DeCure for Immunoglobulin-mediated membranoproliferative glomerulonephritis
DeCure's autonomous Nephrology AI scientist is researching a drug-repurposing hypothesis for immunoglobulin-mediated membranoproliferative glomerulonephritis — screening already-approved drugs against its 2-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleImmunoglobulin-mediated membranoproliferative glomerulonephritis maps to a 2-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 immunoglobulin-mediated 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 H (CFH) — CFH 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 mlidrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 5O32 · 4.20620907647 Å · ligand MALONATE ION (MLI). Experimental structure, not a prediction.
What the evidence adds up to
A 2015 case report describes an elderly man with rapidly progressive renal failure and nephrotic-range proteinuria who was diagnosed with immunoglobulin A dominant membranoproliferative glomerulonephritis after autoimmune disease, cryoglobulinaemia, and infection-associated glomerulonephritis were excluded. Remission was achieved within three months of treatment. The authors note that this diagnosis is rare and described only in case reports.
A 2001 case report describes a 39-year-old man with a ventriculoatrial shunt inserted 15 years earlier who developed nephrotic syndrome with 9 g/24h proteinuria, reduced complement C3 and C4, and type 1 membranoproliferative glomerulonephritis on renal biopsy. Steroid treatment at another hospital had failed to halt progression. Micrococcus roseus/varians was repeatedly cultured from blood and from the shunt itself. Six months after shunt removal and replacement plus treatment of the infection, proteinuria had fallen to 0.45 mg/h and serum creatinine was 1.0 mg/dl. The authors conclude that when membranoproliferative glomerulonephritis is found, secondary causes should be considered, and that specific treatment can in most cases prevent progression.
A 1976 review notes that early classifications of membranoproliferative glomerulonephritis were based on morphology, but modern approaches use immunofluorescence. Glomerular deposits of C3 alone, without immunoglobulin, indicate alternative complement pathway dysregulation and are called C3 glomerulopathy, which includes dense deposit disease and C3 glomerulonephritis. Distinguishing C3 glomerulopathy from immunoglobulin-mediated MPGN is opening the way to better diagnostic, prognostic, and treatment algorithms.
What is still missing is any controlled trial data for immunoglobulin-mediated MPGN; the evidence consists only of single case reports. No randomised treatment comparisons exist, no validated biomarkers to predict which patients will respond to immunosuppression versus those who need complement blockade or infection control, and no prospective cohort that separates immunoglobulin-mediated from C3-dominant forms before assigning therapy. Funding for a multicentre registry and for trials that stratify by immunofluorescence pattern is absent.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Indian Journal of Nephrology · 2015 · 8 citations · open access
Immunoglobulin A dominant membranoproliferative glomerulonephritis in an elderly man: A case report and review of the literature
AbstractImmunoglobulin A (IgA) dominant membranoproliferative glomerulonephritis (MPGN) is rare, described only as case reports. We report a rare case of an elderly man presenting with rapidly progressive renal failure and nephrotic range proteinuria with histological, immunofluorescence, and ultrastructural findings supporting a diagnosis of IgA dominant MPGN. Autoimmune disease, cryoglobulinemia and infection-associated glomerulonephritis were excluded. Remission was achieved within 3 months of treatment. This case highlights an uncommon diagnosis with a good response to therapy. The differential diagnosis of IgA nephropathy with MPGN-like pattern is discussed.
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.
Fluidized bed combustion (citations from the NTIS data base). Report for 1969--Mar 77
AbstractWhereas early classifications of membranoproliferative glomerulonephritis (MPGN) were based on morphologic features, the modern approach is directed at immunofluorescence findings. Glomerular deposits of C3 alone, without immunoglobulin, are the hallmark of alternative complement pathway dysregulation through inherited or acquired defects. These immunoglobulin-negative forms are referred to as C3 glomerulopathy, which encompasses both dense deposit disease and C3 glomerulonephritis. Distinguishing C3 glomerulopathy from immunoglobulin-mediated MPGN is opening the way to better diagnostic, prognostic, and treatment algorithms.
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.
