Molecular Prediction of Development, Progression or Complications of Kidney, Immune or Transplantation-related Diseases (NEPHROGENE2)

Managing patients with renal failure requires an understanding of the molecular mechanisms that lead to its occurrence (i.e. upstream of the disease), its worsening and its persistence (i.e. downstream), while also specifying the risk of worsening renal failure (risk stratification, intolerance to the treatment or complications (infectious, metabolic, cardiovascular, cancer…). Nephrogene 2.0 aims to study these different components of kidney, immune and solid organ transplantation (SOT)-related diseases.

Study Overview

• Status: Recruiting
• Conditions: Cancer; Chronic Kidney Diseases; Acute Kidney Injury; Metabolic Disease; Solid-organ Transplantation; Immune Diseases
• Intervention / Treatment: Biological: Biological samples collection

Detailed Description

Acute renal failure (ARF) and chronic kidney disease (CKD) are frequent pathologies (850 million people are affected worldwide). Renal failure is associated with an increased morbidity and mortality, including an increased risk of infections, drug toxicity and cardiovascular death. The causes of renal failure are numerous: metabolic (diabetes, hypertension), immunological (autoimmune diseases, monoclonal gammopathies), toxic (environment, drugs), genetic, infectious, ischemic, paraneoplastic... Any episode of ARF is also accompanied by a risk of secondary CKD (relative risk multiplied by 9).

The mechanisms leading to renal failure are multiple and combine predisposing genetic factors, inadequate intra-renal or systemic immune response, endothelial and epithelial dysfunctions, and potentially inappropriate regenerative capacity. In addition, renal failure or its treatment itself may be accompanied by additional renal lesions (e.g. nephrotoxicity of calcineurin inhibitors used as anti-rejection treatment in transplantation, hemodynamic intolerance with secondary ARF during hemodialysis sessions, iatrogenic ARF when using diuretics or inhibitors of the renin angiotensin system) or extra-renal complications (e.g. immunosuppression and infections induced by immunomodulatory therapies during autoimmune diseases or for prevention of transplant rejection; vascular diseases secondary to phosphocalcic disorders).

Patients included in the NEPHROGENE 2.0 cohort will be followed during 10 years and clinical data and biological samples will be collected at the inclusion in the cohort, at each monitoring programmed in their usual care and and at each event (infection, acute kidney injury, cancer…). Samples will be collected according to the symptoms of the patients.

• Study Type: Observational
• Enrollment (Estimated): 5000

Contacts and Locations

• Study Contact: Name: Stanislas Faguer, MD, PhD; Phone Number: 0033 561322475; Email: faguer.s@chu-toulouse.fr

Study Locations

• France
  • Toulouse, France, 31059
    • Recruiting
    • Rangueil University Hospital
    • Contact: Stanislas Faguer, MD, PhD; Phone Number: 0033 561322475; Email: faguer.s@chu-toulouse.fr

Participation Criteria

Eligibility Criteria

• Ages Eligible for Study: 18 years to 99 years (Adult, Older Adult)
• Accepts Healthy Volunteers: No

• Sampling Method: Non-Probability Sample

Study Population

Patients who develop or have progression of kidney, immune or transplantation-related diseases, as well as specific complications of these conditions

Description

Inclusion Criteria:

• Patients (> 18 year of age) with kidney disease or at risk to develop a kidney disease,
• Patients followed by a practitioner of the Department of Nephrology and Organ Transplantations of the University Hospital of Toulouse (France)

Exclusion Criteria:

• consent deny
• inability of the patient or its family to give consent.

Study Plan

How is the study designed?

Design Details

• Observational Models: Cohort
• Time Perspectives: Prospective

What is the study measuring?

Primary Outcome Measures

Outcome Measure	Measure Description	Time Frame
Identification of the molecular mechanisms underlying kidney, immune and solid organ transplantation-related diseases.	To identify the molecular mechanisms underlying kidney, immune and solid organ transplantation-related diseases. An unbiased multi-omic approach (including peptidomics, metabolomics, genome sequencing, and flow cytometry and transcriptomic of circulating immune cells) will be performed at the inclusion in the study and correlated to specific end-points (acute kidney injury, kidney failure progression, end-stage kidney disease, infection, cancer according to the underlying condition). Multiple measurements will be studied individually to identify genes variations, gene expression changes, urinary or plasma peptides abundance, immune cells relative abundance in the blood that correlate with the end-point. In a second step, an attempt to combine them in a single predictive signature using artificial intelligence approach.	yearly and up to 10 years after inclusion in the study

Secondary Outcome Measures

Outcome Measure	Measure Description	Time Frame
Identification of the predictive factors (immunological, metabolic, genetic…) for the development or progression of renal diseases	To identify the predictive factors (immunological, metabolic, genetic…) for the development or progression of renal diseases: end-points will be end-stage kidney disease, or a decrease of the estimated glomerular filtration rate (eGFR) > 50%	up to 10 years after inclusion in the study
Identification of the molecular mechanisms (immunological, genetic…) driving complications of kidney, immune and SOT-related diseases	To identify the molecular mechanisms (immunological, genetic…) driving complications of kidney, immune and SOT-related diseases: end-points will the development of bacterial, viral (CytoMégaloVirus, Herpes simplex virus, varicella-zoster virus, BK virus…) or fungal (candidiasis, aspergillosis…) infections, as well as cardiovascular events or other complications	up to 10 years after inclusion in the study
To specify the individual risk of complications secondary to SOT or its treatment	To specify the individual risk of renal and immunological complications secondary to cancer or hematological malignancies, or their treatments: end points will be the development of acute kidney injury, end-stage kidney disease or >50% reduction of the eGFR	up to 10 years after inclusion in the study

Collaborators and Investigators

• Sponsor: University Hospital, Toulouse
• Investigators: Principal Investigator: Stanislas Faguer, MD, PhD, University Hospital, Toulouse

Study record dates

Study Major Dates

• Study Start (Actual): September 5, 2022
• Primary Completion (Estimated): September 1, 2027
• Study Completion (Estimated): September 1, 2032

Study Registration Dates

• First Submitted: March 22, 2022
• First Submitted That Met QC Criteria: March 31, 2022
• First Posted (Actual): April 8, 2022

Study Record Updates

• Last Update Posted (Actual): March 19, 2026
• Last Update Submitted That Met QC Criteria: March 16, 2026
• Last Verified: March 1, 2026

More Information

Terms related to this study

• Keywords: cancer; Chronic kidney disease; Acute kidney injury; risk stratification; solid-organ transplantation
• Additional Relevant MeSH Terms: Urogenital Diseases; Pathologic Processes; Male Urogenital Diseases; Kidney Diseases; Urologic Diseases; Female Urogenital Diseases; Female Urogenital Diseases and Pregnancy Complications; Chronic Disease; Disease Attributes; Renal Insufficiency; Pathological Conditions, Signs and Symptoms; Nutritional and Metabolic Diseases; Neoplasms; Acute Kidney Injury; Renal Insufficiency, Chronic; Metabolic Diseases; Immune System Diseases
• Other Study ID Numbers: RC31/21/0154

Plan for Individual participant data (IPD)

• Plan to Share Individual Participant Data (IPD)?: NO

Drug and device information, study documents

• Studies a U.S. FDA-regulated drug product: No
• Studies a U.S. FDA-regulated device product: No