Submitted on May 21, 2004
Accepted on July 30, 2004
ATTENUATION OF VASOPRESSIN-INDUCED ANTIDIURESIS IN POORLY-CONTROLLED TYPE 2 DIABETES
Amar Agha1, Diarmuid Smith1, Francis Finucane1, Mark Sherlock1, Andrew Morris2, Peter Baylis3, and Christopher J. Thompson1*
1 Academic Department of Endocrinology, Beaumont Hospital, Dublin, Ireland
2 Division of Medicine and Therapeutics, Ninewells Hospital, Dundee, United Kingdom
3 Endocrine Unit, Royal Victoria Infirmary, Newcastle, United Kingdom
* To whom correspondence should be addressed. E-mail: chris.thompson{at}beaumont.ie.
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.
Analysis of variance model (ANOVA) showed that 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, between groups p < 0.001), or
NDCS ( 336.0 ± 123.3 to 786.5 ± 63.3 mOsm/kg, between groups p = 0.019). Total
urine output was higher in the PCDS (794 ± 161 mls) than in WCDS (589 ± 138 mls,
between groups p = 0.014), and NDCS (507 ± 224 mls, between groups p = 0. 004).
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.
