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Hyponatremia in small cell lung cancer. Mechanisms not involving inappropriate ADH secretion
Author(s) -
Kamoi K.,
Ebe T.,
Hasegawa A.,
Sato F.,
Takato H.,
Iwamoto H.,
Kaneko H.,
Ishibashi M.,
Yamaji T.
Publication year - 1987
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19870901)60:5<1089::aid-cncr2820600528>3.0.co;2-u
Subject(s) - vasopressin , hyponatremia , endocrinology , medicine , atrial natriuretic peptide , antidiuretic , plasma renin activity , hypertonic saline , aldosterone , renal cell carcinoma , pathophysiology , arginine vasopressin receptor 2 , renin–angiotensin system , blood pressure , receptor , antagonist
A 62‐year‐old man with small cell carcinoma (oat cell type) of the lung who had hyponatremia and renal sodium loss with inappropriate antidiuresis is reported. Plasma levels of arginine vasopressin (AVP) were not elevated inappropriately. Plasma levels of atrial natriuretic peptide (ANP), however, were high, and increased after water loading and hypertonic saline infusion. The renin‐aldosterone axis was normal, as were adrenal, thyroid, and renal functions. Water restriction to 500 to 700 ml/d resulted in a rise in serum sodium. Analysis of the tumor tissue failed to demonstrate the presence of AVP or ANP. The findings (1) suggest that hyponatremia and renal sodium loss with inappropriate antidiuresis observed in the patient is due to an antidiuretic substance distinct from AVP, and (2) point to the possibility that hypersecretion of ANP may play a role in the pathophysiology.