Читать книгу Disorders of Fluid and Electrolyte Metabolism - Группа авторов - Страница 45

Water retention is by far the most common cause of hypotonic, dilutional hyponatremia. In other words, hypotonic hyponatremia should be considered a disorder of water homeostasis rather than an electrolyte disorder. Dilutional hyponatremia develops if either the kidney’s excretory capacity for water is overwhelmed by excessive water intake (e.g., psychogenic polydipsia, use of electrolyte-free irrigation solutions in transurethral prostatectomy, etc.) or, more frequently, if the regulatory mechanism that physiologically leads to the production of dilute urine is impaired. While the former is mostly (but not entirely) unrelated to the actions of the antidiuretic hormone arginine vasopressin (AVP, also called ADH), the latter (almost) always is [3]. High plasma AVP levels in the presence of hypotonicity can be observed with either a decreased, normal, or increased extracellular fluid volume. Marked reduction of effective arterial blood volume stimulates baroreceptors, which in turn leads to AVP release from the posterior pituitary gland [4]. This scenario can be found in patients with clinical hypovolemia due to true volume depletion as well as in patients with overt hypervolemia due to congestive heart failure [5], liver cirrhosis [6], or nephrotic syndrome. In contrast, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is characterized by euvolemia on clinical examination and comprises a wide range of diverse clinical conditions including cancer, drug side effects, diseases of the central nervous system, pulmonary disorders, stress (e.g., the postoperative state, endurance running), and endocrine disorders such as hypothyroidism and adrenal insufficiency [7]. In addition, several rare gain-of-function mutations of the AVP type 2 receptor have been identified that produce a SIADH-like clinical picture, which has been termed the nephrogenic syndrome of inappropriate antidiuresis [8.] Thiazide-like diuretics, via AVP-independent and -dependent mechanisms, are also a common cause of euvolemic or near-euvolemic hyponatremia [9, 10]. Finally, brain injury can elicit a form of hyponatremia called cerebral salt wasting syndrome that combines aspects of marked volume loss and SIADH [11]. Table 1 gives an overview of hyponatremia etiologies classified by extracellular volume status. For more in-depth information on the various entities, the reader is referred to the respective chapters in this issue of “Frontiers of Hormone Research.”

The relative frequencies of the many types and causes of hyponatremia vary considerably with the patient group studied. Reliable data on the rate of different entities in unselected populations of community-acquired hyponatremia are sparse, mainly because essential criteria for an accurate diagnostic differentiation are often not available in large retrospective analyses and even in most prospective studies. In 121 consecutive patients that were admitted to the University Hospital in Würzburg (Germany) with a serum [Na⁺] <130 mEq/L and that received a proper diagnostic work-up, 35% were diagnosed with SIADH, 32% with hypovolemic hyponatremia, 20% with hypervolemic hyponatremia, 7% with thiazide-induced hyponatremia, 4% with primary polydipsia, and 2% with adrenal insufficiency [12]. In a similar study outline, Cuesta et al. [13] found 43% of 1,323 patients admitted to a tertiary hospital in Dublin (Ireland) with a serum [Na⁺] <130 mEq/L to have SIADH. Of those, 26% were accounted for by disorders of the central nervous system followed by pulmonary disorders (19%), malignancies (18%), drugs (8%), and adrenal insufficiency (4%).