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1. Jacobson HR: Functional segmentation of the mammalian nephron. Am J Physiol 1981, 241:F203.

2. Goldberg M: Water control and the dysnatremias. In The Sea Within Us. Edited by Bricker NS. New York: Science and Medicine Publishing Co., 1975:20.

3. Kokko J, Rector F: Countercurrent multiplication system without active transport in inner medulla. Kidney Int 1972, 114.

4. Knepper MA, Roch-Ramel F: Pathways of urea transport in the mammalian kidney. Kidney Int 1987, 31:629.

5. Vander A: In Renal Physiology. New York: McGraw Hill, 1980:89.

6. Zimmerman E, Robertson AG: Hypothalamic neurons secreting vasopressin and neurophysin. Kidney Int 1976, 10(1):12.

7. Bichet DG: Nephrogenic and central diabetes insipidus. In Diseases of the Kidney, edn. 6. Edited by Schrier RW, Gottschalk CW. Boston: Little, Brown, and Co., 1997:2430

8. Bichet DG : Vasopressin receptors in health and disease. Kidney Int 1996, 49:1706.

9. Dunn FL, Brennan TJ, Nelson AE, Robertson GL: The role of blood osmolality and volume in regulating vasopressin secretion in the rat. J Clin Invest 1973, 52:3212.

10. Rose BD: Antidiuretic hormone and water balance. In Clinical Physiology of Acid Base and Electrolyte Disorders, edn. 4. New York: McGraw Hill, 1994.

11. Cogan MG: Normal water homeostasis. In Fluid & Electrolytes, Physiology and Pathophysiology. Edited by Cogan MG. Norwalk: Appleton & Lange, 1991:98.

12. Halterman R, Berl T: Therapy of dysnatremic disorders. In Therapy in Nephrology and Hypertension. Edited by Brady H, Wilcox C. Philadelphia: WB Saunders, 1998, in press.

13. Veis JH, Berl T, Hyponatremia: In The Principles and Practice of Nephrology, edn. 2. Edited by Jacobson HR, Striker GE, Klahr S. St.Louis: Mosby, 1995:890.

14. Berl T, Schrier RW: Disorders of water metabolism. In Renal and Electrolyte Disorders, edn 4. Philadelphia: Lippincott-Raven, 1997:52.

15. Verbalis JG: The syndrome of ianappropriate diuretic hormone secretion and other hypoosmolar disorders. In Diseases of the Kidney, edn. 6. Edited by Schrier RW, Gottschalk CW. Boston: Little, Brown, and Co., 1997:2393.

16. Berl T, Schrier RW: Disorders of water metabolism. In Renal and Electrolyte Disorders, edn. 4. Edited by Schrier RW. Philadelphia: Lippincott-Raven, 1997:54.

17. Berl T, Anderson RJ, McDonald KM, Schreir RW: Clinical Disorders of water metabolism. Kidney Int 1976, 10:117.

18. Gullans SR, Verbalis JG: Control of brain volume during hyperosmolar and hypoosmolar conditions. Annu Rev Med 1993, 44:289.

19. Zarinetchi F, Berl T: Evaluation and management of severe hyponatremia. Adv Intern Med 1996, 41:251.

20. Lauriat SM, Berl T: The Hyponatremic Patient: Practical focus on therapy. J Am Soc Nephrol 1997, 8(11):1599.

21. Ayus JC, Wheeler JM, Arieff AI: Postoperative hyponatremic encephalopathy in menstruant women. Ann Intern Med 1992,117:891.

22. Laureno R, Karp BI: Myelinolysis after correction of hyponatremia. Ann Intern Med 1997, 126:57.

23. Kumar S, Berl T: Disorders of serum sodium concentration. Lancet 1998. in press.

24. Cogan MG: Normal water homeostasis. In Fluid & Electrolytes, Physiology and Pathophysiology. Edited by Cogan MG. Norwalk: Appleton & Lange, 1991:94.

25. Rittig S, Robertson G, Siggaard C, et al.: Identification of 13 new mutations in the vasopressin-neurophysin II gene in 17 kindreds with familial autosomal dominant neurohypophyseal diabetes insipidus. Am J Hum Genet 1996, 58:107.

26. Lanese D, Teitelbaum I: Hypernatremia. In The Principles and Practice of Nephrology, edn. 2. Edited by Jacobson HR, Striker GE, Klahr S. St. Louis: Mosby, 1995:895.

27. Barrett T, Bundey S: Wolfram (DIDMOAD) syndrome. J Med Genet 1997, 29:1237.

28. Holtzman EJ, Ausiello DA: Nephrogenic Diabetes insipidus: Causes revealed. Hosp Pract 1994, Mar 15:89-104.

29. Bichet D, Oksche A, Rosenthal W: Congential Nephrogenic Diabetes Insipidus. J Am Soc Nephrol 1997, 8:1951.

30. Lieburg van, Verdjik M, Knoers N, et al.: Patients with autosomal nephrogenic diabetes insipidus homozygous for mutations in the aquaporin 2 water channel. Am J Hum Genet 1994, 55:648.

31. Canfield MC, Tamarappoo BK, Moses AM, et al.: Identification and characterization of aquaporin-2 water channel mutations causing nephrogenic diabetes insipidus with partial vasopressin response. Hum Mol Genet 1997, 6(11):1865.

Sodium is the predominant cation in extracellular fluid (ECF); the volume of ECF is directly proportional to the content of sodium in the body. Disorders of sodium balance, therefore, may be viewed as disorders of ECF volume. The body must maintain ECF volume within acceptable limits to maintain tissue perfusion because plasma volume is directly proportional to ECF volume. The plasma volume is a crucial component of the blood volume that determines rates of organ perfusion. Many authors suggest that ECF volume is maintained within narrow limits despite wide variations in dietary sodium intake. However, ECF volume may increase as much as 18% when dietary sodium intake is increased from very low to moderately high levels [1,2]. Such variation in ECF volume usually is well tolerated and leads to few short-term consequences. In contrast, the same change in dietary sodium intake causes only a 1% change in mean arterial pressure (MAP) in normal persons [3]. The body behaves as if the MAP, rather than the ECF volume, is tightly regulated. Under chronic conditions, the effect of MAP on urinary sodium excretion displays a remarkable gain; an increase in MAP of 1 mm Hg is associated with increases in daily sodium excretion of 200 mmol [4].

Guyton [4] demonstrated the importance of the kidney in control of arterial pressure. Endogenous regulators of vascular tone, hormonal vasoconstrictors, neural inputs, and other nonrenal mechanisms are important participants in short-term pressure homeostasis. Over the long term, blood pressure is controlled by renal volume excretion, which is adjusted to a set point. Increases in arterial pressure lead to natriuresis (called pressure natriuresis), which reduces blood volume. A decrease in blood volume reduces venous return to the heart and cardiac output. Urinary volume excretion exceeds dietary intake until the blood volume decreases sufficiently to return the blood pressure to the set point.

Disorders of sodium balance resulting from primary renal sodium retention lead only to modest volume expansion without edema because increases in MAP quickly return sodium excretion to baseline

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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