DeCure for Tubulointerstitial kidney disease, autosomal dominant, 2
DeCure's autonomous Nephrology AI scientist is researching a drug-repurposing hypothesis for tubulointerstitial kidney disease, autosomal dominant, 2 — 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 moduleTubulointerstitial kidney disease, autosomal dominant, 2 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 tubulointerstitial kidney disease, autosomal dominant, 2 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
apolipoprotein A4 (APOA4) — APOA4 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 9HX4 · 3.3 Å · ligand none (apo structure). Experimental structure, not a prediction.
What the evidence adds up to
Autosomal dominant tubulointerstitial kidney disease (ADTKD) is a group of monogenic renal diseases with autosomal dominant inheritance and progressive tubulointerstitial damage. ADTKD–UMOD, caused by pathogenic variants of the UMOD gene, is the most common subtype and is recognised as the most frequent non-polycystic genetic kidney disease. Cohort studies on affected families have deepened understanding of the clinical and genetic spectrum, and research into the pathogenetic mechanism has been extensive. The disease is usually described as showing slowly progressive decline in kidney function without enlarged kidneys.
Three cases from Japan, however, presented with rapidly progressive renal dysfunction in elderly patients who had bilateral kidney enlargement and ADTKD-like histology and who underwent dialysis with rapid progression. Gene panel analysis for target sequences of inherited kidney diseases was performed in those cases. The authors suggested that elderly onset rapidly progressive renal dysfunction with kidney enlargement and tubulointerstitial injury might be a new disease entity of ciliopathy. Histologic findings in tubulointerstitial diseases often have overlapping features, and exact subclassification is difficult; biopsies are frequently performed shortly after symptoms manifest in the acute phase.
No drug treatment is mentioned in any of these abstracts. No clinical trial data, no response rates, no survival figures, and no sample sizes beyond the three Japanese cases are reported. What is still missing is any clinical trial designed to test a therapy for ADTKD–UMOD, funding for such trials, and a reliable way to stratify patients by rate of progression or by the presence of kidney enlargement.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Integrative Medicine in Nephrology and Andrology · 2024 · 2 citations · open access
Autosomal Dominant Tubulointerstitial Kidney Disease–UMOD: A Monogenic Renal Disease that Cannot Be Ignored
AbstractAutosomal dominant tubulointerstitial kidney disease (ADTKD) is a group of monogenic renal diseases characterized by autosomal dominant inheritance and progressive tubulointerstitial damage with bland urinary sediment. With the discovery of pathogenic variants, ADTKD was recognized as the most frequent non-polycystic genetic kidney disease. ADTKD–UMOD is caused by pathogenic variants of UMOD (coding gene of uromodulin) and is the most common subtype of ADTKD. With the improved awareness of the disease and the advance of genetic testing technology, cohort studies on affected families have gradually increased and deepened our understanding of the clinical and genetic spectrum of ADTKD–UMOD. In addition, extensive research has been conducted on the pathogenetic mechanism. This review highlights recent research progress in the genetic and clinical spectrum, as well as the underlying mechanisms of ADTKD–UMOD.
Kidney International Reports · 2020 · 0 citations · open access
SUN-457 ELDERLY ONSET RAPIDLY PROGRESSIVE RENAL DYSFUNCTION WITH KIDNEY ENLARGEMENT AND TUBULOINTERSTITIAL INJURY MIGHT BE A NEW DISEASE ENTITY OF CILIOPATHY
AbstractAutosomal dominant tubulointerstitial kidney disease (ADTKD) is a group of uncommon genetic disorders characterized by slowly progressive decline in kidney function and autosomal dominant inheritance. ADTKD is usually described as not showing enlarged kidneys. However, there have been several reports of rapidly progressive renal dysfunction in elderly patients with bilateral kidney enlargement and ADTKD-like histology in Japan. Here we reported three cases with enlarged kidneys who have undergone dialysis with rapid progression and performed analysis of gene panel for target sequence of inherited kidney diseases.
Cambridge University Press eBooks · 2023 · 0 citations
Hereditary and Acquired Tubulointerstitial Diseases
AbstractMany entities affect specifically the tubulointerstitium, most often sparing the glomeruli and vessels, but exact subclassification is difficult because the histologic findings may have overlapping features. Frequently biopsies are performed shortly after symptoms manifest (in the acute phase). There is controversy in the terminology of chronic lesions; for example the term chronic pyelonephritis, particularly in the pediatric population, has fallen out of favor, replaced by other terms such as reflux nephropathy. However, careful examination and clinicopathologic correlation helps to pinpoint the cause and guide appropriate patient management. In this chapter, the focus is on the histopathology of acquired and hereditary tubulointerstitial diseases in native kidneys.
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.
