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RENOTREAT

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Preventing Alport syndrome with a natural amino acid

Chronic kidney disease (CKD) is a major burden on society, causing significant morbidity and mortality. A typical symptom of CKD is the loss of protein into the urine, also termed proteinuria, which is usually associated with a po... see more

31/03/2026

UKHD

150K€

Project Budget: 150K€

Project leader

UNIVERSITATSKLINIKUM HEIDELBERG No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

PARTICIPATION DEPralty Sin fecha límite de participación.

Financing granted El organismo HORIZON EUROPE notifico la concesión del proyecto The day 2024-09-12

ERC-2024-POC: ERC PROOF OF CONCEPT GRANTS Objective:ObjectivesThe ERC Proof of Concept Grants aim at facilitating exploration of the commercia...

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Este proyecto no cuenta con búsquedas de partenariado abiertas en este momento.

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1 Participantes

UKHD

150.00K€ | Leader

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Project duration: 18 months Date Start: 2024-09-12
End date: 2026-03-31

Project leader

UNIVERSITATSKLINIKUM HEIDELBERG No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Project Budget 150K€

participation deadline Sin fecha límite de participación.

Project description Chronic kidney disease (CKD) is a major burden on society, causing significant morbidity and mortality. A typical symptom of CKD is the loss of protein into the urine, also termed proteinuria, which is usually associated with a poor prognosis. In most cases, a defective glomerulus leads to proteinuria, resulting in damage of the neighboring proximal tubular cells due to protein and lipid overload. In RENOTREAT, we aim to treat Alport syndrome with a natural amino acid, that is known to inhibit the tubular protein uptake receptors cubilin and megalin. This amino acid is already available as a safe treatment in humans, but has never been used for kidney disease. Alport syndrome is a rare disease with underestimated prevalence. It is caused by defective collagen fibers due to pathogenic genetic variants in collagen IV genes. The lack of functional collagen fibers leads to a more permeable glomerular basement membrane, resulting in proteinuria with subsequent proximal tubular damage. In our therapeutic strategy, we will induce tubular proteinuria by blocking protein uptake into the proximal tubule, overturning the paradigm that the degree of proteinuria correlates with kidney damage. First, we will test dosing regimens and bioavailability for three different formulations of the amino acid with regard to the induction of a stable tubular proteinuria in wild-type mice. Using a murine model of Alport syndrome, we will then evaluate these treatments for their potential to slow CKD progression and prolong the survival of the mutant mice. In parallel, we will conduct a pilot trial in healthy human volunteers with the already available form of the amino acid to prepare for a future clinical trial in Alport patients. In summary, we will verify the innovation potential of a novel therapeutic approach of managing Alport syndrome and potentially other proteinuric kidney diseases by performing proof-of-concept preclinical and clinical trials.

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