levels. Examples of these disorders include chronic renal failure and states of mineralocorticoid excess. In this case, the price of a return to sodium balance is hypertension. Disorders of sodium balance that result from secondary renal sodium retention, as in congestive heart failure, lead to more profound volume expansion owing to hypotension. In mild to moderates cases, volume expansion eventually returns the MAP to its set point; the price of sodium balance in this case is edema. In more severe cases, volume expansion never returns blood pressure to normal, and renal sodium retention is unremitting. In still other situations, such as nephrotic syndrome, volume expansion results from changes in both the renal set point and body volume distribution. In this case, the price of sodium balance may be both edema and hypertension. In each of these cases, renal sodium (and chloride) retention results from a discrepancy between the existing MAP and the renal set point.
The examples listed previously emphasize that disorders of sodium balance do not necessarily abrogate the ability to achieve sodium balance. When balance is defined as the equation of sodium intake and output, most patients with ECF expansion (and edema or hypertension) or ECF volume depletion achieve sodium balance. They do so, however, at the expense of expanded or contracted ECF volume. The failure to achieve sodium balance at normal ECF volumes characterizes these disorders.
Frequently, distinguishing disorders of sodium balance from disorders of water balance is useful. According to this scheme, disorders of water balance are disorders of body osmolality and usually are manifested by alterations in serum sodium concentration
(see Chapter 1). Disorders of sodium balance are disorders of ECF volume. This construct has a physiologic basis because water balance and sodium balance can be controlled separately and by distinct hormonal systems. It should be emphasized, however, that disorders of sodium balance frequently lead to or are associated with disorders of water balance. This is evident from Figure 2-24 in which hyponatremia is noted to be a sign of either ECF volume expansion or contraction. Thus, the distinction between disorders of sodium and water balance is useful in constructing differential diagnoses; however, the close interrelationships between factors that control sodium and water balance should be kept in mind.
The figures herein describe characteristics of sodium home-ostasis in normal persons and also describe several of the regulatory systems that are important participants in controlling renal sodium excretion. Next, mechanisms of sodium transport along the nephron are presented, followed by examples of disorders of sodium balance that illuminate current understanding of their pathophysiology. Recently, rapid progress has been made in unraveling mechanisms of renal volume homeostasis. Most of the hormones that regulate sodium balance have been cloned and sequenced. Intracellular signaling mechanisms responsible for their effects have been characterized. The renal transport proteins that mediate sodium reabsorption also have been cloned and sequenced. The remaining challenges are to integrate this information into models that describe systemic volume homeostasis and to determine how alterations in one or more of the well-characterized systems lead to volume expansion or contraction.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...