Abstract
The renal regulation of sodium is intertwined with the extracellular fluid volume (ECFV). Most adjustments in sodium elimination in man are accomplished via alterations in tubular reabsorption. The latter is sensitive to change in ECFV. An expanded ECFV results in less reabsorption and more excretion of sodium, and a contracted ECFV has the converse effect. There are direct and indirect mechanisms whereby ECFV influences sodium reabsorption. Patients with nephrotic syndrome, heart failure, and cirrhosis "behave" physiologically as normal individuals with a contracted ECFV. Water balance is normally determined by intake and losses in sweat which is always hypoosmotic to plasma, by evaporation from skin and lungs, and through renal excretion. The major factors that determine the ability to concentrate the urine are (1) the establishment of a concentrated environment around the collecting ducts, and (2) the elaboration and effects on the kidney of antidiuretic hormone. The evaluation of a patient with abnormalities of sodium and water rests initially and largely on clinical information. The clinical setting provides clues to anticipating, preventing, and interpreting distortions of body sodium and water. The laboratory can detect an abnormality, confirm or refute clinical assessment, and assist in the quantitative aspects of treatment and its efficacy.
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