Project description:Renal failure is characterized by important biological changes resulting in profound pleomorphic physiological effects termed “uremia”, whose molecular causation is not well understood. The data was used to study gene expression changes in uremia using whole genome microarray analysis of peripheral blood from subjects with end-stage renal failure (n=63) and healthy controls (n=20) to obtain insight into the molecular and biological causation of this syndrome. The study was conducted at the University of British Columbia and approved by the human ethics research board. A 3:1 case-control design was employed to compare gene expression in patients with chronic renal failure and healthy controls. Patients with stage 5 renal disease aged 18 to 75 years, who were clinically stable awaiting renal transplantation, were not receiving immunosuppressive medications, and who provided written informed consent were enrolled into the study. Patients were treated according to Canadian Guidelines for Chronic Kidney Disease (13). Normal controls of comparable age and gender to the patients who were screened to ensure freedom from known illness and medical therapy served as comparators.

2012-04-11 | E-GEOD-37171 | biostudies-arrayexpress

Genetic contribution and associated pathophysiology in end-stage renal disease.

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Inflammasome activation in end-stage heart failure-associated atrial fibrillation.

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RMND1 deficiency associated with neonatal lactic acidosis, infantile onset renal failure, deafness, and multiorgan involvement.

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Haploidentical hematopoietic cell and kidney transplantation for hematological malignancies and end-stage renal failure.

Project description: Not available