It is classically taught that when renal function is normal and the secretion of antidiuretic hormone (arginine vasopressin) is fully suppressed, the human kidney has the capacity to excrete large volumes of dilute urine, allowing for a broad range of water intake. This flexibility protects against the development of hyponatremia even in the face of water intake that can approach 20 L/d. What is not as widely recognized is the impact that alterations in solute intake, and therefore excretion, have on this process. As will be illustrated here, a decrement in solute intake markedly reduces the above-mentioned flexibility and puts the individual at risk for the unexpected development of hyponatremia. In contrast, an increment in solute intake can be used therapeutically to treat this electrolyte disorder and allow those prone to it to liberalize their water intake.