More Biomarkers Improve Detection

New diagnostic approach combining skin and blood tests could overhaul Parkinson disease care.

Image Caption: When interpreted together, three biomarkers—4-repeat tau (4R-tau), neurofilament light chain (NfL), and α-synuclein—can help distinguish between Parkinson disease (PD) and related conditions. α-synuclein is commonly found in PD and multiple system atrophy (MSA), while 4R-tau is strongly associated with progressive supranuclear palsy (PSP). Higher levels of NfL in the blood reflect greater nerve cell damage and can help distinguish more aggressive conditions like MSA from PD. Together, these markers provide a more accurate picture than any single test alone.

With the emergence of new disease-modifying therapies that target the specific proteins responsible for neurodegenerative diseases like Alzheimer disease and Parkinson disease (PD), the timing and accuracy of diagnosis are increasingly important. Published in Nature Medicine, a new study led by Drs. Anthony Lang and Ivan Martinez-Valbuena at UHN’s Krembil Brain Institute (KBI), introduces a diagnostic approach that combines multiple biomarkers—biological molecules, often proteins, that can signal disease—to better distinguish between PD and similar neurodegenerative conditions called parkisonian syndromes. This approach could support earlier and more accurate diagnosis, and better care for patients as a result.

The challenge in getting it right 

Current diagnostic methods often misclassify other parkinsonian syndromes, including progressive supranuclear palsy (PSP) and multiple system atrophy (MSA), as PD because of overlapping symptoms. This challenge is especially pronounced in early disease stages, when distinguishing clinical features are not yet present. 

However, despite their similarities, these conditions are driven by different underlying proteins—and identifying which is key to improving diagnosis.

“Misdiagnosis means patients miss the opportunity to use disease-modifying therapies during the critical window in early disease stages when these treatments may have the greatest impact,” says Dr. Martinez-Valbuena, the first author of this study.

A new approach: combining multiple biomarkers

To address this issue, the KBI team developed a diagnostic protocol that integrates three biomarkers associated with parkinsonian syndromes: 4-repeat tau (4R-tau), neurofilament light chain (NfL), and α-synuclein. Each biomarker provides distinct information. α-synuclein identifies the abnormal protein build up seen in diseases like PD and MSA. 4R-tau signals the abnormal protein build up seen in PSP. NfL reflects the extent of damage to nerve cells. The new protocol uses a blood sample to measure NfL, and a single skin biopsy is to perform tests called seeding amplification assays (SAAs) to identify 4R-tau and α-synuclein. Although evaluation of α-synuclein is currently marketed diagnosis of PD, these diagnostic methods do not use SAAs.

The researchers first tested their approach in a sample of 166 participants—40 with PD, 77 with PSP, 29 with MSA, and 20 healthy controls. They then validated their findings in an independent cohort of 63 participants—35 with PD, 17 with PSP, nine with MSA, and two healthy controls. Participants in both groups varied in age and duration since disease onset.

Individually, each biomarker test showed high sensitivity and specificity. Skin tests detected α-synuclein in approximately 85% and 90% of people with PD and MSA, respectively, and 4R-tau in about 88% of people with PSP. Blood levels of NfL were lowest in healthy individuals and highest in people with MSA. The multimodal approach significantly outperformed the diagnostic accuracy—herein defined as the ability to correctly distinguish between MSA, PSP, and PD—of any single biomarker test on its own; receiving a performance score (AUC) of 0.96 for PD, 0.90 for MSA and 0.97 for PSP. AUC describes how well a model, the diagnostic protocol in this case, matches the data it is trying to explain. A perfect model has an AUC of 1.

Importantly, α-synuclein was found in about 23% of patients with PSP. This indicated that diagnostic testing that is limited to this protein, as some companies currently offer, is insufficient as it could misdiagnose PSP as PD.

Notably, the researchers also found that, in addition to better differentiating between PSP and other parkinsonian syndromes, combining biomarkers also enabled doctors to separate patients according to PSP severity. 

To further validate the method, the KBI team compared the results from their diagnostic protocol with findings from brain tissue analysis in a subset of 11 participants. The diagnosis made using the integrated protocol consistently matched brain tissue findings, providing strong real-world validation of the approach. Importantly, in 1 case clinically diagnosed as having PSP—where the individual’s skin SAA tested negative both 4R tau and α-synuclein—brain tissue analysis later revealed a diagnosis of Alzheimer disease. This alternative diagnosis validated the negative skin SAA results. 

A promising (and less invasive) path forward

While researchers emphasize that further testing is required—particularly in patients in earlier disease stages—the findings represent a promising advancement in the diagnosis of parkinsonian syndromes.

“Combining assessment of 4R-tau, NfL, and α-synuclein was a logical step,” says Dr. Lang, the study’s senior author. “These biomarkers complement each other—where one shows limitations, the others provide additional diagnostic value.”

“We are encouraged by the potential of this protocol to address gaps in the clinical evaluation of complex or unclear parkinsonian syndromes,” adds Dr. Martinez-Valbuena.

In addition to performance, the KBI team’s new diagnostic approach is also advantageous because it is less invasive than other approaches. The integrated approach uses a blood sample and one skin biopsy. This contrasts currently marketed testing for α-synuclein, which requires a cerebrospinal fluid sample obtained through a lumbar puncture or multiple skin biopsies. By simplifying sample collection and reducing reliance on specialized equipment and procedures, the integrated diagnostic protocol may make diagnostic testing more widely accessible.

For patients with PD, MSA, and PSP, earlier and more precise diagnosis could enable better disease management and, eventually, an improved quality of life. As new therapies continue to emerge, tools like this may help ensure patients receive the right care at the right time.

The first author of this study, Dr. Ivan Martinez-Valbuena, is a Scientific Associate at UHN’s Krembil Brain Institute.

The senior author of this study, Dr. Anthony E. Lang, is a Senior Scientist at UHN’s Krembil Brain Institute and a Professor at the University of Toronto's Temerty Faculty of Medicine and Institute of Medical Science. He is also the Lily Safra Chair in Movement Disorders, the Director of the Edmond J. Safra Program in Parkinson's Disease, Director of the Rossy PSP Centre, and the Jack Clark Chair for Parkinson’s Disease Research.

This work was supported by the Rossy Family Foundation, the Edmond J. Safra Philanthropic Foundation, the Maybank Foundation, the Blidner Family Foundation, Ajay Virmani, Jen Cerny, the Michael J. Fox Foundation for Parkinson’s Research., the Rainwater Charitable Foundation, the Bay Tree Foundation/Mohammad Al Zaibak Fellowships in Parkinson’s Disease, The Paul and Susan Hansen Foundation, the University Medical Center Goettingen-UMG Clinician Scientist Program, the Mohammad and Najla Al Zaibak Family Parkinson’s Disease Research Fund, the Fonds de Recherche du Québec Santé, and UHN Foundation.

Drs. Martinez-Valbuena, Kovacs, and Lang share a pending patent for movement disorders diagnostic assays, and Dr. Kovacs has a patent for the 5G4 synuclein antibody. 

Dr. Martinez-Valbuena received consulting fees from Ferrer and research funding from the Michael J. Fox Foundation for Parkinson’s Research outside of this work. 

Dr. Lang served as an advisor for AbbVie, Amylyx, Aprinoia, Biogen, BioAdvance, Biohaven, BioVie, BlueRock Therapeutics, Bristol Myers Squibb, Denali, EG427, Ferrer, Janssen, Lilly, Northera, Pharma 2B, Sun Pharma, UCB and Ventyx Bio. He also received honoraria from Sun Pharma and AbbVie and grants from Brain Canada, the Canadian Institutes of Health Research, the Michael J. Fox Foundation for Parkinson’s Research, the Parkinson Foundation, Parkinson Canada, and the Weston Foundation. Dr. Lang also serves as an expert witness in litigation related to paraquat and PD, and has received publishing royalties from Elsevier, Saunders, Wiley-Blackwell, Johns Hopkins Press, and Cambridge University Press.

For a full list of competing interests, see the publication.

Martinez-Valbuena I, Emamikhah M, Olszewska DA, Weber SK, Schnell S, Fereshtehnejad SM, Reyes NGD, Sousa M, Di Luca DG, Ta J, Anastassiadis C, Li J, Sasitharan J, Bhakta P, Visanji NP, Fox SH, Mollenhauer B, Tartaglia MC, Kovacs GG, Lang AE. Dermal α-Synuclein and 4R-Tau SAAs Combined with Serum NfL: Enhancing Diagnostic Precision in Neurodegenerative Parkinsonism. Nat Med. 2026 May 19. doi: 10.1038/s41591-026-04398-3

Decoding Pancreatic Differentiation

Study identifies molecular cues to improve development of pancreatic cells in the lab.

Image Caption: Scientists are investigating ways to better refine how to develop specific pancreatic cell types in the lab. In doing so, this work contributes to ongoing efforts towards creating cell-based therapies for diabetes.

In a recent study from UHN’s McEwen Stem Cell Institute (McEwen), Senior Scientist Dr. M. Cristina Nostro and her team identified key factors that drive the development of various pancreatic cell types, like insulin-producing beta cells. This work aims to improve how stem cells can be used to develop a cellular therapy for type 1 diabetes.

During fetal development, pancreatic progenitors (PPs) are precursor cells that give rise to multiple pancreatic cell types, including exocrine and endocrine cells. Exocrine cells produce digestive enzymes, and endocrine (islet) cells, like beta cells, produce the hormones important for controlling blood sugar levels. The endocrine or exocrine fate of PPs is regulated by a complex set of biological signals, including the duration and timing of exposure to these biological signals.

Reproducing the developmental conditions that results in endocrine cells, including beta cells, in the lab is essential to the study of diabetes and the generation of new, cell-based therapies that could be used to replace a patient’s lost and nonfunctional beta cells. To achieve this, scientists use a technique called in vitro differentiation, in which they expose human pluripotent stem cells—cells that can become any cell type in the body—to key biological factors to guide their development into pancreatic islet cells.

However, knowledge of how PPs develop into specific lineages, such as islet cells, is still limited. As a result, differentiation toward pancreatic beta cells remains difficult to control and frequently produces other cell types, such as intestinal enterochromaffin cells (ECs), as unintended and unwanted byproducts.

To address this challenge, Dr. Nostro’s team modulated key signals used during differentiation towards pancreatic beta-like cells and analyzed the characteristics of the resulting cells over time. They also collaborated with Dr. Gabriela Pavlínková from the Czech Academy of Sciences to compare the process of fetal pancreatic cell development in a lab model to the process of in vitro pancreatic cell differentiation.

Researchers found that distinct populations of PPs preferentially develop into beta cells or EC cells. They identified several key regulatory proteins—including NKX6-1 and Neurogenin 3 (NGN3)—that influenced the fate of the progenitors. 

Importantly, the McEwen showed that these PP populations respond differently to various developmental cues. By carefully adjusting these conditions in their differentiation protocol, the researchers were able to control which pancreatic cell type developed.

These findings may help refine stem cell differentiation protocols produce more consistent and defined cell populations. As cell-based therapies for type 1 diabetes advance to clinical trials, achieving precise control over differentiation outputs will be critical. “This work brings us closer to generating highly purified islet cell populations,” says Dr. Paraish Misra, first author of this study. “Purer populations can make this therapy safer and more effective for patients and streamline their production as they reduce the need to remove any non-beta cells from the cell population before transplantation into patients.” Overall, this work provides important insights that may support the development of more consistent and scalable cell-based therapies for diabetes.

The first author of this study is Dr. Paraish Misra, a former Postdoctoral Researcher in the Nostro Lab and currently an Assistant Professor and researcher at McGill University.

The senior author of this study is Dr. M. Cristina Nostro, a Senior Scientist at UHN’s McEwen Stem Cell Institute and Associate Professor in the Department of Physiology at the University of Toronto.

This work was supported by the Canadian Institutes of Health Research, the Howard Webster Foundation, the Kidney Foundation of Canada, the Canadian Society of Transplantation, the Temerty Faculty of Medicine at the University of Toronto, the Banting and Best Diabetes Centre, the Natural Sciences and Engineering Research Council of Canada, Breakthrough T1D International (formerly JDRF), The Leona M. and Harry B Helmsley Charitable Trust, Eli Lilly Canada, the Canadian Islet Research Training Network, the Canadian Clinical Trial Network, the Czech Science Foundation, the Grant Agency of Charles University, the Czech Academy of Sciences, and UHN Foundation. 

Drs. Misra, McGaugh, and Nostro are co-inventors on two patent applications related to this work.

Misra PS, McGaugh EC, Huang H, Cho A, Lin J, Sarangi F, Oakie A, Sambathkumar R, Song Y, Fabríciová V, Bohuslavová R, Pavlínková G, Nostro MC. Efficient control of enterochromaffin versus islet differentiation from human pluripotent stem cell-derived pancreatic progenitors. Nat Commun. 2026 Mar 18;17(1):4137. doi: 10.1038/s41467-026-70666-y. PMID: 41851084; PMCID: PMC13149693. 

Advancing Care with Digital Lungs

Scientists at UHN develop digital twins of human lungs using Ex Vivo Lung Perfusion data.

Image Caption: Scientists are building “digital twins” of organs through the use of real-world data and AI, creating virtual lungs that accurately reflect the complexity of how a real human lung works. (Image: Ariadna Villalbi)

The concept of a “digital twin”—a virtual representation of physical objects, such as an organ—is emerging as a way to accelerate medical research and improve patient care. Researchers from UHN’s Toronto Lung Transplant Program within the Ajmera Transplant Centre have developed a digital twin of a human lung using data from Ex Vivo Lung Perfusion (EVLP).

In the medical field, digital twins are comprehensive computer models that integrate molecular, physiological, functional, and clinical data to create virtual representations of biological systems. However, due to the lack of large datasets that combine these different types of data, creating a digital twin for health research has been difficult to achieve.  

EVLP is a biomedical technique in which a donated lung is preserved at normal body temperature, enabling the lung to breathe on its own outside of the body. Invented at UHN, EVLP enables clinicians to safely assess donor lungs before transplant. The lung function data generated during EVLP—spanning imaging, physiological monitoring, and molecular assays—serves as a foundation for the development of a digital twin for the human lung, or a “digital lung”.

The research team, led by Drs. Andrew Sage, Assistant Scientist, and Shaf Keshavjee, Chief of Innovation, Senior Scientist, and Donald K. Jackson Chair in Lung Transplant Research at UHN, analyzed the largest known EVLP dataset and developed a method to generate a digital lung. Their model accurately simulated over 75 parameters of lung biology and health, including physiology, biochemical and gene-expression markers.

To determine how effective the digital lung model could be in assessing therapeutic treatment results, the team compared real-world results from EVLP lungs treated with alteplase, a drug that dissolves blood clots, to predictions from the digital twin. Results showed that the digital lungs were better at assessing therapy in human lungs.

These findings show that virtual lungs can accurately simulate lung function and predict treatment outcomes. Digital twins could become a powerful tool for evaluating therapies, improving drug development, and ultimately improving patient care.

Xuanzi Zhou is a Doctoral Candidate at the University of Toronto and UHN and the first author of the study.

Dr. Andrew Sage, an Assistant Scientist at UHN and Assistant Professor in the Department of Surgery at the University of Toronto, is the co-senior author of the study.

Dr. Shaf Keshavjee is a Senior Scientist and Chief of Innovation at UHN. He is also a Professor of Thoracic Surgery and Biomedical Engineering and Vice Chair for Innovation in the Department of Surgery at the University of Toronto. He is the co-senior author of the study.

This work was supported by the Canadian Institutes of Health Research (CIHR), the J.P. Bickell Foundation, and UHN Foundation.

Dr. Shaf Keshavjee serves as Chief Medical Officer of Traferox Technologies and receives personal fees from Lung Bioengineering, outside the submitted work. Xuanzi Zhou, Andrew, Sage, Shaf Keshavjee, and other authors declare ongoing patent applications with the University Health Network related to ex vivo digital twin machine learning models used in this study.

Zhou X, Wang B, Wei Y, Hacker S, Kim S, Borrillo T, McCaig A, Ahmed H, Ren Y, Hough O, Orsini L, Chao BT, McInnis M, Cypel M, Liu M, Yeung JC, Del Sorbo L, Keshavjee S, Sage AT. Digital twins of ex vivo human lungs enable accurate and personalized evaluation of therapeutic efficacy. Nat Biotechnol. 2026 May 4. doi:10.1038/s41587-026-03121-4.

New Centre for Clinical Research

UHN’s Toronto Western Hospital opens a new facility, expanding access to clinical research.

Image Caption: (Pictured L-R) Dr. Sheila Riazi, Dr. Amit Oza, Dr. Susan Fox, Marnie Escaf, Dr. Carmela Tartaglia, Dr. Antonio Strafella, Briar Coman, and Anam Islam.

The Toronto Western Hospital Centre for Clinical Research project team pictured in the main treatment room alongside images of the new Centre facilities.

Decoding a Rare Genetic Heart Threat

Study reveals how mutations can trigger arrhythmias and cardiac arrest in a rare condition.

Image Caption: In short QT syndrome, the electrical recovery of the heart muscle after each heart beat is accelerated and creates a risk of sudden arrhythmia.

Short QT syndrome (SQTS) is a rare, inherited condition that can cause sudden cardiac death. A new study from UHN, the University of Toronto, and collaborators in Germany provides insight into the molecular mechanisms behind SQTS using patient-derived lab models.

In SQTS, problems with the heart’s electrical system increase the risk of heart rhythm problems, called arrhythmias, which can lead to sudden death. Despite improved awareness and diagnosis of SQTS over the years, scientists still do not entirely understand the underlying molecular causes or how to optimally treatment the condition.

Several genes have been implicated in this condition, including SLC4A3 (Solute Carrier Family 4 Member 3)—involved in mediating the exchange of ions (charged atoms) across cell membranes and, ultimately, the pH inside cells. However, analyses of mutations in SLC4A3 have yet to explain how altered pH leads to arrhythmias and cardiac death.

To address this knowledge gap, the team examined two new SLC4A3 mutations by generating lab-grown models of cardiomyocytes—heart muscle cells—from patient samples. They found that in models with mutated SLC4A3, the disruption of ion movement across the cell membrane caused the cells to have a higher pH or be more alkaline. The increased pH resulted in a fewer calcium ions moving into the cells, which led to the shortening of the heart’s electrical recovery after each heart beat and irregular, arrhythmia-like beating.

This study reveals, for the first time, the mechanisms underlying SQTS related to pH imbalance and how SLC4A3 gene mutations lead to heart problems. These findings open the door to potential new, targeted drug treatments.

Dr. Michael Gollob is a Senior Scientist at UHN and a Professor in the Department of Physiology in the Temerty Faculty of Medicine at the University of Toronto. He is the co-senior author of this study.

Dr. Ibrahim Akin, from the University Medical Centre Mannheim (UMM), University of Heidelberg, and Dr. Ibrahim El-Battrawy, from Ruhr University Bochum, are also co-senior authors of the study.

The first authors of the study are:

● Zenghui Meng – University Medical Centre Mannheim (UMM), University of Heidelberg

● Chen Yan – University Medical Centre Mannheim (UMM), University of Heidelberg

● Christina Holscher – University Medical Centre Mannheim (UMM), University of Heidelberg

● Boldizsar Kovacs – Inselspital University Hospital of Bern

● Saltanat Zhazykbayeva – Ruhr University Bochum

● Oliver Jarkas – Ruhr University Bochum

This work was supported by the Ian Copland Arrhythmia and Sudden Death Research Fund at the University of Toronto, the German Center for Cardiovascular Research, the Hector- Stiftung, Else-Kröner-Fresenius Foundation, German Heart Foundation, EU Horizon 2020 research and innovation program, and UHN Foundation.

See the manuscript for competing interests.

Meng Z, Kovacs B, Yan C, Hölscher C, Zhazykbayeva S, Jarkas O, Zou C, Cyganek L, Zorio E, Braza-Boils A, Pablo Ochoa J, Rehbehn N, Fan X, Lei X, Liu R, Tong S, Liu F, Xue Z, Bober SL, Zhao B, Duru F, Aweimer A, Köppel A, Burau K, Mügge A, Berger W, Hamdani N, Zhou X, Saguner AM, Akin I, Gollob MH, El-Battrawy I. SLC4A3-related short QT syndrome assessed in human induced pluripotent stem cell-derived cardiomyocytes: mechanisms of ventricular arrhythmia and sudden cardiac death. Eur Heart J. 2026 Mar 5:ehag068. doi: 10.1093/eurheartj/ehag068. Epub ahead of print.

Canadian Honour for Chem Innovator

UHN researcher awarded SCI’s Canada Medal for lifetime contributions to biotech and pharma.

Image Caption: Dr. Donald Weaver is a Senior Scientist at UHN’s Krembil Brain Institute, a Professor of Neurology at the University of Toronto’s Temerty Faculty of Medicine, and a Professor (Status Only) in the Department of Chemistry at the University of Toronto.

The Society of Chemical Industry (SCI) has awarded its Canada Medal to Dr. Donald Weaver, Senior Scientist at UHN’s Krembil Brain Institute, recognizing his productive career translating chemistry into real-world health solutions. 

The SCI Canada Medal recognizes a scientific business leader whose lifetime contributions have advanced a Canadian industry rooted in chemistry, including fields such as biotechnology and pharmaceuticals, two areas in which Dr. Weaver has had lasting global impact. 

Dr. Weaver is internationally recognized for his research focused on understanding and treating Alzheimer disease (AD). His commitment to medicinal chemistry is rooted in his clinical experience—he is among a small handful of people worldwide with credentials as a medicinal chemist and neurologist. His first encounter with a patient with AD in 1981 sparked a lifelong determination to design drugs capable of altering the course of the condition. Dr. Weaver’s more than 40-year career, grounded in both chemistry and neuroscience, has bridged molecular science, drug development, and patient care.  

“Papers are nice. Products are nicer. Canadian products are nicest of all,” says Dr. Weaver. This motto reflects his philosophy that research should not stop at publications but move decisively toward solutions that benefit patients. 

Throughout his illustrious career, Dr. Weaver has sat at the helm of several innovative organizations. In 1994, Dr. Weaver co‑founded Neurochem Inc., which later became Bellus Health, in Montreal. Here he invented two amyloid-targeting drugs that both eventually went to phase 3 clinical trials: tramiprosate—one of the first drugs ever tested with the intent to modify the disease course of AD—and eprodisate. In 2023, GlaxoSmithKline (GSK) acquired Bellus Health for approximately $2 billion.  

In Halifax in 2006, Dr. Weaver co‑founded DeNovaMed Inc. to develop novel antibiotics. He continues to serve as their Chief Medical Officer.  

Most recently, Dr. Weaver co‑founded Treventis Corporation in Toronto, a spin‑out from his UHN laboratory, where he also serves as Chief Medical Officer. In 2023, Treventis entered a major collaboration and licensing agreement with Takeda to advance small‑molecule therapies targeting toxic tau protein in AD.  

Beyond commercial work, Dr. Weaver has authored more than 400 peer‑reviewed publications, including Medicinal Chemistry (Oxford University Press), a widely used reference in the field. He holds 47 patents, all focused on therapeutic applications. He has received numerous honours for his work, including the Bernard Belleau Award in Medicinal Chemistry, the Merck Frosst Award in Organic Chemistry, and the Oskar Fischer Prize. The SCI Canada Medal adds a distinct recognition celebrating the translation of fundamental science to industry. 

“I am genuinely thrilled to receive the SCI Canada Medal,” says Dr. Weaver. “I have spent my career working at the interface between chemistry and clinical neurology, which is not a typical place to stand; you are never quite sure whether your feet are planted in chemistry or medicine. Recognitions are usually discipline specific, so it is especially meaningful to receive this award from a chemistry society that values translation and real-world outcomes.” 

New Drug for Kidney Health

Trial finds finerenone improves kidney health in adults with diabetes & kidney disease.

Results of an international clinical trial, where UHN was a Canadian site, showed that the drug finerenone may help improve kidney health in adults with type 1 diabetes and chronic kidney disease (CKD).  

Type 1 diabetes affects approximately 9.5 million people worldwide. CKD—the long-term and progressive loss of function in the kidneys—remains a common and serious complication of type 1 diabetes. Some drugs, like finerenone—which blocks the activity of certain hormones that can damage the heart and kidneys—have been shown to help people with CKD caused by type 2 diabetes. But until now, these medications haven’t been used in clinical trials in people with type 1 diabetes and kidney disease.

To address this, a team of international researchers ran a clinical trial to test finerenone on 242 adults with type 1 diabetes and CKD. Dr. David Cherney, Senior Scientist at UHN and Professor at the University of Toronto’s Temerty Faculty of Medicine, was the lead investigator at the UHN site in Toronto.

Published in The New England Journal of Medicine, results showed that participants receiving finerenone had a significantly greater decrease in the urinary albumin-to-creatinine ratio than those who received the placebo, suggesting kidney protection with finerenone. Healthy kidneys prevent albumin—a type of protein in the blood—from being excreted in the urine, resulting in a lower ratio. Therefore, a reduction in urinary albumin levels is consistent with a lower risk of developing worsening kidney disease.

These findings highlight the potential of finerenone as an additional therapeutic option for adults with type 1 diabetes and CKD. More research will be needed to understand long-term effects on diverse populations.

This study was led by the FINE-ONE Investigators, including the following authors:

• Hiddo Heerspink, Andreas Birkenfeld, David Cherney, Helen Colhoun, Per-Henrik Groop, Linong Ji, Niels Jongs, Chantal Mathieu, Richard Pratley, Sylvia Rosas, Peter Rossing, Jay S Skyler, Katherine Tuttle, Robert Lawatscheck, Meike Brinker, Markus Scheerer, Julie Russell, Patrick Schloemer, and Janet B McGill

Dr. David Cherney is a Senior Scientist at UHN and Professor in the Department of Medicine at the University of Toronto. He is also the Gabor Zellerman Chair of Nephrology Research at the University of Toronto. He was a member of the international steering committee for the trial and the lead investigator for the UHN site of the trial.

This study was supported by Bayer.        

Research at UHN is supported by UHN Foundation, and Dr. Cherney was supported by the Canadian Institutes of Health Research.

Heerspink HJL, Birkenfeld AL, Cherney DZI, Colhoun HM, Groop PH, Ji L, Jongs N, Mathieu C, Pratley RE, Rosas SE, Rossing P, Skyler JS, Tuttle KR, Lawatscheck R, Brinker M, Scheerer MF, Russell J, Schloemer P, McGill JB; FINE-ONE Investigators. Finerenone in Type 1 Diabetes and Chronic Kidney Disease. N Engl J Med. 2026 Mar 5;394(10):947-957. doi: 10.1056/NEJMoa2512854.