This study validates and identifies the optimal early predictive parameter available for kidney transplant recipients, with implications for refining early postoperative management and potential utility in organ allocation policy.

Abstract. We have investigated the prevalence of proteinuria in patients with Graves' disease and chronic autoimmune thyroiditis attending a routine thyroid clinic. Using the urine protein creatinine index, proteinuria was found in 29.8% of patients with autoimmune thyroid disease and in 9.5% of patients attending the same clinic but without these conditions. When patients with Graves' disease were treated with 131I, proteinuria measured by 24 h collections developed in 9 of 14 patients without pre-existing proteinuria and appeared to diminish in 4 patients in whom proteinuria had been present before treatment. The prevalence and fluctuation of proteinuria was independent of thyroglobulin and microsomal antibody levels. We were unable to confirm previous reports of a high prevalence of circulating immune complexes in autoimmune thyroid disease; complexes were detected in only 7.9% of patients and did not correlate with proteinuria. The causes of mild proteinuria in autoimmune thyroid disease are not apparent, but previous case reports suggesting that membranous glomerulonephritis is associated with Graves' disease, albeit rarely, indicate that immunological mechanisms may be implicated.

The diabetogenic agent streptozotocin (STZ) was injected intraperitoneally in Long-Evans and arginine vasopressin (AVP)-deficient Brattleboro rats. Twenty-eight days later both strains had a bradycardia and systolic hypotension; STZ-treated Brattleboro rats also had diastolic hypotension. The vasopressin (V1-receptor) antagonist, d(CH2)5[Tyr(Et)]DAVP, had no effect on resting blood pressure (BP) or heart rate (HR) in either strain of rat, indicating the relative maintenance of diastolic BP in STZ-treated Long-Evans rats was not dependent on acute vascular actions of AVP. Captopril caused a modest hypotension in all groups of rats, indicating that BP was not differentially dependent on the renin-angiotensin system in the different groups. In the presence of captopril and the ganglion blocker, pentolinium tartrate, the AVP-mediated recovery in BP was impaired in STZ-treated Long-Evans rats. During administration of d(CH2)5[Tyr(Et)]DAVP and pentolinium, the angiotensin II (ANG II)-mediated BP recovery was smaller in both groups of STZ-treated rats, indicating that this abnormality was not likely to be caused by inhibition of renin release by AVP. The abnormalities in ANG II- and AVP-mediated recovery were prevented by insulin treatment.

IA patients who choose to travel overseas for kidney transplantation have poor clinical outcomes and should be counseled accordingly.

Because plasma arginine vasopressin (AVP) levels are raised during streptozotocin (STZ)-induced diabetes mellitus (DM), it is possible that AVP contributes to the pattern of change in fluid and electrolyte handling and cardiovascular status after STZ treatment. Therefore we have made daily measurements of cardiovascular and metabolic variables in normal (Long-Evans) and AVP-deficient (Brattleboro) rats treated with saline or STZ. Twenty-four days after STZ, both strains had similar weight loss and increases in fluid intake, but the increase in food intake was greater in Long-Evans than in Brattleboro rats. After STZ, bradycardia developed in both strains, but only Brattleboro rats had reduced blood pressure. Plasma variables were measured 25 days after STZ. Packed cell volume and plasma sodium concentration were reduced in STZ-treated Long-Evans rats compared with saline-treated controls but were unchanged in STZ-treated Brattleboro rats. The results indicate that although AVP deficiency does not seriously affect the ability to maintain fluid and electrolyte balance after STZ treatment, there may be consequences for cardiovascular control.