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. Under conditions of euglycaemia, PCDS 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 PCDS.