1
Disorders of body water homeostasis

https://doi.org/10.1016/S1521-690X(03)00049-6Get rights and content

Abstract

Disorders of body fluids are among the most commonly encountered problems in the practice of clinical medicine. This is in large part because many different disease states can potentially disrupt the finely balanced mechanisms that control the intake and output of water and solute. It therefore behoves clinicians treating such patients to have a good understanding of the pathophysiology, the differential diagnosis and the management of these disorders. Because body water is the primary determinant of the osmolality of the extracellular fluid, disorders of body water homeostasis can be divided into hypo-osmolar disorders, in which there is an excess of body water relative to body solute, and hyperosmolar disorders, in which there is a deficiency of body water relative to body solute. The classical hyperosmolar disorder is diabetes insipidus (DI), and the classical hypo-osmolar disorder is the syndrome of inappropriate antidiuretic hormone secretion (SIADH). This chapter first reviews the regulatory mechanisms underlying water and sodium metabolism, the two major determinants of body fluid homeostasis. The major disorders of water metabolism causing hyperosmolality and hypo-osmolality, DI and SIADH, are then discussed in detail, including the pathogenesis, differential diagnosis and treatment of these disorders.

Section snippets

Body fluid compartments

Water constitutes approximately 55–65% of body weight, varying somewhat with age, sex and amount of body fat, and therefore constitutes the largest single constituent of the body. Total body water (TBW) is distributed between the intracellular fluid (ICF) and the ECF compartments. Estimates of the relative sizes of these two important pools differ significantly depending on the tracer used to measure the ECF volume, but most studies in animals and man have suggested that 55–65% (or just under

Total and effective osmolality

Osmolality is defined as the concentration of all of the solutes in a given weight of water. Plasma osmolality can be measured directly (via determination of freezing point depression or vapour pressure because each of these are colligative properties of the number of free solute particles in a given volume of plasma), or estimated as:Posm(mOsm/kgH2O)=2×serum[Na+](mmol/l)+glucose(mmol/l)+breadureanitrogen(BUN)(mmol/l)Both methods produce comparable results under most conditions, as will simply

Water metabolism

Water metabolism represents a balance between the intake and excretion of water. Each side of this balance equation can be considered to consist of a ‘regulated’ and an ‘unregulated’ component, the magnitudes of which can vary quite markedly under different physiological and pathophysiological conditions. The unregulated component of water intake consists of the intrinsic water content of ingested foods, the consumption of beverages primarily for reasons of palatability or desired secondary

Sodium metabolism

Maintenance of sodium homeostasis requires a simple balance between intake and excretion of Na+. As in the case of water metabolism, it is possible to define regulated and unregulated components of both Na+ intake and Na+ excretion. Unlike water intake, however, there is little evidence in humans to support a significant role for regulated Na+ intake, with the possible exception of some pathological conditions. Consequently, there is an even greater dependence on mechanisms for regulated renal

Pathogenesis

Hyperosmolality indicates a deficiency of water relative to solute in the ECF. Because water moves freely between the ICF and ECF, this also indicates a deficiency of TBW relative to total body solute. Although an excess of body sodium can cause hypernatraemia, the vast majority of cases are due to losses of body water in excess of body solutes, caused by either insufficient water intake or excessive water excretion. Consequently, most of the disorders causing hyperosmolality are those

Pathogenesis

Hypo-osmolality indicates excess water relative to solute in the ECF; because water moves freely between ECF and ICF, this also indicates an excess of TBW relative to total body solute. Imbalances between body water and solute can be generated either by depletion of body solute more than body water, or by dilution of body solute from increases in body water more than body solute (Table 4).3 This represents an oversimplification, because most hypo-osmolar states include components of both solute

References (65)

  • C.L. Fraser et al.

    Epidemiology, pathophysiology, and management of hyponatremic encephalopathy

    American Journal of Medicine

    (1997)
  • D.D. Fanestil

    Compartmentation of body water

  • J.G. Verbalis

    The syndrome of inappropriate antidiuretic hormone secretion and other hypoosmolar disorders

  • T.P. Vokes et al.

    Effect of insulin on osmoregulation of vasopressin

    American Journal of Physiology

    (1987)
  • J.G. Verbalis

    Body water and osmolality

  • J.T. Fitzsimons

    Physiology and pathophysiology of thirst and sodium appetite

  • E.M. Stricker et al.

    Water intake and body fluids

  • G.L. Robertson

    Thirst and vasopressin function in normal and disordered states of water balance

    Journal of Laboratory and Clinical Medicine

    (1983)
  • C.J. Thompson et al.

    The osmotic thresholds for thirst and vasopressin release are similar in healthy man

    Clinical Science (London)

    (1986)
  • P.A. Phillips et al.

    Angiotensin II-induced thirst and vasopressin release in man

    Clinical Science (London)

    (1985)
  • G.L. Robertson

    Posterior pituitary

  • M.A. Knepper

    Molecular physiology of urinary concentrating mechanism: regulation of aquaporin water channels by vasopressin

    American Journal of Physiology

    (1997)
  • G.L. Robertson

    The regulation of vasopressin function in health and disease

    Recent Progress in Hormone Research

    (1976)
  • J.G. Verbalis

    Body sodium and extracellular fluid volume

  • D. Denton

    The Hunger for Salt: An Anthropological, Physiological and Medical Analysis

    (1982)
  • L. Wilkins et al.

    A great craving for salt by a child with cortico-adrenal insufficiency

    JAMA

    (1940)
  • D.N. Orth et al.

    The adrenal cortex

  • K.A. Kirchner et al.

    Sodium metabolism

  • W.B. Reeves et al.

    Tubular sodium transport

  • C. Baylis et al.

    Glomerular filtration

  • S. Masilamani et al.

    Aldosterone-mediated regulation of ENaC alpha, beta, and gamma subunit proteins in rat kidney

    Journal of Clinical Investigation

    (1999)
  • E.G. Schneider et al.

    Effect of osmolality on aldosterone secretion

    Endocrinology

    (1985)
  • Cited by (348)

    • Etiology and Management of Edema: A Review

      2023, Advances in Kidney Disease and Health
    • Participation of the angiotensinergic and vasopressinergic mechanisms in the maintenance of cardiorespiratory parameters in sodium depleted rats

      2022, Heliyon
      Citation Excerpt :

      Disruption of body fluids regulation is a very common issue encountered in the medical practice. This is mainly due to several illness and conditions that may potentially affect the control of intake and output of water and electrolytes, such as hyponatremia, disrupting this finely balanced mechanism [1]. Hyponatremia occurs when the concentration of sodium in the blood is low, causing a hydroelectrolyte imbalance in the body.

    View all citing articles on Scopus
    View full text