DeCure's autonomous Nephrology AI scientist is researching a drug-repurposing hypothesis for interstitial nephritis — screening already-approved drugs against its 6-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleInterstitial nephritis maps to a 6-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 interstitial nephritis 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
adenine phosphoribosyltransferase (APRT) — APRT 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 ampdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 4X45 · 1.75 Å · ligand ADENOSINE MONOPHOSPHATE (AMP). Experimental structure, not a prediction.
What the evidence adds up to
Five patients diagnosed with acute interstitial nephritis after excluding other causes all presented with severe renal failure but improved clinically and biochemically within several months. Two improved spontaneously, three improved after starting corticosteroid therapy. No cause was identified in any of these patients. Drug-induced acute interstitial nephritis is described as a rare, potentially correctable cause of acute renal failure; early recognition and appropriate therapy are considered essential. Several drug classes are associated, including antibiotics and nonsteroidal anti-inflammatory agents, each with characteristic mechanisms of toxicity.
A single-centre study from India covering ten years reports that acute interstitial nephritis is a major cause of acute kidney injury, with patients mainly presenting as non-oliguric. The authors state that tissue diagnosis is necessary to decide on therapy in cases that do not show spontaneous recovery of renal function, and that this may prevent disease progression. The study focuses on clinical presentations, causes, outcomes, and prognostic indicators, but the abstract provides no numerical results, no response rates, and no survival data.
The evidence base for acute interstitial nephritis remains limited to small case series and descriptive reviews. The 2008 series of five patients shows that spontaneous recovery occurs in some cases, and that corticosteroids are used in others, but no controlled comparison exists. The 2024 Indian study promises outcome data but the abstract gives none. What is still missing is prospective, controlled trials that compare steroid therapy against supportive care alone, with clearly defined patient stratification by cause, severity, and timing of diagnosis. Funding for such trials, and standardised diagnostic criteria, remain 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.
BMJ · 1998 · 45 citations · open access
Late onset interstitial nephritis associated with mesalazine treatment
AbstractPatients taking mesalazine should have renal function monitored regularly to avoid nephrotoxicity
Mesalazine is widely prescribed for the treatment of inflammatory bowel disease. It is a single molecule of 5-aminosalicylic acid (5-ASA), and is structurally similar to phenacetin and aspirin. Occasionally, treatment with mesalazine may lead to a severe indolent interstitial nephritis causing appreciable morbidity. Unless detected and treated early this may progress to end stage renal failure despite withdrawal of the drug.1 It is obvious from the increasing number of reports of nephritis and renal failure occurring after treatment with mesalazine that the premise that “there is no need for routine monitoring of renal function”2 needs to be reviewed; the need for a review has been suggested by a number of recent reports. 1 3–9 We report two cases of late onset interstitial nephritis induced by mesalazine (Asacol); the first presented after at least 5 years of continuous treatment with the drug and the second after 1 year.
### Case 1
A 38 year old laboratory technician began taking mesalazine for ulcerative colitis. After 2 years of continuous treatment he remained well with normal renal function (serum creatinine concentration 76 μmol/l; normal range 71-133 μmol/l) and negative results on urinalysis. He had an exacerbation of his colitis during the third and fourth years of treatment. On each occasion he responded to a combination of oral prednisolone treatment and an increase in the dose of mesalazine to 1.2 g twice a day. Each time, steroid treatment lasted for 3 months and began with 40 mg a day of prednisolone which was rapidly tapered down to a maintenance dose of 10 mg a day. Repeat serum creatinine concentration measured after 3 years of mesalazine treatment was 79 μmol/l. Thereafter the dose of mesalazine fluctuated between 800 …
Acute Interstitial Nephritis A Distinct Clinico-Pathological Entity?
AbstractThe term acute interstitial nephritis (AIN) has generally been used to describe the pathologic changes observed in the kidney after a variety of ‘insults’, but many authorities have questioned whether AIN constitutes a distinct clinico-pathological entity. This report describes 5 patients in whom the diagnosis of AIN was established after ruling out other processes which could have produced similar clinical or pathologic findings. All patients presented with severe renal failure but improved both clinically and biochemically within several months. Two patients improved spontaneously and 3 improved in association with the institution of corticosteroid therapy. No etiologic agent was readily apparent in any of the patients.
Pharmacotherapy The Journal of Human Pharmacology and Drug Therapy · 1992 · 31 citations
Review of Drug‐Induced Acute Interstitial Nephritis
AbstractDrug-induced acute interstitial nephritis (AIN) is a rare, potentially correctable cause of acute renal failure. Early recognition and appropriate therapy are essential to its management. Several drugs have been associated with the development of AIN, including antibiotics and nonsteroidal antiinflammatory, agents, all with characteristic mechanisms of toxicity.
Kidney International Reports · 2024 · 0 citations · open access
WCN24-1592 CLINICAL PROFILE, OUTCOMES AND ROLE OF STEROIDS IN ACUTE INTERSTITIAL NEPHRITIS : A SINGLE CENTRE EXPERIENCE OF 10 YEARS FROM INDIA
AbstractAcute interstitial nephritis (AIN) is one of the major causes of Acute kidney injury who mainly present with non-oliguria. It is imperative to have tissue diagnosis of AIN in order to decide on therapy in cases who are not showing self-recovery of renal function and prevent them from disease progression. This study focuses on the clinical presentations, causes of AIN, outcomes and prognostic indicators.
5-ASA induced interstitial nephritis in patients with inflammatory bowel disease: a systematic review
AbstractAbstract Background Acute interstitial nephritis (AIN) is an important cause of kidney injury accounting for up to 27% of unexplained renal impairment. In up to 70% of cases, drugs, including aminosalicylates, are reported as the underlying cause. Following two recent paediatric cases of suspected mesalazine induced AIN within our own department, we performed a systematic review of the literature to address the following question: In patients with inflammatory bowel disease (IBD), is interstitial nephritis associated with 5-aminosalicylate (5-ASA) treatment? Our primary objective was to identify the number of cases reported in the literature of biopsy-proven 5-ASA induced interstitial nephritis, in children and adults with IBD. We also aimed to identify which variables influence the onset, severity and recovery of 5-ASA interstitial nephritis. Methods Embase and PubMed databases were searched from inception to 07/10/20. Search terms had three main themes: “inflammatory bowel disease”, “interstitial nephritis” and “aminosalicylates”. Studies were included if they reported an outcome of AIN, confirmed on biopsy, suspected to be secondary to a 5-ASA drug in those with IBD. A narrative synthesis was performed. Results Forty-one case reports were identified. Mesalazine was the most frequently reported aminosalicylate associated with AIN (95%). The median duration of treatment before AIN was diagnosed was 2.3 years (Interquartile Range (IQR) 12–48 months). The median rise in creatinine was 3.3 times the baseline measurement (IQR 2.5–5.5). Aminosalicylate withdrawal and steroids were the most frequently used treatments. Despite treatment, 15% of patients developed end-stage renal failure. Conclusions AIN is a serious adverse drug reaction associated with aminosalicylates, with mesalazine accounting for most reports. The current guidance of annual monitoring of renal function may not be sufficient to identify cases early. Given the severity of AIN and reports in the literature that early treatment with steroids may be beneficial, we would recommend at least 6 monthly monitoring of renal function. PROSPERO registration number CRD42020205387.
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.
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