BES2005 Poster Presentations Endocrine tumours and neoplasia (46 abstracts)
Attenuation of vasopressin-induced antidiuresis in poorly-controlled type 2 diabetes
A Agha 1 , D Smith 1 , F Finucane 1 , M Shelock 1 , A Morris 2 , P Baylis 3 & CJ Thompson 1
1Academic Department of Endocrinology, Beaumont Hospital, Dublin, Ireland; 2Division of Medicine and Therapeutics, Ninewells Hospital, Dundee, Scotland, UK; 3Endocrine Unit, Royal Victoria Infirmary, Newcastle, UK.
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, HbA1c > 9 %), 10 subjects with well-controlled type 2 diabetes (WCDS, HbA1c < 7 %), and 10 matched non-diabetic control subjects (NDCS), during a euglycaemic 8-hour water deprivation test. None of the subjects had nephropathy or arterial hypertension.
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 mOsm/kg) was lower than in WCDS (360.7 +/- 142.8 to 794.1 +/- 77.3 mOsm/kg), p < 0.001, or NDCS (336.0 +/- 123.3 to 786.5 +/- 63.3 mOsm/kg), 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 threshold for thirst (291.9 +/- 4.6 mOsm/kg) and vasopressin release (291.1 +/- 2.9 mOsm/kg) were higher compared to WCDS (286.6 +/- 1.8 and 286 +/- 3.6 mOsm/kg, respectively), and to NDCS (286.0 +/- 2.4 and 284.1 +/- 4.7 mOsm/kg, respectively); between groups p < 0.001 for both variables.
Under conditions of euglycaemia, patients with poorly-controlled type 2 diabetes have impaired renal response to vasopressin, and elevated osmotic threshold for thirst and vasopressin release in response to dehydration. Under conditions of chronic hyperglycaemia, these abnormalities may have significant contribution to the development of dehydration in poorly-controlled diabetes.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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