At this year’s American Diabetes Association (ADA) congress, while obesity and diabetes treatments took the limelight, there were sessions focused on kidney disease.
This included real-world analysis of contributors to metabolic dysfunction-associated kidney diseases and insulin delivery.
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Diabetes is the leading cause of kidney failure globally, accounting for nearly half of all chronic kidney disease (CKD) cases.
XOR promoter linked to kidney disease
During an oral presentation at ADA, researchers presented findings on whether variants in the xanthine oxidoreductase (XOR) promoter influence susceptibility to metabolic dysfunction-associated kidney disease. The findings suggest that XOR promoter variation may be a meaningful genetic contributor to metabolic kidney disease, with potential implications for both disease stratification and future target validation in chronic kidney disease (CKD)
Clinically, the findings strengthen the case that kidney disease in metabolic contexts is not just a downstream consequence of diabetes or obesity but may also reflect inherited regulatory biology that influences progression risk.
By leveraging All of Us and Million Veteran Program data, the researchers found reproducible associations between XOR promoter variants and kidney-related as well as endocrine/metabolic phenotypes across ancestry groups.
This is clinically significant because replication across large, diverse datasets improves confidence that the signal is not an artefact of a single cohort. The association with proteinuria, glomerular disease, nephrotic syndrome, and diabetic renal manifestations is especially relevant because these are phenotypes that often define high-risk CKD populations and drive escalation to specialist care.
From a mechanistic perspective, the finding that several variants sit in predicted CCAAT/enhancer-binding protein beta (CEBPβ) transcription factor binding sites adds biological plausibility. This drives the narrative beyond generic association and supports a potential regulatory pathway linking XOR expression to kidney injury and metabolic inflammation. It also expands the narrative around precision nephrology, a space that is increasingly attractive to pharma because it offers potential differentiation in a crowded CKD market dominated by sodium-glucose co-transporter-2 inhibitors, glucagon-like peptide-1 receptor agonists (GLP-1RAs), and non-steroidal mineralocorticoid receptor antagonists. The broader implication is that XOR could sit at an intersection of metabolism, oxidative injury, and kidney structural damage, making it relevant to both biomarker development and future targeted therapy.
AID more beneficial
Automated insulin delivery (AID) systems link a pump and continuous glucose monitor (CGM) to an algorithm that adjusts insulin dosing in near real time. That matters because insulin needs change minute-to-minute with stress hormones, illness, meals, steroids, and sleep.
In a randomised inpatient trial of adults with diabetes and advanced kidney disease (eGFR <30), AID delivered a striking improvement: time in the target glucose range (70–180 mg/dL) was 69% with AID versus 36% with multiple daily injections (MDI) plus CGM, with lower average glucose as well. Time spent low (<70 mg/dL) was equivalent to AID and MDI, suggesting the system does not improve hypoglycaemia impact.
Insulin delivery isn’t just about convenience, plays a role in the drug’s impact on the body. By turning insulin dosing into a responsive, data-driven process, AID can increase time in a healthy range and reduce extreme highs, even in medically complex settings like advanced kidney disease. This will lead to more stable and comfortable patients, especially in a hospital setting where both can play a role in recovery.
Insulin is a hormone that must be responsive to blood sugar levels, and diabetes patients deal with the consequences when this system is disrupted. The insulin delivery system they use (syringes, pens, pumps, or automated “closed-loop” systems) can change how quickly it starts working, how predictably it peaks, and how safely a healthy glucose range is achieved.
