Captopril stimulation of differential renins in renovascular hypertension.

Twenty-six patients being evaluated for renovascular hypertension were studied to assess the diagnostic value of enhancing the differential between renal venous renins (PRA) by a single 25 mg oral dose of converting enzyme inhibitor (CEI, captopril). Antihypertensive medications were not discontinued prior to the study, and renal venous effluent was sampled before and 30 minutes after CEI. Eight patients without stenosis who did not have surgery had post-CEI ratios of less than 3.0. The other 18 patients had operative intervention, with 14 subsequently having improved blood pressure control. Of these 14, seven patients with unilateral stenosis, four patients with bilateral stenosis, and one patient without overt stenosis but with other evidence of reduced renal blood flow had 30-minute PRA ratios of 3.0 or greater. Five of these 14 patients had prestimulation ratios of less than 1.5 and might not be considered operative candidates by conventional criteria. Four other patients unimproved by surgery had post-CEI ratios of less than 3.0 despite a baseline ratio of greater than 1.5 in two of four. Only two patients with post-CEI ratios of less than 3.0 were improved with surgery. We conclude that a 30-minute post-CEI renal venous ratio of 3.0 or greater enhances the probability that patients with renovascular disease, and hypertension will respond to surgical intervention with improved blood pressure control.

Hepatic osteodystrophy after liver transplantation in a patient with primary biliary cirrhosis.

A patient is presented who developed hepatic osteodystrophy after orthotopic liver transplantation in association with persistently low serum 25-hydroxyvitamin D levels. After successful liver transplantation there was a delay in the return to normal of the serum 25-hydroxyvitamin D levels until oral supplementation with vitamin D was instituted. This case emphasizes the need for effective treatment of hepatic osteodystrophy with vitamin D especially in patients considered for transplantation.

Glucocorticoid effects in vitamin D intoxication.

Calcium balance studies and measurement of 25-hydroxyvitamin D3 (25[OH]D3) levels were performed on a vitamin D intoxicated, hypoparathyroid patient before, during, and after successful management of hypercalcemia with oral prednisone therapy. Prednisone effected a dramatic reduction in both mean serum calcium levels and mean 24-hour urinary calcium excretion within four days on two separate occasions. No changes were apparent in fecal calcium excretion. Calcium balance became less negative with prednisone treatment. Levels of 25(OH) D3 during the same period did not change. Decreased calcium mobilization from bone best accounted for the glucocorticoid-mediated amelioration of hypercalcemia.

Pituitary adrenal recovery following short-term suppression with corticosteroids.

To provide clinical guidelines for the use of high-dose short-term glucocorticoid therapy, we studied recovery of the hypothalamic-pituitary-adrenal axis in 10 normal men following the administration of suppressive doses of prednisone (25 mg twice daily for five days). Cortisol responses to insulin-induced hypoglycemia and synthetic ACTH before treatment were compared with responses two and five days after concluding the prednisone course when adrenal function was not influenced by the presence of exogenous steroid. Two days after prednisone therapy, peak cortisol responses to both hypoglycemia (11.0 +/- 0.9 microgram/dl mean +/- SEM) and synthetic ACTH (13.3 +/- 1.4 microgram/dl) were significantly reduced compared to pretreatment (20.6 +/- 1.6 and 27.3 +/- 2.5 microgram/dl, respectively, p less than 0.001). Five days after concluding the prednisone therapy, peak cortisol response to hypoglycemia had returned to near pretreatment levels although peak cortisol response in the adrenal gland to synthetic ACTH (22.3 +/- 1.1 microgram/dl) remained reduced (p less than 0.05). These data suggest that brief courses of high-dose prednisone therapy may limit the adrenal component of the hypothalamic-pituitary-adrenal response to stress for up to five days.