Renal Athersosclerotic reVascularization Evaluation (RAVE Study): Study protocol of a randomized trial [NCT00127738]

BACKGROUND: It is uncertain whether patients with renal vascular disease will have renal or mortality benefit from re-establishing renal blood flow with renal revascularization procedures. The RAVE study will compare renal revascularization to medical management for people with atherosclerotic renal vascular disease (ARVD) and the indication for revascularization. Patients will be assessed for the standard nephrology research outcomes of progression to doubling of creatinine, need for dialysis, and death, as well as other cardiovascular outcomes. We will also establish whether the use of a new inexpensive, simple and available ultrasound test, the renal resistance index (RRI), can identify patients with renal vascular disease who will not benefit from renal revascularization procedures[1]. METHODS/DESIGN: This single center randomized, parallel group, pilot study comparing renal revascularization with medical therapy alone will help establish an infrastructure and test the feasibility of answering this important question in clinical nephrology. The main outcome will be a composite of death, dialysis and doubling of creatinine. Knowledge from this study will be used to better understand the natural history of patients diagnosed with renal vascular disease in anticipation of a Canadian multicenter trial. Data collected from this study will also inform the Canadian Hypertension Education Program (CHEP) Clinical Practice Guidelines for the management of Renal and Renal Vascular Disease. The expectation is that this program for ARVD, will enable community based programs to implement a comprehensive guidelines based diagnostic and treatment program, help create an evidence based approach for the management of patients with this condition, and possibly reduce or halt the progression of kidney disease in these patients. DISCUSSION: Results from this study will determine the feasibility of a multicentered study for the management of renovascular disease

Procedimento e sistema er assemblare una forma di dosaggio orale e forma di dosaggio orale

La presente invenzione si riferisce alla produzione di medicamenti orali, ed in particolare di medicamenti costituiti da più principi attivi combinati in una singola forma di dosaggio, le cosiddette polypil

A ROLE FOR LH IN ALDOSTERONE SECRETION: PRELIMINARY RESULTS OF AN IN VITRO STUDY ON CONN ADENOMAS AND NORMAL ADRENALS

Objective: Recent studies identified overexpression of G-protein coupled receptors in adrenal adenomas, among which luteinizing hormone receptor (LHR). Clinically, its is known that plasma aldosterone levels may increase under LH stimulation, at least in females (Fommei, 2009). Aim of the study was to confirm LHR presence in aldosterone producing adenomas and assess the direct LH effect on aldosterone production in vitro, in a comparison with normal adrenals. Design and Method: After informed consent, adrenal fragments were collected from 16 hypertensive patients (7F/9M, mean age 66 years) during laparoscopic unilateral adrenalectomy for clinically confirmed primary aldosteronism due to unilateral adenoma and from normal adrenal glands of 6 cadaveric kidney normotensive donors (3F/3M, mean age 59 years). LHR was assayed by Western blotting analysis. Adrenal cell cultures from 12 hypertensive patients were also obtained and cortisol levels in supernatant measured as a marker of cell viability.Cells were then splitted and investigated both in the absence or presence of LH (300 ng/ml) in serum free-DMEM/F12 medium for 6 h. The supernatant was then assayed for aldosterone levels (Aldoctk-2RIA, Diasorin, Italy). Results: Western blotting analysis demonstrated LHR proteins as single bands at 85 kDa in all the explored adrenal tissues; however, LHR were more expressed in hypertensive patients than in normotensive kidney donors (1.71 ± 0.57 vs. 0.72 ± 0.21 mean ± SD of LHR/beta-actin; p < 0.001). LH stimulation of adrenal cells significantly increased aldosterone levels compared to unstimulated cultures in 5/12 patients, by a mean of 1.5 folds (p < 0.05). Conclusion: The results confirm LHR presence in human adrenal cortex and demonstrate an increased expression in Conn adenomas compared to normal adrenals. They also suggest the presence of LH dependent mechanism(s) on aldosterone secretion at least in subsets of human hyperaldosteronism