sodium excretion from spot urinary sodium/urinary creatinine (UNa/UCr) ratio as a surrogate, on renal function using two-sample Mendelian randomization (MR). Genetic instruments for UNa/UCr were derived from a recent genome-wide association study of 218,450 European-descent individuals in the UK Biobank. Kidney outcomes were creatinine-based estimated glomerular filtration rate (eGFRcrea) (N = 567,460) and CKD (eGFRcrea < 60 ml/min/1.73 m2, N cases = 41,395, N controls = 439,303) from the CKDGen consortium. Cystatin C-based eGFR (eGFRcys) and eGFRcrea single-nucleotide polymorphisms associated with blood urea nitrogen (BUN) were used for sensitivity analyses. MR revealed a causal effect of UNa/UCr on higher eGFRcrea [ß = 0.14, unit change in log ml/min/1.73 m2 per UNa/UCr ratio; 95% confidence interval (CI) = 0.07 - 0.20, P = 2.15 × 10-5] and a protective effect against CKD risk (odds ratio = 0.24, 95% CI = 0.14 to 0.41, P = 1.20 × 10-7). The MR findings were confirmed by MR-Egger regression, weighted median MR, and mode estimate MR, with less evidence of existence of horizontal pleiotropy. Consistent positive causal effect of UNa/UCr on eGFRcys was also detected. On the other hand, bidirectional MR suggested inconclusive results of CKD, eGFRcrea, eGFRcrea (BUN associated), and eGFRcys on UNa/UCr. The average 24-h sodium excretion was estimated to be approximately 2.6 g per day for women and 3.7 g per day for men. This study provides evidence that sodium excretion, well above the recommendation of <2 g per day of sodium intake, might not have a harmful effect on kidney function. Clinical trials are warranted to evaluate the sodium restriction target on kidney function.

Blood pressure control status and relationship between salt intake and lifestyle including diet in hypertensive outpatients treated at a general hospital.

The purpose of the present study was to investigate blood pressure (BP) control and salt intake in hypertensive outpatients treated at a general hospital and to examine the relationship between their lifestyles and amount of salt intake. Subjects comprised 429 hypertensive patients (206 males, 223 females, and average age of 71 ± 11 years). We estimated 24-hour salt excretion using spot urine samples and assessed lifestyle using a self-description questionnaire. Average clinic BP and the number of antihypertensive drugs were 132 ± 11/73 ± 8 mmHg and 1.8 ± 0.9, respectively. In all subjects, average estimated salt intake was 9.2 ± 2.8 g/day and the rate of achievement of the estimated salt intake of <6 g/day was 11.2%. In patients with chronic kidney disease or cardiovascular disease, these values were 8.6 ± 2.6 g/day and 15.5%, and 9.1 ± 3.3 g/day and 18.2%, respectively. Estimated salt intake was lower in patients living alone than in those with a family. In a multivariate analysis, estimated salt intake correlated positively with body mass index and negatively with age. Among patients with an excessive salt intake (≥10 g/day), 75.2% answered that they made an effort to reduce their salt intake. The amount of food and processed food consumption correlated with estimated salt intake. In conclusion, the rate of achievement of salt restriction was low in hypertensive patients treated at a general hospital. It may be important to provide data on actual salt intake and guide salt restriction in the individual management of hypertension.