Major Activation Of NCC in Graft Urinary Exosomes

Overview

Hypertension is common disorder after renal transplantation and is associated with mortality. Calcineurin Inhibitor (CNI), by activating NCC cotransporter, may be a major determinant of hypertension, included in a "Gordon like" syndrome. However, prevalence of NCC activation by CNI is unknown. Our objective is to determine the prevalence of NCC activation three months after transplantation in patient treated by CNI.

Hypertension is common disorder after renal transplantation and is associated with mortality. Calcineurin Inhibitor (CNI), by activating NCC cotransporter, may be a major determinant of hypertension, included in a "Gordon like" syndrome. Gordon syndrome is a rare genetic disorder where NCC cotransporter is overactivated and cause hypertension, metabolic acidosis and tendency to hyperkaliemia. Few studies evaluated NCC expression by exosomes techniques in human kidney transplant, and mostly compared NCC expression in specific subpopulation (for example with or without hypertension). Thus, prevalence of NCC activation by CNI is unknown. To determine it, we will include prospective patients in Bordeaux and la Réunion who undergo urine and blood tests three months after transplantation, and a control group with no transplantation and no use of CNI. First, we will compare kidney recipients and control and use immunoblot to quantify NCC expression in urinary exosomes to identify the population of transplanted with a high activation. Then, we will analyze the relationship between NCC activation and clinicobiological features of Gordon's syndrome.

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