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Carpal Tunnel Syndrome clinical trials

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NCT ID: NCT01382966 Not yet recruiting - Clinical trials for Chronic Kidney Disease

Serum Sclerostin Levels, Cardiovascular Parameters and Carpal Tunnel Syndrome in Maintenance Hemodialysis Patients

Start date: July 2011
Phase: N/A
Study type: Observational

Sclerostin, the product of the SOST gene, located on chromosome 17, locus q11.2 in humans, was originally believed to be a non-classical Bone morphogenetic protein (BMP) antagonist.Sclerostin was recently identified as a component of parathyroid hormone (PTH) signal transduction. Chronic kidney disease (CKD) is associated with abnormalities in bone and mineral metabolism.New advances in the pathogenesis of renal osteodystrophy (ROD) change the perspective from which many of its features and treatment are viewed. Calcium, phosphate, parathyroid hormone (PTH), and vitamin D have been shown to be important determinants of survival associated with kidney diseases. Now ROD dependent and independent of these factors is linked to survival more than just skeletal frailty.Furthermore, ROD is shown to be an underappreciated factor in the level of the serum phosphorus in CKD. The discovery and the elucidation of the mechanism of hyperphosphatemia as a cardiovascular risk in CKD change the view of ROD. Emerging current data suggests a promising role for serum measurements of sclerostin in addition to iPTH in the diagnosis of high bone turnover in chronic kidney disease-5D patients (dialysis patients). Because of the close relationship between ROD and cardiovascular disease, the aim of this study is to investigate the association between sclerostin, arteriovenous fistula thrombosis, echocardiography and carpal tunnel syndrome in maintenance hemodialysis patients.

NCT ID: NCT01081860 Not yet recruiting - Clinical trials for Carpal Tunnel Syndrome

Stiffness of the Skin and Joints in Relation to Carpal Tunnel Syndrome

STIF-CTS
Start date: May 2010
Phase: N/A
Study type: Observational

The exact etiology of CTS remains yet unknown. A rise in carpal tunnel pressure is well documented, but why this phenomenon occurs is yet unknown in most patients. There is an absolute or relative narrowing of the carpal tunnel, which results in a compression of the median nerve. The investigators postulate, that a stiffer flexor retinaculum (roof of carpal tunnel) will be less compliant. As a consequence of this stiffer retinaculum the pressure in the carpal tunnel will rise more quickly in stiff patients resulting in CTS-complaints. A relation between connective tissue composition and joint stiffness is proven. This relationship possibly extends to a relation between stiffness of the skin, joint stiffness and the prevalence of CTS.