Major Activation Of NCC in Graft Urinary Exosomes

Evaluation of the Prevalence of an Hyperactivation of NCC Cotransporter Three Months After Kidney Transplantation in Recipients Treated by Calcineurin Inhibitors

Status

Completed

Phases

Unknown

Study type

Observational

Source

ClinicalTrials.gov

Registry ID

NCT03503461

Acronym

MANGUE

Enrollment

Registered

2018-04-19

Start date

2018-06-21

Completion date

2018-08-31

Last updated

2018-11-14

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Kidney Transplantation

Keywords

Calcineurin inhibitors, hypertension, kidney transplant, acidosis, Gordon syndrome

Brief summary

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.

Detailed description

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.

Interventions

OTHERexosomes analysis

Perform exosomes analysis in urine sample obtain from usual urine testing in both kidney transplant and control group.

Study design

Observational model

CASE_CONTROL

Time perspective

PROSPECTIVE

Eligibility

Sex/Gender

ALL

Age

18 Years to No maximum

Healthy volunteers

Yes

Inclusion criteria

For kidney transplant group : * inclusion criteria: * Age≥18years * Recipients three months after kidney transplantation using calcineurin inhibitors * Glomerular Filtration Rate\>15ml.mn.m2 CKD-EPI * Renal ultrasound underwent before inclusion * No opposition at participating at the research *

Exclusion criteria

* Use of diuretic thiazides or aldosterone receptor antagonists in the month preceding inclusion * Graft artery stenosis with indication of interventional radiology or surgery For control group : * Inclusion criteria * No previous transplantation * Age≥18years * No hypertension * No metabolic disorders (dysnatremia, dyskaliemia, acidosis or alkalosis) * No opposition at participating at the research *

Design outcomes

Primary

Measure	Time frame	Description
NCC cotransporter expression	Inclusion day	Dosage of NCC cotransporter expression in urinary exosomes samples in both groups.

Secondary

Measure	Time frame	Description
Phosphorylated NCC cotransporter expression	Inclusion day	Dosage of phosphorylated NCC cotransporter expression in urinary exosomes samples in both groups.
pendrine expression in kidney transplant group	Inclusion day	Dosage of pendrine expression in urinary exosomes samples in kidney transplant group.

Countries

France, Reunion

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026