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Salt and its effect on blood pressure and target organ damage: new pieces in an old puzzle Titze J; Ritz EJ Nephrol 2009[Mar]; 22 (2): 177-89For centuries, salt has been regarded as essential to human health. Recent work, however, has provided further evidence that the current dietary intake of salt in Western societies is an important factor in the genesis of essential hypertension and may even partly cause blood pressure-independent target organ damage including renal damage. Accordingly, recent guidelines recommend reduction of daily consumption of salt to 6 g/day. Individuals vary with respect to the increase of blood pressure with increasing salt intake (salt sensitivity); individuals with renal disease are particularly salt sensitive. Salt causes major alterations of renal hemodynamics and accelerates progression. Despite some opinions to the contrary, salt restriction and volume control is particularly important in dialyzed patients. Understanding of how salt affects blood pressure and renal function has recently been advanced in 2 respects. The past concept that salt acts by expanding the extracellular fluid space has been challenged by the demonstration of water-free sodium storage of salt in tissues. Furthermore, salt promotes the secretion of cardiotonic steroids, i.e., mammalian "digitalis." Initial observations suggest a causal role for cardiotonic steroids in the genesis of cardiac abnormalities in advanced renal disease.|*Hypertension/etiology/physiopathology/prevention & control[MESH]|Blood Pressure/*drug effects[MESH]|Diet, Sodium-Restricted/*methods[MESH]|Humans[MESH]|Prognosis[MESH]|Sodium, Dietary/*adverse effects[MESH] |