Left-Sided Living Kidney Donation Leads to Transiently Reduced Adrenocortical Responsiveness.

Living kidney donation is safe and established, but can lead to long-term complications such as chronic fatigue. Since the adrenal vein is usually transected during left-sided donor nephrectomy-which is not necessary on the right-we hypothesized that venous congestion might lead to an impairment of adrenal function, offering a possible explanation. In this prospective open label, monocentric cohort study, adrenal function was compared in left- and right-sided living kidney donors. The primary endpoint was plasma cortisol response to low-dose adrenocorticotropic hormone (ACTH) stimulation. Secondary endpoints included plasma renin and ACTH concentration as well as adrenal volume in response to donor nephrectomy. A total of 30 healthy donors-20 left- and 10 right-sided donations-were included. On postoperative day 1, response to low-dose ACTH stimulation was intact, but significantly lower after left-sided donor nephrectomy. After 28 days, adrenal responsiveness to ACTH stimulation did not differ any longer. Magnetic resonance imaging volumetry showed no significant adrenal volume change over 4 weeks, neither after left- nor after right-sided nephrectomy. In conclusion, left-sided living kidney donation entails a transiently reduced adrenocortical responsiveness, which returns to baseline after 28 days.

[A 47-year-old patient with paroxysmal arterial hypertension and gastric tumors]. / 47-jährige Patientin mit paroxysmaler arterieller Hypertonie und gastralen Raumforderungen.

Arterial hypertension caused by a paraganglioma is rare and approximately one third of all cases of paraganglioma occur as part of a hereditary syndrome. Among these the Carney-Stratakis syndrome is characterized by the occurrence of paraganglioma/pheochromocytoma and gastrointestinal stromal tumors caused by germline mutations of the succinate dehydrogenase subunit genes (B-D). We report the case of a 47-year-old female patient suffering from Carney-Stratakis syndrome with an endocrine active thoracic paraganglioma which was successfully resected with the assistance of a heart-lung machine and the gastric stromal tumors were removed in a second surgical intervention.

The prevalence of familial hyperaldosteronism in apparently sporadic primary aldosteronism in Germany: a single center experience.

Primary aldosteronism (PA) is the most frequent cause of secondary arterial hypertension. To date 3 forms of familial hyperaldosteronism (FH) have been described accounting for a small percentage of all PA cases. In Germany, the prevalence of FH is currently unknown. Our aim was to determine the prevalence of familiarity in a large cohort of patients with PA. A total of 166 patients with apparently sporadic PA in Munich were investigated. FH types I, II, and III were identified using established clinical, biochemical, and molecular criteria. Among the 166 patients with PA, 2 patients (1.2%) reported a family history suggestive of FH. None of the 166 patients showed clinical, endocrine, or genetic evidence of FH type I. The 2 families had characteristic features of FH type II. Family A had 3 subjects affected out of 11 evaluated family members. Family B had 3 out of 4. Bilateral adrenal hyperplasia and unilateral adrenal adenoma were found within the same family. FH type I and FH type III are rare in Germany. With a prevalence of 1.2%, FH type II seems to be more common in apparently sporadic PA than had been assumed so far.

Cardiovascular and cerebrovascular comorbidities of hypokalemic and normokalemic primary aldosteronism: results of the German Conn's Registry.

CONTEXT: Primary aldosteronism (PA) is associated with vascular end-organ damage. OBJECTIVE: Our objective was to evaluate differences regarding comorbidities between the hypokalemic and normokalemic form of PA. DESIGN AND SETTING: This was a retrospective cross-sectional study collected from six German centers (German Conn's registry) between 1990 and 2007. PATIENTS: Of 640 registered patients with PA, 553 patients were analyzed. MAIN OUTCOME MEASURES: Comorbidities depending on hypokalemia or normokalemia were examined. RESULTS: Of the 553 patients (61 +/- 13 yr, range 13-96), 56.1% had hypokalemic PA. The systolic (164 +/- 29 vs. 155 +/- 27 mm Hg; P < 0.01) and diastolic (96 +/- 18 vs. 93 +/- 15 mm Hg; P < 0.05) blood pressures were significantly higher in hypokalemic patients than in those with the normokalemic variant. The prevalence of cardiovascular events (angina pectoris, myocardial infarction, chronic cardiac insufficiency, coronary angioplasty) was 16.3%. Atrial fibrillation occurred in 7.1% and other atrial or ventricular arrhythmia in 5.2% of the patients. Angina pectoris and chronic cardiac insufficiency were significantly more prevalent in hypokalemic PA (9.0 vs. 2.1%, P < 0.001; 5.5 vs. 2.1%, P < 0.01). Overall, cerebrovascular comorbidities were not different between hypokalemic and normokalemic patients, however, stroke tended to be more prevalent in normokalemic patients. CONCLUSIONS: Our data indicate a high prevalence of comorbidities in patients with PA. The hypokalemic variant is defined by a higher morbidity than the normokalemic variant regarding some cardiovascular but not cerebrovascular events. Thus, PA should be sought not only in hypokalemic but also in normokalemic hypertensives because high-excess morbidity occurs in both subgroups.

[Epidemiology and etiology of therapy-resistant hypertension]. / Epidemiologie und Atiologie der therapieresistenten Hypertonie.

Uncontrolled arterial hypertension is a frequent clinical problem, affecting 1/10 of hypertensive subjects, and can lead to severe renal, cerebral and cardiovascular damage. Common causes of poorly controlled blood pressure include lack of compliance, inadequate antihypertensive medication and white-coat hypertension, all referred to as "false" therapy-resistant hypertension. 4-19% of patients with arterial hypertension suffer from "true" therapy-resistant hypertension: this is defined as failure to achieve target blood pressure values despite full-dose triple drug regimen including a diuretic. In most cases, its etiology is multifactorial. Frequent causes include interfering medication, volume overload, chronic kidney disease, obstructive sleep apnea and secondary causes such as primary aldosteronism. Factors such as obesity, high salt intake and excessive alcohol ingestion contribute to poor blood pressure control. This article reviews the literature and describes epidemiology and etiology of therapy-resistant hypertension.