DeCure for Membranoproliferative glomerulonephritis
DeCure's autonomous Nephrology AI scientist is researching a drug-repurposing hypothesis for membranoproliferative glomerulonephritis — screening already-approved drugs against its 3-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleMembranoproliferative glomerulonephritis maps to a 3-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 membranoproliferative 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
complement factor B (CFB) — CFB 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 apo structuredrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 3HRZ · 2.2 Å · ligand none (apo structure). Experimental structure, not a prediction.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Terapevticheskii arkhiv · 2018 · 8 citations · open access
Membranoproliferative glomerulonephritis in Russian population
AbstractAIM: Analysis of etiology, clinical and morphological manifestations, approaches to therapy and prognosis of membranoproliferative glomerulonephritis (MPGN). MATERIALS AND METHODS: Cases of MPGN were retrospectively identified in the period 2000-2017 with subsequent analysis of etiology, clinical data and morphology (including deposits of immunoglobulins (Ig) and C3 complement fractions). The achievement of complete and partial remissions (PR, CR), overall survival, progression (by composite endpoint: decrease in the estimated GFR (eGFR) ≥50% from the baseline or eGFR <15 ml/min/1.73 m2 or the onset of dialysis). RESULTS: 214 cases of MPGN entered the study with the average age of 44±16 years. Most patients had nephrotic syndrome and significant hematuria. In 58.4% of cases, eGFR was <60 mL/min/1.73 m2, and every fifth patient had CKD 4 or 5 stages. The prevalence of MPGN among all biopsy-confirmed glomerulopathies was 9.3%. Idiopathic MPGN (iMPGN) was detected in 30.4% of cases, secondary MSGN (sMPGN) - in 69.6% (autoimmune diseases - 34.1%, infectious diseases - 16.4%, monoclonal gammopathies - 9.3%, complement-mediated damage - 9.8%). Ig+C3+MPGN was mainly associated with autoimmune diseases and infections; C3-glomerulopathy or thrombotic microangiopathy were most often causes of Ig-C3+MPGN; Ig-C3-/Ig+C3-MPGN had heterogeneous etiology. The median follow-up period was 28 [7; 37] months. The 10-year total cumulative patient and renal survival rates were 71 and 50%, respectively (without differences between sMPGN and iMPGN). The frequency of the PR/CR was 50% (iMPGN - 46.2%, sMPGN - 51.3%) depending on the etiology of the MPGN (p=0.049). The cumulative 10-year progression-free renal survival was nearly 100% in cases with PR/CR and 0% in non-responders. CONCLUSION: MPGN is a severe variant of glomerular damage with a heterogeneous etiological structure and an unfavorable prognosis. Targeted clinical and morphological diagnostics of MPGN allows to identify the cause of the disease in most cases. This approach is reliable for the adequate treatment choice and improvement of outcomes in MPGN.
DMW - Deutsche Medizinische Wochenschrift · 2001 · 1 citations
Sekundäre Glomerulonephritis bei chronischer Infektion eines ventrikuloatrialen Shunts
AbstractHISTORY AND ADMISSION FINDINGS: A 39-year-old man was referred for assessment of a nephrotic syndrome. He reported deteriorating health with bouts of fever and microhaematuria and proteinuria in the past year. At the age of 24 years a ventriculoatrial shunt had been inserted for an internal hydrocephalus. At another hospital he was given steroids for a nephrotic syndrome suspected of being associated with membranoproliferative glomerulitis, but the disease progressed. On admission he had severe generalised oedema with a temperature of 38,5;C. His general condition was poor. He had no neck stiffness. INVESTIGATIONS: Parameters of inflammation were raised. Serum creatinine and creatinine clearance were normal. Levels of complements C3 and C4 were reduced. The proteinuria was 9g/24h. Renal biopsy revealed type 1 membranoproliferative glomerulonephritis. Micrococcus roseus/varians was demonstrated several times by aerobic blood cultures. TREATMENT AND COURSE: The findings suggested chronically infected ventriculoatrial shunt as cause of the glomerulonephritis. The shunt was, therefore, removed. The same pathogens were grown from it on aerobic culture medium. Six months after removal and replacement of the shunt and treatment of the infection the proteinuria had fallen to 0.45 mg/h; serum creatinine was 1.0 mg/dl. CONCLUSION: When membranoproliferative glomerulonephritis has been demonstrated, secondary forms should be considered in the differential diagnosis. In most cases specific treatment can prevent progression of the renal disease.
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.
