Mostly, our gut microbes are beneficial or at least neutral because we have co-evolved and reached an accommodation. One benefit we derive from their presence is that they make life difficult for potentially harmful organisms, if only by monopolising the available resources and occupying the niches in our gut.
There is a downside, of course, as in any evolved system, which is inevitably a compromise and can tip over into pathology under certain circumstances. But overall, because the disadvantages are more than compensated for by the benefits, the system has evolved and been maintained.
However, a newly discovered downside is that a Staphylococcus species may be implicated in one of the serious complications of diabetes mellitus (DM) — kidney fibrosis and ultimately kidney failure. The discovery was made by researchers at the University of Illinois Urbana-Champaign and Mie University in Japan, co-led by Professor Isaac Cann of Illinois and Professor Esteban Gabazza of Mie University. The bacterium is believed to produce corisin — a small peptide — which is found at high levels in patients with diabetic kidney fibrosis. The researchers have just published their findings, open access, in Nature Communications.
For creationists, this sort of discovery is always a problem, one they normally ignore or blame on “Eve’s sin,” revealing ID creationism for what it is — Bible literalism in a lab coat — which must retreat into mystical theology when faced with problems ID cannot address. Yet creationists also claim that their omniscient creator god is personally responsible for the design of organisms such as Staphylococcus. That would mean it knowingly endowed Staphylococcus with the genes to make corisin, along with all the harmful consequences.
Taking William A. Dembski’s “complex specified genetic information,” which supposedly produces a specific outcome, at face value, the staphylococcal genes are equally “proof” of intelligent design. And so we end up with an unresolved paradox for ID creationism: “complex specified” genes that do us harm, standing as evidence of malevolent design.
Background^ The Human Microbiome.The research is explained in a University of Illinois Urbana-Champaign news bureau item.
- What it is - The microbiome is the community of bacteria, fungi, and other microbes that live in and on the human body, especially in the gut.
- Numbers game - There are trillions of microbes in our intestines, roughly equal in number to our own cells, and together they contain far more genes than the human genome.
- Why they matter - Gut microbes help break down food, make vitamins (such as vitamin K and some B vitamins), and train our immune system.
- First line of defence - By occupying space and consuming resources, they prevent harmful organisms from gaining a foothold.
- Not always friendly - While mostly beneficial or harmless, some microbes can cause problems if the balance is disrupted or if they find a way into parts of the body where they don’t belong.
Kidney fibrosis linked to molecule made by gut bacteria
A molecule made by bacteria in the gut can hitch a ride to the kidneys, where it sets off a chain reaction of inflammation, scarring and fibrosis — a serious complication of diabetes and a leading cause of kidney failure — according to a new study from researchers at the University of Illinois Urbana-Champaign and Mie University in Japan.
After finding high levels of corisin — a small peptide produced by Staphylococcus bacteria in the gut — in the blood of patients with diabetic kidney fibrosis, the researchers used computer simulations and tissue and mouse experiments to track how corisin affects the kidneys, how it gets there from the gut, and a possible method of countering it with antibody treatment.
Our earlier studies showed corisin can damage cells and worsen tissue scarring and fibrosis in other organs, so we suspected it might be a hidden driver of kidney fibrosis. Our new findings suggest corisin is indeed a hidden culprit behind progressive kidney damage in diabetes, and that blocking it could offer a new way to protect kidney health in patients.
Professor Isaac Cann, co-corresponding author
Carl R. Woese Institute for Genomic Biology (Microbiome Metabolic Engineering)
University of Illinois Urbana-Champaign
Urbana, IL, USA.
[Professor Isaac Cann and Professor Dr. Esteban Gabazza] are affiliates of the Carl R. Woese Institute for Genomic Biology at Illinois.
The researchers published their findings in the journal Nature Communications.
Diabetic kidney fibrosis is a major cause of kidney failure worldwide, yet the key drivers of it have remained a mystery, and no treatments can stop the process, said Dr. Taro Yasuma of Mie University, a medical doctor and the first author of the manuscript.
Many people with longstanding diabetes eventually develop kidney fibrosis, and once it progresses, there are limited options beyond dialysis or kidney transplantation. Current treatments mainly focus on controlling blood sugar and blood pressure, but there’s no cure that stops or reverses the scarring or fibrotic process.
Dr. Taro Yasuma, co-first author
Department of Immunology
Mie University Faculty and Graduate School of Medicine
Edobashi, Tsu, Mie, Japan.
The researchers began by screening the blood and urine of patients with diabetic kidney disease. They found that patients had significantly more corisin than their healthy counterparts, and that the amount of corisin in the blood correlated with the extent of kidney damage.
Upon seeing the same results in mice with kidney fibrosis, the researchers tracked what corisin was doing in the kidneys of the mice. They found that corisin speeds up aging in kidney cells, setting off a chain reaction from inflammation to cell death to a buildup of scar tissue, eventually resulting in the loss of kidney function and worsening fibrosis.
But how was corisin getting from the gut to the kidneys? Cann and Gabazza’s groups collaborated with U. of I. chemical and biomolecular engineering professor Diwakar Shukla’s group to produce computer simulations and laboratory experiments to follow corisin’s journey from the gut to the bloodstream. They found that corisin can attach to albumin, one of the most common proteins in blood, and ride it through the bloodstream. When it reaches the kidneys, corisin detaches from the albumin to attack the delicate structures that filter blood and urine.
To confirm that corisin was the main culprit behind the kidney damage, the researchers gave the mice antibodies against corisin. They saw a dramatic reduction in the speed of kidney damage.
Diabetes increases corisin release from the microbiome into the bloodstream, where it binds to the protein albumin. The corisin-albumin complex reaches the kidney, where corisin detaches from albumin and enters kidney cells. Corisin accelerates cell aging and death, resulting in scarring and fibrosis. However, an anticorisin antibody binds to corisin peptides, blocking their aging activity and mitigating disease progression.Image from Yasuma et al. (2025).When we treated the mice with an antibody that neutralizes corisin, it slowed the aging of kidney cells and greatly reduced kidney scarring. While no such antibody is currently approved for use in humans, our findings suggest it could be developed into a new treatment.
Professor Dr. Esteban C. Gabazza, Department of Immunology
Mie University Faculty and Graduate School of Medicine
Edobashi, Tsu, Mie, Japan.
Diabetes increases corisin release from the microbiome into the bloodstream, where it binds to the protein albumin. The corisin-albumin complex reaches the kidney, where corisin detaches from albumin and enters kidney cells. Corisin accelerates cell aging and death, resulting in scarring and fibrosis. However, an anticorisin antibody binds to corisin peptides, blocking their aging activity and mitigating disease progression. Image from Yasuma et al., Microbiota-derived corisin accelerates kidney fibrosis by promoting cellular aging, 2025.
Next, the researchers plan to test anticorisin treatments in more advanced animal models, such as pigs, to explore how they could be adapted for safe use in humans. The U. of I. and Mie University have a joint invention disclosure on corisin antibodies.
Our work suggests that blocking corisin, either with antibodies or other targeted therapies, could slow down or prevent kidney scarring in diabetes and thus enhance the quality of life for patients.
Professor Isaac Cann.
Publication:
AbstractCreationists are fond of claiming that the intricacies of life point to the hand of a benevolent designer. Yet discoveries like this corisin-producing Staphylococcus illustrate the opposite: genetic information carefully tuned not to promote life, but to damage it. Within their own framework, this is not random misfortune but an intentional feature, deliberately included in the microbial genome by an omniscient creator fully aware of the outcome — kidney fibrosis, suffering, and early death.
The increasing global prevalence of diabetic nephropathy poses substantial health and economic burdens. Currently, effective anti-fibrotic therapies for managing kidney fibrosis associated with chronic kidney disease are lacking. This study reveals corisin, a microbiota-derived peptide, as a central driver in the progression of diabetic kidney fibrosis. Corisin levels were found to be markedly elevated in the serum of diabetic chronic kidney disease patients relative to healthy controls, with strong correlations to advanced disease stages and declining renal function. In a murine model of kidney fibrosis, corisin levels were similarly heightened, directly contributing to increased inflammation and worsening fibrosis and renal impairment. Notably, the use of a monoclonal anti-corisin antibody significantly reduced nephropathy severity in diabetic mice. Through molecular dynamics simulations and experimental validation, we demonstrated that corisin interacts with human serum albumin, potentially enhancing its renal accumulation and pathological impact. The pathogenic mechanism of corisin involves the acceleration of cellular senescence and the induction of epithelial-mesenchymal transition and apoptosis in kidney cells. These findings underscore the critical role of corisin in progressive diabetic nephropathy and suggest a promising new target for therapeutic intervention.
Introduction
The rising prevalence of diabetes mellitus (DM) has emerged as a critical global health challenge, imposing a substantial economic burden on societies worldwide1,2,3. Recent epidemiological data underscore the alarming magnitude of this issue, revealing that 536.6 million individuals, constituting an estimated prevalence of 10.5%, were affected by DM worldwide in 20214. The prevalence is expected to rise to 12.2%, affecting 783.2 million individuals, by 20454. The seriousness of the situation is compounded by the association of DM with elevated morbidity and mortality rates. According to the World Health Organization (WHO), there was a 3% increase in mortality rates due to DM across different age groups between 2000 and 2019, resulting in approximately 1.5 million deaths globally in 2019 directly attributed to DM3. The primary culprits contributing to the high morbidity and mortality rates associated with DM are microangiopathy and macroangiopathy5,6,7,8,9,10. Notably, diabetic nephropathy stands out as one of the most prevalent complications, assuming the role of the leading cause of chronic kidney disease and end-stage kidney disease6,9,11,12. This expanding diabetic population and the associated complications, particularly diabetic nephropathy, underscore the pressing need for comprehensive strategies to manage and mitigate the impact of diabetes on global health.
The unique functional and histopathological features of diabetic nephropathy include proteinuria, enhanced cell proliferation, elevated matrix deposition in the mesangium and renal interstitium, tubular atrophy, and thickening of the glomerular basement membrane, resulting in glomerulosclerosis and tubulointerstitial fibrosis, collectively contributing to a reduced glomerular filtration rate13,14. These fibrotic changes in the kidneys can lead to irreversible damage, ultimately culminating in end-stage kidney disease. Currently, there is no definitive cure for DM-associated kidney fibrosis. Treatment options primarily revolve around controlling hyperglycemia, proteinuria, and arterial hypertension, decreasing cardiovascular risk, alleviating symptoms, and implementing renal replacement therapies in cases of severely impaired kidney function. The primary effects of dysglycemia on the kidneys include injury, activation, and/or apoptosis of glomerular endothelial cells, podocytes, and tubular epithelial cells, as well as overactivation of the intrarenal renin-angiotensin-aldosterone system13,15. Recent studies suggest that alterations in the microbiome or dysbiosis may play a role in the progression of diabetic nephropathy16,17,18. Dysbiosis has been linked to excessive production and accumulation of bacterial metabolites, including urease, p-cresol, and acetate, potentially contributing to oxidative stress, kidney cell apoptosis, inflammation, and profibrotic activity19,20,21,22. Notably, recent studies demonstrated the presence of gut-derived bacteria within the kidneys of spontaneously hypertensive rats, and patients with arterial hypertension23. Dysbiosis has also been implicated in the sudden exacerbation of renal failure or acute kidney injury24,25,26. Additionally, our recent research identified corisin, a microbiota-derived peptide, as a potential contributor to podocyte and renal tubular cell apoptosis, further implicating the microbiome in the pathogenesis of kidney fibrosis27,28.
Building upon this foundation, we hypothesized that corisin contributes to the progression of kidney fibrosis, a key pathological feature of diabetic CKD. Overall, our study demonstrates that elevated circulating corisin levels correlate with disease severity and renal dysfunction in DM patients and with increased kidney fibrosis in murine models. Systemic administration of corisin was associated with kidney fibrosis, while its inhibition attenuates the progression of diabetic nephropathy in experimental animal models. Mechanistically, corisin interacts with human serum albumin, facilitating its transport to the kidneys, where it accelerates cellular senescence and induces apoptosis or epithelial-mesenchymal transition, promoting fibrogenesis. These findings underscore the potential of targeting the corisin pathway as a promising strategy to mitigate the progression of diabetic nephropathy.
Yasuma, T., Fujimoto, H., D’Alessandro-Gabazza, C.N. et al.
Microbiota-derived corisin accelerates kidney fibrosis by promoting cellular aging. Nat Commun 16, 7591 (2025). https://doi.org/10.1038/s41467-025-61847-2
Copyright: © 2025 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
If one accepts William Dembski’s claim that “complex specified information” is evidence of design, then the genes coding for corisin qualify every bit as much as those coding for insulin or haemoglobin. The question, then, is what kind of designer intentionally crafts peptides whose primary consequence is organ failure in vulnerable hosts? To call this “benevolent” stretches language past breaking point.
Creationists often retreat into theology when confronted with such examples, blaming “the Fall” or “Eve’s sin.” But that explanation only underscores the point: the supposed designer left humanity saddled with a microbial arsenal of molecular weapons, pre-programmed to exploit disease states. A designer who builds misery into the very fabric of biology looks less like a source of goodness and more like a figure of calculated malice.
In evolutionary biology, by contrast, no such moral paradox arises. Harmful traits emerge because of the messy compromises of natural selection, where what benefits one organism can damage another. Suffering is not planned, but an unavoidable consequence of blind processes. The creationist position leaves its followers with a cruel irony: the better the science, the darker their “designer” appears.
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