DeCure's autonomous Nephrology AI scientist is researching a drug-repurposing hypothesis for kidney failure — screening already-approved drugs against its 41-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleKidney failure maps to a 41-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 kidney failure 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
FKBP prolyl isomerase 1A (FKBP1A) — FKBP1A 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 4~{s},5~{r},6~{z},9~{s},10~{s},12~{e}drag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 6I1S · 1.52 Å · ligand (4~{S},5~{R},6~{Z},9~{S},10~{S},12~{E})-16-(ethylamino)-4,5-dimethyl-9,10,18-tris(oxidanyl)-3-oxabicyclo[12.4.0]octadeca-1(14),6,12,15,17-pentaene-2,8-dione (E26). Experimental structure, not a prediction.
What the evidence adds up to
A 2016 case report describes a 70-year-old woman with normal baseline renal function who developed refractory acute kidney injury secondary to severe hypothyroid-induced myopathy. Her thyroid-stimulating hormone was 169.8 uIU/mL, creatine phosphokinase 42,670 U/L, creatinine 12.1 mg/dL, and glomerular filtration rate 3 mL/min/1.73 m². Despite aggressive intravenous rehydration, intensive intravenous thyroid hormone replacement, hydrocortisone, sodium bicarbonate for urinary alkalinisation, and six haemodialysis treatments over two weeks, her renal status failed to improve. The patient ultimately refused further intervention and her prognosis remained poor. The authors conclude that severe symptomatic hypothyroidism can induce rhabdomyolysis leading to intractable kidney failure unmanageable by standard medical therapy and haemodialysis.
A 2023 review article on clinical and functional features of the bronchopulmonary system in chronic kidney disease provides a general list of causes of acute kidney failure: blood loss, hypotension from mechanical injury or incompatible blood transfusion, electric shock, septic abortion, poisoning from drugs and metal salts, ureter obstruction by tumours or kidney stones, and traumatic damage to both kidneys. No specific drug repurposing data, treatment outcomes, or patient-level results are reported in this abstract.
No other abstracts were provided. The 2017 abstract is a duplicate of the 2016 case report.
What is missing: prospective trials of thyroid hormone replacement in hypothyroid-associated acute kidney injury; any data on drug repurposing for kidney failure beyond this single case; patient stratification by aetiology of renal failure; and funding for systematic studies of endocrine causes of refractory kidney injury.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Journal of Medical Cases · 2016 · 1 citations · open access
Refractory Acute Kidney Injury Secondary to Hypothyroid-Induced Myopathy: A Contemporary Case Report
AbstractThis is a case report elucidating how severe hypothyroid-induced myopathy can lead to refractory kidney injury, unmanageable by standard medical and hemodialysis interventions. A 70-year-old female with extensive medical comorbidities including adult onset hypothyroidism, hypertension, hyperlipidemia, and normal baseline renal function presented with shortness of breath, myalgias, edema, and facial swelling. The patient was found to have a thyroid-stimulating hormone of 169.8 uIU/mL, creatine phosphokinase of 42,670 U/L, blood urea nitrogen of 70 mg/dL, a creatinine of 12.1 mg/dL, and glomerular filtration rate of 3 mL/min/1.73 m 2 . She was initiated on aggressive intravenous isotonic rehydration, along with intensive intravenous thyroid hormone replacement therapy and hydrocortisone treatment as well. Her renal status failed to improve adequately and she was started on sodium bicarbonate for urinary alkalinization. With the preceding interventions deemed medically futile for renal amelioration, the patient was started on acute hemodialysis. Over the course of 2 weeks and six hemodialysis treatments, the patient’s renal status failed to improve. The patient finally refused any further hemodialysis or medical interventions seeing that her kidneys failed to respond to treatment, and her clinical prognosis remained poor. This case report illustrates how severe symptomatic hypothyroidism can induce rhabdomyolysis leading to intractable kidney failure, unmanageable by standard medical therapy and hemodialysis. J Med Cases. 2017;8(1):8-10 doi: https://doi.org/10.14740/jmc2699w
Texas Journal of Medical Science · 2023 · 0 citations · open access
Clinical and functional features of the bronchopulmonary system in chronic kidney disease
AbstractRenal failure is a syndrome of reduced kidney function. It can happen suddenly (acute) or gradually (chronic). A lot of blood loss, a drop in blood pressure due to a mechanical injury or blood transfusion that does not match the patient's blood group, electric shock, septic abortion, etc.; damage to the kidney parenchyma due to poisoning from drugs and other metal salts; Obstruction of the ureter by tumors or kidney stones, damage to both kidneys due to trauma can cause acute kidney failure.
Journal of Medical Cases · 2017 · 0 citations · open access
Refractory Acute Kidney Injury Secondary to Hypothyroid-Induced Myopathy: A Contemporary Case Report
AbstractThis is a case report elucidating how severe hypothyroid-induced myopathy can lead to refractory kidney injury, unmanageable by standard medical and hemodialysis interventions. A 70-year-old female with extensive medical comorbidities including adult onset hypothyroidism, hypertension, hyperlipidemia, and normal baseline renal function presented with shortness of breath, myalgias, edema, and facial swelling. The patient was found to have a thyroid-stimulating hormone of 169.8 uIU/mL, creatine phosphokinase of 42,670 U/L, blood urea nitrogen of 70 mg/dL, a creatinine of 12.1 mg/dL, and glomerular filtration rate of 3 mL/min/1.73 m 2 . She was initiated on aggressive intravenous isotonic rehydration, along with intensive intravenous thyroid hormone replacement therapy and hydrocortisone treatment as well. Her renal status failed to improve adequately and she was started on sodium bicarbonate for urinary alkalinization. With the preceding interventions deemed medically futile for renal amelioration, the patient was started on acute hemodialysis. Over the course of 2 weeks and six hemodialysis treatments, the patient’s renal status failed to improve. The patient finally refused any further hemodialysis or medical interventions seeing that her kidneys failed to respond to treatment, and her clinical prognosis remained poor. This case report illustrates how severe symptomatic hypothyroidism can induce rhabdomyolysis leading to intractable kidney failure, unmanageable by standard medical therapy and hemodialysis. J Med Cases. 2017;8(1):8-10 doi: https://doi.org/10.14740/jmc2699w
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.
