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This Article Full Text Full Text (PDF) All Versions of this Article: 287/6/E1100    most recent 00214.2004v2 00214.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Agha, A. Articles by Thompson, C. J. Search for Related Content PubMed PubMed Citation Articles by Agha, A. Articles by Thompson, C. J.

Attenuation of vasopressin-induced antidiuresis in poorly controlled type 2 diabetes

¹Academic Department of Endocrinology, Beaumont Hospital, Dublin 9, Ireland; ²Division of Medicine and Therapeutics, Ninewells Hospital, Dundee DD1 9SY, Scotland; and ³Endocrine Unit, Royal Victoria Infirmary, Newcastle NEI 4LP, England

Submitted 21 May 2004 ; accepted in final form 30 July 2004

Renal resistance to vasopressin has been demonstrated in type 1 diabetes and in type 2 diabetes with nephropathy. However, renal response to vasopressin in type 2 diabetes without nephropathy has not been studied. We studied 10 subjects with poorly controlled type 2 diabetes (PCDS; Hb A_1c >9%), 10 subjects with well-controlled type 2 diabetes (WCDS; Hb A_1c <7%), and 10 matched nondiabetic control subjects (NDCS) during a euglycemic 8-h water deprivation test. None of the subjects had nephropathy. Water deprivation caused similar rises in plasma vasopressin concentrations in all three groups, but the rise in urine osmolality in PCDS (280.3 ± 49.7 to 594.4 ± 88.5 mosmol/kgH₂O) was lower than in WCDS (360.7 ± 142.8 to 794.1 ± 77.3 mosmol/kgH₂O, P < 0.001) or NDCS (336.0 ± 123.3 to 786.5 ± 63.3 mosmol/kgH₂O, P = 0.019). Total urine output was higher in the PCDS than in WCDS and NDCS (P < 0.05). Linear regression analysis showed that, in PCDS, the osmotic thresholds for thirst (291.9 ± 4.6 mosmol/kgH₂O) and vasopressin release (291.1 ± 2.9 mosmol/kgH₂O) were higher compared with WCDS (286.6 ± 1.8 and 286.0 ± 3.6 mosmol/kgH₂O, respectively) and NDCS (286.0 ± 2.4 and 284.1 ± 4.7 mosmol/kgH₂O, respectively) (between groups P < 0.001 for both variables). Under conditions of euglycemia, PCDS have impaired renal response to vasopressin and elevated osmotic threshold for thirst and vasopressin release in response to dehydration. Under conditions of chronic hyperglycemia, these abnormalities may significantly contribute to the development of dehydration in PCDS.

osmoregulation