A new study has identified the circulating protein INHBC as a possible link between type 2 diabetes and chronic kidney disease. It is an early research lead, not a treatment, validated blood test, or reason to change medication.
The actionable message remains familiar: kidney disease can develop without obvious symptoms, so regular blood and urine testing matters. The ADA recommends checking urine albumin-to-creatinine ratio (UACR) and estimated glomerular filtration rate (eGFR) at least yearly in people with type 2 diabetes. These tests, blood-pressure management, and individualized medication decisions remain the foundation of kidney care.
What the study found
The researchers used a method called Mendelian randomization. In plain language, this approach uses genetic variants that are associated with an exposure—in this case, type 2 diabetes risk or circulating proteins—to explore whether a relationship may be more consistent with causation than a simple observational association. It is a powerful tool for prioritizing research, but it depends on assumptions and does not substitute for a clinical trial.
The research team first looked for proteins associated with genetically proxied type 2 diabetes. They identified 71 candidates. Next, they examined how genetically proxied levels of several proteins related to kidney traits, including eGFR, blood urea nitrogen (BUN), and chronic kidney disease risk. Five proteins stood out in different analyses: INHBC, GNPTG, LPO, AGRN, and CTSD.
INHBC received the most attention. Higher genetically proxied levels of INHBC were associated with lower eGFR and higher BUN across several datasets. In a separate observational analysis of nearly 38,000 people from UK Biobank, higher measured INHBC was associated with a higher likelihood of kidney-disease diagnosis. The authors also estimated that INHBC mediated about 1.3% of the association between type 2 diabetes and kidney-disease diagnosis.
That 1.3% figure is easy to misunderstand. It is a model-based estimate about one possible pathway in this genetic analysis. It does not mean that 1.3% of people could be treated by lowering INHBC. It does not mean INHBC “causes” 1.3% of diabetic kidney disease. And it does not show that blocking INHBC would prevent dialysis, kidney failure, or death.
Why this is a research lead—not a therapy
The study did not give participants an INHBC-lowering drug or test a supplement, diet, exercise program, existing diabetes medicine, or diagnostic blood test. Its main outcomes were kidney-related markers and disease-risk definitions in genetic datasets. eGFR estimates filtration and BUN is a blood measure influenced by kidney function and other factors. Associations with these markers do not demonstrate fewer cases of kidney failure, dialysis, transplant, symptoms, or death.
Mendelian randomization strengthens a hypothesis only when important assumptions hold. A protein-related genetic variant may affect more than one pathway, and a blood measurement may not reflect the relevant tissue or disease stage. Replication across datasets makes INHBC more interesting for future work, but not clinically actionable. An earlier integrative genomics study also nominated INHBC as a potential kidney-function determinant while calling for follow-up rather than clinical adoption.
The screening that matters now
Diabetic kidney disease is often silent. A person can feel well while albumin begins to appear in urine or filtration declines. UACR measures urine albumin relative to creatinine, and eGFR estimates filtration. Together, they help clinicians stage risk, watch trends, and decide how often monitoring is needed. The ADA recommends at least annual UACR and eGFR assessment for people with type 2 diabetes; established chronic kidney disease may require more frequent testing.
NIDDK likewise notes that diabetic kidney disease is usually found through blood and urine testing rather than symptoms. Testing matters because kidney status can change which medicines fit, how drugs are dosed, and how closely blood pressure, potassium, and glucose should be followed.
A useful appointment question is: “What are my current UACR and eGFR, how have they changed over time, and what does that mean for my risk and treatment plan?” That focuses the conversation on established information rather than a speculative biomarker.
Current kidney protection is individualized, evidence-based care
Research on INHBC should not distract from treatments and monitoring strategies that already have outcome evidence. Kidney protection in type 2 diabetes usually involves several connected pieces: glucose management, blood-pressure management, smoking cessation when relevant, physical activity, nutrition support, medication review, and regular kidney testing.
For people with diabetes, hypertension, and albuminuria, an ACE inhibitor or angiotensin receptor blocker (ARB) may be indicated. These medicines require individualized monitoring of blood pressure, kidney function, potassium, and pregnancy considerations. For appropriate people with type 2 diabetes and chronic kidney disease, SGLT2 inhibitors have evidence supporting kidney and cardiovascular benefit, and other treatments may be added according to kidney function, albuminuria, cardiovascular risk, and patient preferences.
This is not a one-size-fits-all medication checklist. Some treatments are not appropriate in every circumstance, and medicines that protect the kidneys in one setting can require careful monitoring in another. For example, SGLT2 inhibitors can cause an initial reversible change in eGFR and have other precautions related to acute illness, volume status, and infections. ACE inhibitors and ARBs also need clinical follow-up. The decision belongs with a clinician who knows the person’s laboratory results, comorbidities, goals, and full medication list.
Over-the-counter medicines and supplements deserve mention here. Some products can affect kidneys, blood pressure, glucose, or interactions with prescriptions. NIDDK advises people to review both prescription and nonprescription medicines with a health professional or pharmacist. A new genetic study is not a basis for self-directed supplement use or for stopping established treatment.
What patients, clinicians, and investors can take from this paper
For patients, the takeaway is calm and practical: the study gives researchers a possible new pathway to investigate, but the steps that protect kidney health today are regular UACR/eGFR testing, a personalized plan for glucose and blood pressure, and a medication review with the care team.
For clinicians, the study is a useful distinction between genetic causal-inference methods, biomarkers, and outcome trials. It can guide hypotheses, especially when replicated across datasets, but it does not establish an actionable target without disease-specific functional research and clinical testing.
For investors and innovators, INHBC is a research lead rather than a validated asset. There is no clinical biomarker standard, no proven intervention, no human safety package, and no evidence yet that altering the pathway reduces kidney failure, dialysis, transplant, symptoms, mortality, or healthcare use. Those gaps are precisely what future research would need to address.
Whole-person care while science advances
At Diabetes Reversal Group, we welcome research that seeks to understand why type 2 diabetes can affect kidneys and other organs. We also believe people deserve a clear boundary between promising science and proven care. A genetic signal is not a treatment, but it can deepen the questions researchers ask next.
Whole-person type 2 diabetes care remains central: food, movement, sleep, stress management, support systems, and clinical monitoring all shape health.
For some people, type 2 diabetes remission may be possible with sustained changes and clinical oversight. Remission is not a cure, and monitoring remains important because glucose levels and complication risk can change over time. New genetic research does not alter those principles.
Dr. Dr. Jeffrey Hockings, CEO/Founder & Kristine Burke, MD, Chief Operation Officer
This article is educational and does not replace individualized medical care. Do not start, stop, or change diabetes, blood-pressure, kidney, or supplement treatment without guidance from the clinician managing your care. Discuss meaningful medication or supplement changes with your diabetes care team or pharmacist.