Leptin and Adipokine Dynamics in Chronic Kidney Disease
Summary
Chronic kidney disease (CKD) is marked by progressive loss of renal function accompanied by profound disturbances in adipose‐tissue signalling. Adipokines such as leptin and adiponectin circulate at altered levels in CKD, reflecting both reduced renal clearance and dysregulated production. Hyperleptinaemia arises from impaired renal elimination and heightened adipocyte secretion driven by insulin resistance and low‐grade inflammation. Conversely, adiponectin often increases as a compensatory anti‐inflammatory response but may also reflect malnutrition‐inflammation syndromes in advanced CKD. The resulting imbalance in adipokine networks contributes to endothelial dysfunction, hypertension, proteinuria and cardiovascular risk, while also influencing nutritional status, muscle wasting and systemic inflammation. Emerging work highlights bidirectional crosstalk between the kidney and adipose tissue—termed the adipose‐renal axis—whereby uremic toxins, cellular senescence and inflammatory mediators perpetuate adipocyte dysfunction and fuel renal injury. Understanding these dynamics offers avenues for biomarker development and targeted interventions to mitigate CKD progression and its cardiometabolic sequelae.
Research from Nature Portfolio
Investigations into severe secondary hyperparathyroidism in end‐stage renal disease have revealed that surgical correction by parathyroidectomy restores adipocyte leptin production via upregulation of Akt signalling. Postoperative rises in circulating leptin correlate with improvements in anaemia and nutritional markers, suggesting leptin’s therapeutic potential in reversing CKD‐associated wasting. Complementary in vitro and in vivo studies of uremic serum exposure demonstrate that renal failure primes adipocytes and macrophages toward a proinflammatory phenotype through activation of NF-κB and HIF-1 pathways. This interaction promotes macrophage infiltration into adipose depots in both human samples and murine models, with interleukin-6 emerging as a critical mediator of adipose inflammation in uremia.
Leptin and Adipokine Dynamics in Chronic Kidney Disease publication trend
The graph below shows the total number of articles in leptin and adipokine dynamics in chronic kidney disease across all publications each year (not limited to Nature Index journals).
Technical terms
Leptin: Hormone secreted by adipocytes that regulates appetite, energy expenditure and immune responses.
Adipokine: Bioactive proteins released by adipose tissue with roles in metabolism, inflammation and vascular function.
Adiponectin: Adipokine with insulin-sensitising, anti-inflammatory and anti-atherogenic properties.
Uremic toxins: Metabolic by-products that accumulate with declining renal function and provoke systemic inflammation.
eGFR: Estimated glomerular filtration rate, a clinical measure of kidney filtration capacity.
References
- Adiponectin‐to‐leptin ratio and incident chronic kidney disease: Sex and body composition‐dependent association. Journal of Cachexia Sarcopenia and Muscle (2024).
- Clinical Study of Metabolic Parameters, Leptin and the SGLT2 Inhibitor Empagliflozin among Patients with Obesity and Type 2 Diabetes. International Journal of Molecular Sciences (2023).
- Advanced Oxidation Protein Products Contribute to Chronic-Kidney-Disease-Induced Adipose Inflammation through Macrophage Activation. Toxins (2023).
- Pro-Inflammatory Profile of Adipokines in Obesity Contributes to Pathogenesis, Nutritional Disorders, and Cardiovascular Risk in Chronic Kidney Disease. Nutrients (2022).
- New Insights into Adiponectin and Leptin Roles in Chronic Kidney Disease. Biomedicines (2022).
- The Causes and Potential Injurious Effects of Elevated Serum Leptin Levels in Chronic Kidney Disease Patients. International Journal of Molecular Sciences (2021).
- Association of Increased Serum Leptin with Ameliorated Anemia and Malnutrition in Stage 5 Chronic Kidney Disease Patients after Parathyroidectomy. Scientific Reports (2016).
- Macrophage and adipocyte interaction as a source of inflammation in kidney disease. Scientific Reports (2021).
Turn complex research questions into confident strategic decisions
When you're under pressure to set direction, justify investment, or understand your competitive position, you need more than raw data — you need trusted insights you can act on.
Benchmark your performance against global peers using robust, methodologically sound analysis.
Combine quantitative metrics with qualitative expert insight to uncover strengths, gaps and emerging opportunities.
Gain tailored, decision-ready recommendations aligned to your strategic priorities.
Talk to us to learn more about our data dashboards and bespoke strategy reports.
Grow research skills, confidence and careers with training built for every stage of the research lifecycle.
Developed with Nature Portfolio journal Editors and internationally renowned experts. Discover three ways to learn:
Self-paced, online courses in convenient bite-sized units, covering key skills across scientific writing, publishing, grant writing, data analysis, and more.
Expert trainer-led workshops with hands-on exercises and real-time feedback across core research skills, delivered via interactive group sessions.
Editor-led workshops combining core principles in writing and publishing, personalised 1:1 feedback from Nature Portfolio Editors and hands-on exercises.
Explore course catalogues and workshop agendas, enquire about the options or request institutional pricing.