DeCure for Nephrolithiasis susceptibility caused by SLC26A1
DeCure's autonomous Nephrology AI scientist is researching a drug-repurposing hypothesis for nephrolithiasis susceptibility caused by SLC26A1 — 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 moduleNephrolithiasis susceptibility caused by SLC26A1 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 nephrolithiasis susceptibility caused by slc26a1 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
alpha-L-iduronidase (IDUA) — IDUA 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 1~{r},2~{r},3~{r},4~{s},6~{s}drag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 6I6R · 2.02 Å · ligand (1~{R},2~{R},3~{R},4~{S},6~{S})-6-azanyl-2,3,4-tris(oxidanyl)cyclohexane-1-carboxylic acid (H62). 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.
Mini-Reviews in Medicinal Chemistry · 2016 · 7 citations
Research Progress of Mechanisms of Ceftriaxone Associated Nephrolithiasis
AbstractBACKGROUND: Urinary calculi can be caused by a variety of reasons, such as metabolic abnormalities, urinary tract infection and obstruction. Certain medications can induce urinary stone disease. Ceftriaxone, a third generation cephalosporin with broad spectrum antibiotic activity, primarily eliminated by the kidneys, has now been widely used for treatment of infection. It has been long considered safe, especially in children. However, more and more cases about ceftriaxone induced nephrolithiasis as a rare side effect have been reported. CONCLUSION: This complication generally resolves spontaneously with cessation of the drug. Severe nephrolithiasis can cause post renal acute renal failure (PARF). There is limited information about how this complication develops, though high doses and extended treatment periods are generally considered to be responsible. Understanding the mechanisms would help the doctors to be aware of this rare complication and respond with proper treatment. The primary goal of this review is to discuss the possible mechanisms based on the most recent literatures.
Journal of the American Society of Nephrology · 2022 · 1 citations
Don't Miss Mesalamine! Mesalamine-Induced Focal Segmental Glomerulosclerosis in a Patient With Ulcerative Colitis
AbstractIntroduction: Renal manifestation in UC and Crohn's disease is not uncommon. It's suggested to be a combination of genetic factors, infectious agents, bacterial endotoxins, and immune complex depositions. The most frequent renal disease in patients with IBD are nephrolithiasis, TIN, GN, and amyloidosis. Mesalamine is a 5-ASA compound which is the mainstay drug for UC. It is known to cause hypersensitivity reactions which may even cause aggravation of UC. Case Description: We present a case of a 23 year old male with a history of UC for 8 years who went to the ED for worsening generalized edema for 3 days. His UA with 3+ protein and no RBCs. UPCR was 7.2 and albumin 1.6 g/dL. Nephrology was consulted for nephrotic syndrome. IV diuresis was started for anasarca. The patient had been taking mesalamine for many years and did not have recent UC flare ups. He did not have history of premature birth, hypertension, or obesity, and had normal kidney size. Urine microscopy showed oval fat bodies. Serological work up was significant for elevated ESR, + MPO and +PR3 antibodies. HIV, CMV, EBV, and parvovirus B19 were negative. A native kidney biopsy was done and it revealed negative IF findings and evidence against active immune complex mediated GN. EM confirmed diffuse podocyte effacement and ultimately glomerular tip lesion variant Focal Segmental Glomerulosclerosis. The patient was started on immunosuppression with corticosteroids, RAAS blockade with ARB, Calcium/ Vitamin D supplementation, PPI, diuretics, and salt restriction. With close outpatient monitoring and tapering of steroids, the patient's proteinuria and edema improved. He continues to follow up with GI and will pursue other treatments for UC once steroids have been completely tapered. Discussion: IBD renal manifestations are usually associated with disease activity and improve with remission of bowel inflammation. Lack of viral causes or UC activity, as well as postive MPO and PR3 antibodies, was more suggestive of a drug induced reaction. Mesalamine is renally excreted and the most common reported kidney related adverse reactions is acute or chronic interstitial nephritis due to hypersensitivity reaction usually occurring in the first 6 months of use. Mesalamine induced FSGS must be considered in the differential early on presentation of a patient with nephrotic syndrome to ensure adequate and appropriate treatment to preserve kidney function.
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.
