Renal pathology in patients with primary hyperaldosteronism secondary to an adrenal cortical adenoma.

OBJECTIVES: The cause of persistent hypertension following the removal of an aldosterone-producing adrenal adenoma is unknown. The purpose of this study was to determine whether this occurrence is due to existing renal histopathologic damage. METHODS: Thirty-two patients with primary hyperaldosteronism due to an aldosterone-secreting adrenal cortical adenoma underwent open renal biopsy at the time of unilateral adrenalectomy. Biopsy results were correlated with the duration and severity of hypertension before and after surgery. RESULTS: Nineteen patients were cured of their hypertension postoperatively, whereas 13 patients had persistent diastolic hypertension. Statistical analysis of these two groups revealed no difference when renal histopathologic variables, preoperative severity of hypertension, or preoperative duration of hypertension were compared. CONCLUSIONS: Persistent hypertension in these patients does not appear to be due to renal histopathologic changes; coexisting essential hypertension is a more likely cause.

Reversal of end stage renal failure with surgical revascularization in patients with atherosclerotic renal artery occlusion.

A total of 9 patients with end stage renal failure caused by atherosclerotic renal artery occlusion underwent surgical revascularization with subsequent recovery of renal function. The duration of dialysis preoperatively ranged from 1 week to 13 months. In all cases renal viability was being maintained by collateral vascular supply. Postoperatively, renal function improved immediately and no patient required subsequent dialysis. Excellent over-all rehabilitation was achieved in all patients. Six patients currently are alive at a mean interval of 4.0 years postoperatively and with satisfactory renal function (mean serum creatinine 2.7 mg. per dl.). Three patients died at a mean interval of 6.8 years postoperatively and they all maintained satisfactory renal function (mean serum creatinine 3.0 mg. per dl.) until death. In some patients with end stage renal failure caused by atherosclerotic arterial occlusion surgical renal revascularization can yield extended survival with freedom from chronic dialysis.

The effect of estrogen on monoamine systems in the fetal rat brain.

The effect of a pharmacologic dose of estrogen on brain monoamine systems in the rat fetus was determined using a semiquantitative measure of histofluorescence. Pregnant rats received a subcutaneous injection of cottonseed oil alone or estradiol (E2) in cottonseed oil just before the monoamine systems began to develop. The fetuses were delivered abdominally and killed on day 22 of gestation. A study of four major monoamine areas of the brain with a glyoxilic acid preparation showed that intrauterine exposure to E2 has a significant effect on the monoamine organization of the fetal hypothalamus. No treatment effects were noted in the areas of locus coeruleus, substantia nigra and corpus striatum. The litter sizes of the E2-treated rats and the body weights of the fetuses were much lower than those of the control group. The effect of E2 on monoamine distribution in the fetal hypothalamus may explain the reported disturbances of reproductive function and sexual behavior seen after perinatal exposure to high doses of estrogen in humans.

Induction of severe intrauterine growth retardation in the Sprague-Dawley rat.

A noninvasive technique in an animal model that consistently produces severe intrauterine growth retardation in the Sprague-Dawley rat is described. Maternal rats were exposed continuously to a hypoxic environment (9.5% oxygen) between days 10 and 22 of gestation. This oxygen concentration was marginal for the survival of the Sprague-Dawley rat fetus. The results demonstrate decreases of 61% in litter size, 36% in fetal body weight, and 23% in fetal brain weight. The effect of hypoxia was differentiated from that of a reduced voluntary food intake by the maternal rats occurring simultaneously during the period of hypoxic exposure.