UK study highlights harmful connection between obesity, kidney disease
LEXINGTON, Ky. (April 24, 2025) — A comprehensive new review by researchers at the University of Kentucky sheds light on the intricate and damaging relationship between obesity and kidney disease.
The review, recently published in the prestigious Nature Reviews Nephrology, details the multiple ways in which excess fat tissue disrupts kidney function and even triggers changes in the brain that further exacerbate renal damage. Conversely, when the kidneys aren’t working properly, that can also affect adipose tissue (or body fat).
“Our review shows that the link between obesity and kidney disease is far more complex than previously understood. This work underscores the urgent need for new therapeutic strategies to combat the growing epidemic of obesity-related kidney problems,” said Analia S. Loria, Ph.D., an associate professor in the Department of Pharmacology and Nutritional Sciences in the UK College of Medicine and principal investigator of the grant from the National Heart, Lung, and Blood Institute that funded some of the studies highlighted in this publication.
The review emphasized that obesity doesn’t just add extra weight — it triggers a cascade of harmful effects on the kidneys. These include direct physical compression, disruption of blood flow and increased pressure within the kidney, and the release of inflammatory signals and hormones from expanded fat tissue.
“Expanded fat tissue acts like an active neuroendocrine organ, sending signals that directly harm the delicate structures of the kidney. Our lab showed that adipose tissue also sends signals to the brain, increasing renal sympathetic outflow, and contributing to the development of chronic kidney disease,” said Carolina Dalmasso, Ph.D., a research scientist in the Department of Pharmacology and Nutritional Sciences and one of the lead authors of the review. “Investigating therapeutic targets to reduce these signals from adipose tissue may offer a promising strategy for mitigating obesity-related hypertension and chronic kidney disease.”
The study also highlights the role of the communication network connecting adipose tissue, the brain and the kidneys via nerves, hormones and inflammatory factors.
“Notably, pre-existing kidney disease can contribute to the dysfunction of fat tissue through the accumulation of waste products in the body,” said Nermin Ahmed, Ph.D., a registered dietician, recent graduate of the Loria Lab and one of the lead authors. “These toxins can lead to fat tissue loss and the abnormal storage of fats, potentially worsening kidney function.”
The researchers emphasize that a deeper understanding of all these interactions is crucial for developing effective treatments.
“Understanding the impact of fat-derived signals will pave the way for innovative therapies that can prevent or slow the progression of kidney disease in individuals with obesity,” said Loria.
The review explored current and emerging therapeutic strategies, including drugs targeting a crucial hormonal pathway that regulates blood pressure, fluid and electrolyte balance in the body — the renin-angiotensin-aldosterone system — along with inflammation, lipid metabolism, lifestyle interventions and bariatric surgery.
“It was a great experience to develop figures summarizing the most up-to-date information in the field and see them highlighted in such a prestigious journal,” said Meghan Turner, a Ph.D. candidate in the Loria Lab.
This research provides critical insights into the dangerous connection between obesity and kidney disease, highlighting the need for continued investigation and the development of novel therapeutic interventions.
You can find the full paper in Nature Reviews Nephrology online.
Research reported in this publication was supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health under Awards Numbers R01HL142969 and R01HL135158, and by the National Institute of General Medical Sciences of the National Institutes of Health under Award Number P30GM127211. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
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