After organic disease had been excluded as far as possible by clinical examination, including laboratory tests, analysis of faeces, and X-ray examination or endoscopy of the upper and lower gastrointestinal tract, 61 patients were given either 50 mg trimipramine at bedtime or identically looking coded placebo in a prospective study for 4 weeks. The complaints were graded on an analogue scale by both the patients and the physicians. The results showed that the complaint scores were significantly reduced to about half in the placebo group. In the group treated with trimipramine a significantly greater reduction was found for the scores of vomiting, sleeplessness, depression, and for the mucus content of stools. The scores for tiredness during treatment had decreased less in the group receiving trimipramine than in the one receiving placebo. These improvements occurred already during the first week of treatment. No adverse side effect was recorded.

In the present study 43 patients with unilateral parenchymatous kidney disease and hypertension were investigated. 20 patients were nephrectomized, 23 treated with antihypertensive drugs. Both therapeutic approaches showed an excellent and sustained blood pressure-(BP)-lowering effect. BP fell from 185 ± 27/116 ± 13 to 138 ± 20/86 ± 10 mm Hg in the operated and from 194 ± 32/116 ± 13 to 149 ± 22/95 ± 12 mm Hg in the medically treated patients after 2 and 6 weeks, respectively (p < 0.001). BP was 142 ± 16/89 ± 11 and 136+ 16/90 ± 10 mm Hg at the long-term follow-up in the 2 subgroups. In the operated group 70% (n = 14) were cured, 20% (n = 4) were improved and 10% (n = 2) unimproved. In the medically treated group 65% (n = 15) were normotensive, 26% (n = 6) improved and 9% (n = 2) treatment resistant. No significant correlation between postoperative BP reduction and lateralization of renin secretion (PRA-ratio > 1.5) was found. Although cured patients showed a higher mean PRA-ratio, 4 patients with a PRA-ratio < 1.5 were cured (n = 2) or improved (n = 2) postoperatively. Our results document an excellent and sustained antihypertensive effect of both nephrectomy and medical treatment in patients with unilateral parenchymatous kidney disease and hypertension. They further limit the predictive value of renal venous renin determination in the preoperative workup.

The effect of unilateral adrenalectomy in primary aldosteronism was analyzed in 38 patients with unilateral adenoma, 12 cases with idiopathic bilateral hyperplasia and 1 patient suffering from an aldosterone-producing carcinoma. Responses to surgery differed markedly. In all 38 adenoma cases plasma aldosterone dropped to normal levels and remained within normal range during a mean follow-up period of 75 ± 12 months. 23 (61 %) of these patients became normotensive without medication and thus could be classified as definitely cured. 34% (13 patients) improved (normotensive under medical treatment) and only 2 cases (5 %) remained hypertensive despite sufficient medical treatment. In the hyperplasia group, however, the effect of adrenalectomy was disappointing. None of these subjects showed a long-lasting normalization of aldosterone secretion. A temporary remission for no more than 3–4 months was achieved in only 3 patients. In a fourth case with macronodular hyperplasia, primary aldosteronism relapsed after a 6-year period of normal blood pressure and aldosterone values. Therefore, 6 years after adrenalectomy no hyperplasia patient was definitely cured in contrast to 61 % of the adenoma cases. The problems in the management of hypertension in adrenal hyperplasia are furthermore documented by a poorer blood pressure control despite antihypertensive medication and a high rate of vascular complications. During the follow-up, 3 of 12 hyperplasia patients experienced a cerebrovascular event and 1 a myocardial infarction.

Trilostane, an inhibitor of the 3β-hydroxysteroid dehydrogenase enzyme sytem of steroid biosynthesis, was applied to 18 patients with primary aldosteronism (9 patients with adrenal adenoma, 9 patients with bilateral adrenal hyperplasia) for 12 weeks. A marked decrease in plasma aldosterone was observed during therapy combined with a reduction in blood pressure and a rise in serum potassium levels. Except for slight diarrhea in 4 patients, which did not require cessation of trilostane medication, no further side effects were observed. Trilostane proved to be an effective inhibitor of aldosterone biosynthesis and was found useful in the treatment of primary aldosteronism both in patients with adrenal adenoma and in those with bilateral adrenal hyperplasia.