Our genes were selected to adapt us to life in the African continent where the climate is hot and dry, perspiration substantial, and dietary salt intake was low. Presently, individuals living in rural African communities have very low levels of blood pressure until they migrate to an urban environment, where salt intake rises steeply and, with it, the incidence of hypertension. These observations suggest that we are adapted to retain, rather than eliminate, salt through a salt appetite and renal mechanisms for avid salt retention. Despite these evolutionary adaptations, most normal subjects maintain an extracellular fluid volume that changes by less than 1 liter (1 kilogram of body weight) and a blood pressure that changes by less than 10%, despite wide variations in daily salt intake. These subjects are termed “salt resistant” and encompass the majority of healthy adolescents and young adults. However, a minority are unable to maintain a normal, low level of blood pressure in face of a steep rise in salt intake and are termed “salt-sensitive.” Salt sensitivity precedes hypertension. It is a cardiovascular risk factor, complicates antihypertensive therapy, contributes to progressive loss of kidney function in patients with chronic kidney disease (CKD), exacerbates proteinuria, and diminishes the antiproteinuric response to drugs in those with renal disease. Thus, the evaluation and management of dietary salt intake is an essential component of care for patients with high blood pressure, kidney disease, or cardiovascular risk. Regrettably, many physicians erroneously believe that dietary salt intake does not require attention in the era of modern diuretics. This chapter will outline arguments for a more comprehensive assessment of dietary salt intake than is presently customary and provide goals and steps to appropriate management.

Most sodium is ingested as salt. Moreover, the increase in blood pressure in salt-sensitive subjects fed salt is not apparent if an equivalent quantity of sodium is given with another anion. However, intake is usually quantitated as sodium. A daily intake of 100 mmol of sodium is equivalent to 5.8 g of salt.

Daily sodium intake varies widely in modern Western societies but is generally between 80 and 250 mmol. A multinational INTERSALT study concluded that the mean level of blood pressure of individuals in a country increases with ambient salt intake. Because hypertension is the leading cause of cardiovascular death and cardiovascular disease is the leading cause of death, any increase in population blood pressure is a cause for concern.

A reduction of salt intake in patients with pre- or established hypertension is recommended by the World Health Organization and the Joint National Commission on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC). Clandestine promotion of high salt intake by food and beverage companies in the United States, for example by the Salt Institute, has unfortunately been highly successful. Whereas prior to 1980, the total sales of food salt and the prevalence of hypertension in the United States were decreasing, since then the use of salt has increased by as much as 90%. This has been accompanied by an increase in age-adjusted prevalence of high blood pressure in the U.S. population. The relationship between salt intake and blood pressure varies between individuals. This obscures the overall effect of dietary salt on blood pressure and cardiovascular disease and has complicated the public health case for salt restriction in food.

Salt sensitivity is defined arbitrarily as a greater than 10% increase in blood pressure on passing from a low to a high salt intake. Salt-sensitive individuals constitute approximately 30% of the young adult population. A shortened protocol to assess salt sensitivity has been developed whereby individuals are given dietary advice to achieve a 150 mmol per day sodium intake for 3 days. They then receive 2 L of 0.9% saline intravenously over 4 hours to provide high salt intake. The following day, they receive a salt-restricted diet of 10 mmol daily and 3 oral doses of 40 mg furosemide. The blood pressure is compared at the end of the high and low salt periods. This shortened protocol is reproducible in defining salt-sensitive and salt-resistant individuals. However, there is a normal distribution of salt-induced blood pressure. Therefore, division into salt resistant and salt sensitive is arbitrary.

Unfortunately, this protocol is too cumbersome for routine clinical use. The proportion of subjects who are salt sensitive is rather greater in African Americans than Caucasians, is associated with a low plasma renin activity, increases with age, and increases markedly with declining renal function. Salt sensitivity is more frequent in hypertensive than normotensive subjects. Therefore, elderly or African American hypertensives, and especially those with chronic kidney disease can reasonably be assumed to be salt sensitive. In practice, salt sensitivity often becomes apparent as a large fall in blood pressure with dietary salt restriction and thiazide diuretic therapy.

The degree of salt sensitivity increases exponentially with declining kidney function. As patients approach end-stage renal disease, the great majority are salt sensitive. The exceptions are those with primary tubulointerstitial disease who typically do not retain sodium chloride (NaCl) and have normal blood pressure.

Because the level of blood pressure determines the progression of kidney disease in those with more than 1-3 g/24 hours of protein excretion, attention to dietary salt and proper use of diuretics
are essential in hypertensive patients with chronic proteinuric kidney disease. Moreover, a high level of dietary salt increases protein excretion in patients with proteinuric kidney disease and appears to enhance the progression of underlying CKD. Therefore, dietary salt restriction and proper use of diuretics are an important component of the management of the great majority of patients with CKD. Indeed, because proper management of blood pressure (often with a lower than normal blood pressure goal) is required for optimum control of progressive proteinuric kidney disease, control of salt intake and proper use of diuretics should be a part of the initial clinical management of these patients. This follows from the observations that salt intake determines blood pressure, whereas blood pressure determines not only the progression of chronic kidney disease but the rapidity and severity with which cardiovascular events develop in this high-risk population.

Current estimates suggest that the high level of dietary salt in the United States presently accounts for up to 15% of strokes and 8% of coronary artery disease. In countries such as Finland where national programs to reduce salt intake have been effective, there is a reduction in blood pressure and a greater than 70% decrease in stroke and coronary heart mortality in the population younger than 65 years.