{'fraction_non_alphanumeric': 0.045081967213114756, 'fraction_numerical': 0.028005464480874317, 'mean_word_length': 5.599099099099099, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Pathogenesis of clinical hyponatremia: observations of vasopressin and fluid intake in 100 hyponatremic medical patients

Abstract. The pathogenesis of hyponatremia remains debated; therefore, we determined the roles of plasma vasopressin, fluid intake and renal free water excretion in hyponatremic medical patients. We evaluated 100 consecutive hypo‐osmolar hyponatremic patients (PNa = 127 ± 0·7 mm l−1) in a prospective manner. We observed: (i) hyponatremia was often found in association with advanced congestive cardiac failure (twenty‐five of 100 patients), liver cirrhosis (16%) and primary volume contraction (29%). There was a 17% in‐hospital mortality of hyponatremic patients. This was primarily related to the severity of underlying illnesses rather than to hyponatremia per se. (ii) The most consistently observed laboratory finding of hyponatremia was non‐osmotic vasopressin stimulation; mean observed PADH was 4·7 ± 0·7 pg ml−1 and vasopressin was detectable by radioimmunoassay (RIA) in 91% of all patients. (iii) In addition to vasopressin stimulation we also found evidence of advanced ‘circulatory underfilling’ in most hyponatremic patients. (iv) Mean urinary osmolality was hypertonic to plasma (441 ± 17·4 mOsm kg H2O−1). This applied to patients with hyponatremic cardiac failure, liver cirrhosis and volume contraction. Almost all of these patients received high ceiling diuretics. (v) Spontaneous mean daily fluid intake was 2·4 ± 0·2 1.