Sodium and Its Multiorgan Targets

Abstract

ase Presentation: A 66-year-old retired man presented to his physician with complaints of shortness of breath and weight gain over 1 week's time during a recent cruise. He was not short of breath in the supine position, although his neck veins were distended. The blood pressure was 196/ 104 mm Hg; his heart rate was 92 bpm; and his cardiac rhythm was normal. He had a large habitus and was 76 in tall and 248 lb, which was 27 lb heavier than when he was evaluated 6 weeks previously in the office. The lungs revealed fine crackling rales bilaterally and posteriorly, but no wheezes or other sounds were noted. A fourth heart sound was heard at the apex. The ECG revealed left atrial abnormality and left ventricular hypertrophy with a normal sinus rate and rhythm. The echocardiogram confirmed left ventricular hypertrophy, increased left atrial size, and evidence of impaired diastolic function, and the left ventricular ejection fraction was 32%. Pulse wave velocity and aortic distensibility were impaired. There was severe 4ϩ bilateral edema of both lower extremities to the knees. Although the hemogram was normal, his blood urea nitrogen and creatinine concentrations were 28 and 1.2 mg/dL, respectively. The urinalysis revealed 4ϩ proteinuria, and a 24-hour urine collection for sodium content (at the time when his appointment was made) was Ͼ13 g. Brief CommentaryThe patient had been a long-time patient of ours, with well-controlled hypertension (receiving an angiotensin II receptor blocker, a calcium antagonist, a ␤-adrenergic receptor blocker, furosemide, spironolactone, and a statin). He controlled his diet at home, but always was tempted by the cuisine on his frequent vacation cruises. His dietary indiscretion actually produced his 27-lb weight gain within the first 3 days of his cruise and was lost 2 days after his office visit after a temporary increase in the dose of furosemide and spironolactone. This clinical experience was not at all unusual over the years that we followed him up, despite maintaining a workable therapeutic program designed for him. He had reduced his body weight from 293 to 260 lb on a calorie-and sodiumrestricted diet, but over these many years of follow-up, his dietary indiscretions always took a holiday, and its toll. He always apologized to me and his wife, but never to himself. He fully understood the basis of the development of heart failure and cardiovascular disease and the potential for endstage renal disease, vowing not to let this gain happen again.His is one of the major health problems of our society, prompting repeated recurrences of heart failure, and is the basis of many revisions of the dietary recommendations by the American Heart Association, the Institute of Medicine, and the National High Blood Pressure Education Program. Despite his awareness of dietary indiscretions, he knew our recommendations and followed them when at home. What is necessary is our continued patience and education, coupled with careful attention to nutritional guidelines. When reasonable dietary programs w...

Sodium, Blood Pressure, and Cardiovascular Disease

“…25 Excess sodium intake in experimental animals also promotes left and right ventricular hypertrophy and fibrosis, perivascular fibrosis of the coronary arteries, and diastolic dysfunction. 24,26 These findings in animal studies are strikingly similar to those seen in patients with similarly impaired left ventricular function, the most common basis for cardiac and renal failure and hospitalization in Medicare patients. 27 Even in young healthy adults with clinically normal BP, those who consume more sodium and less potassium are more likely to have increased left ventricular mass; this is especially prominent when BP is elevated, suggesting that excess dietary sodium sensitizes the heart, large arteries, and kidneys to hypertrophic and fibrotic stimuli.…”

“…For example, high sodium intake results in massive albumin excretion, oxidative stress, severe renal arteriolar damage, interstitial fibrosis, increased glomerular hydrostatic pressure, glomerular hyalinization, fibrosis, and end-stage renal disease independently of increased BP. [21][22][23][24] Moreover, excess sodium intake attenuates the beneficial effects of many antihypertensive drugs, including blockers of the renin-angiotensin-aldosterone system, whereas reducing sodium intake enhances these effects. 25 Excess sodium intake in experimental animals also promotes left and right ventricular hypertrophy and fibrosis, perivascular fibrosis of the coronary arteries, and diastolic dysfunction.…”

Mortality Benefits From US Population-wide Reduction in Sodium Consumption

“…It is plausible that there are effects on the renal system and vasculature that are not captured by BP alone. 33 The magnitudes of these effects are drawn from the long-term observational followup of the TOHP trial. This found a 25% reduction in CVD, although the CI was wide (95% CI, 1-43).…”

Effect of Dietary Sodium Restriction on Human Urinary Metabolomic Profiles

“…Reducing sodium intake induces benefits beyond and independent of BP lowering alone (7,8), suggesting that additional physiologic mechanisms also contribute to associated cardiovascular benefits. We recently demonstrated that DSR improves vascular endothelial function in middle-aged and older adults with moderately elevated systolic BP (SBP) via a reduction in vascular oxidative stress (8), while also reducing large elastic artery stiffness (9).…”