DeCure's autonomous Nephrology AI scientist is researching a drug-repurposing hypothesis for glomerulonephritis — screening already-approved drugs against its 37-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleGlomerulonephritis maps to a 37-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.
Research record
01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash
Current lead
No approved-drug candidate for glomerulonephritis is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.
Molecular view
ubiquitin C-terminal hydrolase L1 (UCHL1) — UCHL1 is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.
Loading structure…
helix sheet 4-chlorophenyldrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 8EDE · 1.799 Å · ligand 2-[(4-chlorophenyl)-methyl-amino]-~{N}'-ethanoyl-ethanehydrazide (WEU). Experimental structure, not a prediction.
What the evidence adds up to
Treatment of primary glomerulonephritis remains empirical and differs by subtype, as no etiological therapy exists. For minimal change nephropathy, glucocorticoids are standard, with cytotoxic drugs or cyclosporin reserved for steroid-dependent patients. In focal glomerulosclerosis, 40–60% of patients may respond to prolonged glucocorticoids, immunosuppressive drugs, or cyclosporin. Membranous nephropathy may benefit from a six-month course of glucocorticoids and alkylating agents, which can favour remission and protect renal function. For IgA nephritis, ongoing trials in 1999 suggested possible benefit from glucocorticoids alone or with azathioprine. Membranoproliferative glomerulonephritis is described as still elusive to treatment.
Recurrent primary glomerulonephritis after kidney transplantation is a frequent and severe disease, representing the second or third leading cause of graft loss. A 2025 review of studies and meta-analyses confirms that recurrence rates, characteristics, and treatments differ among glomerulonephritis variants. The review distinguishes pre-transplant, peri-transplant, and post-transplant periods, and notes that new drugs are being discovered, with some ongoing trials having shown important results already.
The immune mechanisms underlying glomerulonephritis involve both humoral and cell-mediated adaptive responses, which cause injury to resident glomerular cells. Despite decades of clinical studies, treatment remains empirical and subtype-specific, with no curative or universally effective regimen established.
What is still missing are controlled trials that stratify patients by histological subtype and immune profile, adequate funding for such trials, and a reliable way to predict which patients will respond to glucocorticoids, alkylating agents, or newer drugs before graft loss occurs.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
BMJ · 1971 · 71 citations · open access
Controlled Trial of Azathioprine and Prednisone in Chronic Renal Disease
AbstractPatients with various forms of glomerulonephritis, but excluding those with minimal glomerular changes, were admitted to a controlled trial of a regimen which combined azathioprine in a dosage of 2·5 mg/kg/day with prednisone in a dosage of 20 mg/day (adults) or 0·5 mg/kg/day (children). Of 149 patients included, 32 of them under the age of 15, 72 were randomly allocated to the “treatment” group and 77 to the “control” group. There was no evidence of benefit from the treatment group as a whole; and the mortality was in fact higher in the treated group.
Oxford University Press eBooks · 2009 · 4 citations
Glucocorticoids and immunomodulating agents
AbstractAlthough the rationale for an etiological treatment of primary glomerulonephritis is still lacking, a number of clinical studies have shown that some subtypes of these diseases may benefit from empirical treatment based upon the use of glucocorticoids or immunomodulating agents. In this chapter the clinical pharmacology, the mechanisms of action, and the toxic effects of these drugs will be reviewed.
Current Opinion in Nephrology & Hypertension · 1999 · 1 citations
Immunosuppressive therapy in primary glomerulonephritis
AbstractThe treatment of glomerulonephritis is empirical and is different for the various subtypes. The treatment of minimal change nephropathy rests on glucocorticoids, reserving cytotoxic drugs and cyclosporin for steroid-dependent patients. Some 40-60% of patients with focal glomerulosclerosis may respond to prolonged therapy with glucocorticoids, immunosuppressive drugs or cyclosporin. In membranous nephropathy a 6 month course of glucocorticoids and alkylating agents may favour remission and protect renal function. Ongoing trials are showing the possible benefit of glucocorticoids alone or with azathioprine in IgA nephritis. The treatment of membranoproliferative glomerulonephritis is still elusive.
Transplantology · 2025 · 0 citations · open access
Recurrence of Primary Glomerular Diseases After Kidney Transplantation: Incidence, Predictors, Characteristics and Treatment
AbstractRecurrent primary glomerulonephritis is a frequent and severe disease that represents the second or third leading cause of graft loss. The purpose of this study is to address the rates of recurrence for all types of glomerulonephritis, detailing their characteristics and the treatments adopted. The authors collected the main studies and meta-analyses published on PubMed. In addition, the main clinical trials ongoing on the topic were collected. The results highlighted the different frequency of recurrence in relation to the glomerulone-phritis considered, assessing the different characteristics and the different treatments adopted. In conclusion, this review confirms the severity of this disease. The treatment possibilities differ among glomerulonephritis variants. Frequently, a pre-transplant period should be distinguished from a peri-transplant period and a post-transplant period. Fi-nally, new drugs are being discovered to treat recurrent glomerulonephritis and several ongoing trials are also discussed. Some of them have shown important results already.
The Role of Humoral and Cell-Mediated Adaptive Immune Response
AbstractGlomerulonephritis is a major cause of chronic kidney disease worldwide and presents with various histological and clinical manifestations in terms of severity and duration, resulting in diverse clinical outcomes. Immune-mediated injury of the resident glomerular cells plays a critical role in many forms of glomerular injury and mounting evidence indicates that both humoral and cell-mediated mechanisms are involved.
AbstractFifty years ago, the prospects for treatment of glomerulonephritis were dim. Beginning around 1950 the field of "glomerular therapeutics" was begun by the introduction of new agents (adrenocorticotrophic hormone, cortisone, nitrogen mustard) as possible disease-modifying therapies for the various forms of glomerular disease. For the next several decades these and other agents (azathioprine, cyclophosphamide, chlorambucil, prednisone) were used therapeutically in a largely uncontrolled and anecdotal fashion. The application of randomized, controlled trials led to the adoption of some forms of therapy as both effective and reasonably safe, and the rejection of others as either ineffective or hazardous. New regimens involving different routes of administration or dosing schedules were adopted. After about another two decades, new and increasingly selective agents began to be introduced into the therapeutic armamentarium (cyclosporine, mycophenolate mofetil). Diseases previously associated with a very poor outcome were transformed into manageable disorders. The consequences of glomerular disease (e.g., nephrotic syndrome, chronic renal failure) were now subject to control and alleviation in many circumstances. The next transformation of "glomerular therapeutics" is now under way. The revolution in molecular genetics and pharmacogenomics will allow new agents to be developed that target specific aspects of the pathogenic mechanisms underlying glomerular disease. This transformation will not be an easy one, because development, testing, approval, and application of these new concepts in therapeutics (e.g., somatic gene therapy) will be time consuming and expensive. Eventually, the understanding of the genetic basis of susceptibility to glomerular disease and its progression will allow a preventative and curative, rather than palliative, strategy to emerge.
GLOBAL JOURNAL FOR RESEARCH ANALYSIS · 2024 · 0 citations · open access
A RARE CASE OF FIBRILLARY GLOMERULONEPHRITIS PRESENTED AS NEPHROTIC SYNDROME IN A PATIENT WITH TYPE 2 DIABETES MELLITUS
AbstractFibrillary Glomerulonephritis is a rare form of glomerulonephritis with poor prognosis and less proven therapeutic options. My patient, a 42 year old recently diagnosed Diabetic but non-hypertensive who presented as adult onset nephrotic syndrome and kidney biopsy showed presence of Fibrillary Glomerulonephritis. She got remission with injection Rituximab.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.
