Public Health Perspectives on Kidney-resident Immune Cells and Chronic Disease

Arielle Cohen^*
*Correspondence: Arielle Cohen, Arielle Cohen Department of Nephrology and Dialysis Unit, University of Genova, 16126 Genoa, Italy, Email:

Introduction

Chronic Kidney Disease (CKD) has emerged as a significant global health issue, with an estimated 10% of the worldâ??s population affected by some form of kidney dysfunction. This widespread prevalence is driven by factors such as the aging population, poor dietary habits, sedentary lifestyles and a rising incidence of comorbid conditions like diabetes and hypertension. CKD not only burdens individuals with poor health and diminished quality of life but also strains healthcare systems worldwide. While much attention has been paid to the traditional risk factors of kidney disease, a lesser-discussed but increasingly important area is the role of kidney-resident immune cells. These immune cells, which include macrophages, dendritic cells and T lymphocytes, are crucial in maintaining kidney function and response to injury. However, in chronic diseases, such as CKD, these same cells can become a source of damage. When immune responses go awry, persistent inflammation, fibrosis and tissue remodeling can accelerate the progression of kidney dysfunction. Moreover, kidney-resident immune cells do not operate in isolation they interact with other systems in the body, particularly the cardiovascular and metabolic systems, exacerbating the overall morbidity of CKD and associated conditions such as diabetes and hypertension. This paper aims to explore the relationship between kidney-resident immune cells and chronic disease, with a specific focus on how these interactions influence public health. By understanding the mechanisms of kidney immunity, we can improve disease prevention strategies, develop new therapeutic interventions and raise awareness about the importance of kidney health in preventing the broader burden of chronic diseases [1].

Description

Kidney-resident immune cells, including macrophages, dendritic cells and T lymphocytes, are critical to the kidney's ability to function and respond to injury. These cells reside in various compartments of the kidney, such as the glomeruli, interstitial spaces and tubules, where they play essential roles in tissue surveillance, immune defense and tissue repair. Macrophages are the most abundant immune cells in the kidney and they are involved in maintaining tissue homeostasis by phagocytosing dead cells, removing pathogens and resolving inflammation. Dendritic cells are also present in smaller numbers, but they are essential for activating the adaptive immune response, presenting antigens and modulating immune tolerance. T lymphocytes, which are recruited to the kidney during inflammation, can either contribute to tissue repair or exacerbate injury, depending on the type of immune response activated. Under normal conditions, these immune cells help prevent excessive inflammation, facilitate wound healing and maintain kidney function. However, in the context of Chronic Kidney Disease (CKD), these same immune cells can drive disease progression. In CKD, persistent immune activation leads to chronic inflammation, fibrosis and tissue remodeling, which are hallmarks of kidney damage [2].

Kidney-resident immune cells play a central role in the progression of CKD. In patients with CKD, immune cells are persistently activated by factors such as hyperglycemia in diabetes, high blood pressure in hypertension, or the presence of chronic infections. Macrophages, in particular, release pro-inflammatory cytokines (e.g., TNF-ÃÂ?±, IL-6) that amplify inflammation and promote fibrosis. These inflammatory cytokines cause an imbalance between tissue repair and destruction, resulting in scarring and progressive loss of kidney function. Additionally, immune cells contribute to vascular remodeling in the kidneys, which worsens blood flow and accelerates the damage to renal tissues. In diabetic nephropathy, for instance, elevated blood glucose levels increase the production of Reactive Oxygen Species (ROS), which in turn activate immune cells and trigger inflammatory pathways. Similarly, in hypertensive nephropathy, sustained high blood pressure can directly damage the renal vasculature, leading to immune cell infiltration and exacerbation of kidney injury [3].

The link between kidney-resident immune cells and metabolic diseases, particularly diabetes and hypertension, further complicates the management of CKD. In diabetic individuals, kidney-resident immune cells contribute to the development of diabetic nephropathy by amplifying inflammatory responses and altering kidney tissue architecture. The immune systemâ??s chronic activation in the face of hyperglycemia accelerates kidney fibrosis, leading to a decline in kidney function. Similarly, in hypertensive individuals, kidney-resident immune cells play a role in mediating nephrosclerosis, a condition in which the kidneys become stiff and scarred due to the effects of prolonged high blood pressure. These immune responses also intersect with systemic inflammation, further contributing to the development of cardiovascular diseases, which are commonly seen in CKD patients [4].

Understanding the role of kidney-resident immune cells in chronic diseases like CKD, diabetes and hypertension opens the door to novel public health interventions. Public health initiatives focused on educating communities about the interconnectedness of kidney health and immune system function can help in preventing CKD or slowing its progression in high-risk populations. Additionally, translating findings from immunological research into clinical practice offers the potential for new treatment modalities that target the immune system to halt or reverse kidney damage. For instance, drugs that modulate macrophage activity or inhibit the release of pro-inflammatory cytokines could offer therapeutic benefits to CKD patients. Moreover, public health campaigns that raise awareness about the importance of controlling blood pressure, managing diabetes and reducing oxidative stress could mitigate the risk of CKD, especially in vulnerable groups [5].

Conclusion

The research on kidney-resident immune cells offers a wealth of knowledge with profound implications for both clinical practice and public health. These immune cells are central to maintaining kidney health, but when dysregulated, they become key contributors to the pathogenesis of Chronic Kidney Disease (CKD) and its related comorbidities, including hypertension and diabetes. By studying the mechanisms through which immune cells affect kidney function, we gain valuable insights into the progression of CKD and the potential for targeted therapies. From a public health standpoint, it is crucial to integrate this knowledge into disease prevention strategies. Community-based education programs can raise awareness of the critical role of kidney health and the impact of lifestyle factors such as diet, exercise and blood pressure management on kidney function. Moreover, public health policies aimed at improving access to early diagnosis and treatment for at-risk populations could significantly reduce the burden of CKD. Moving forward, further research into the immune systemâ??s involvement in kidney disease will pave the way for new treatments and preventative measures. As the global burden of CKD continues to rise, it is imperative to address this challenge through comprehensive public health strategies that emphasize prevention, early intervention and the integration of kidney immunology into healthcare practices. Ultimately, improving kidney health on a population level will not only reduce the incidence of CKD but also improve the overall quality of life for millions of people worldwide.

Acknowledgement

None.

Conflict of Interest

None.

References

1. Munro, David AD and Jeremy Hughes. "The origins and functions of tissue-resident macrophages in kidney development." Front Physiol 8 (2017): 837.

Google Scholar Cross Ref Indexed at

2. Gottschalk, Catherine and Christian Kurts. "The debate about dendritic cells and macrophages in the kidney." Front Immunol6 (2015): 435.

Google Scholar Cross Ref Indexed at

3. Puranik, Amrutesh S., Irina A. Leaf, Mark A. Jensen and Ahmad F. Hedayat, et al. "Kidney-resident macrophages promote a proangiogenic environment in the normal and chronically ischemic mouse kidney." Sci Rep 8(2018): 13948.

Google Scholar Cross Ref Indexed at

4. Kumar, Mahendra, Shah Dev, Muhammad Usman Khalid and Sowmya Manjari Siddenthi, et al. "The bidirectional link between diabetes and kidney disease: Mechanisms and management." Cureus 15 (2023).

Google Scholar Cross Ref Indexed at

5. Sundaram, Arunkumar, Lee Siew Keah, Kuttulebbai Nainamohamed Salam Sirajudeen and Harbindar Jeet Singh. "Upregulation of catalase and downregulation of glutathione peroxidase activity in the kidney precede the development of hypertension in pre-hypertensive SHR." Hypertens Res36 (2013): 213-218

Google Scholar Cross Ref Indexed at