Kamal Kishor Maru¹, Deepak Kumar², Rajasri Bhattacharyya¹ and Dibyajyoti Banerjee^1*

¹ Department of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India
² School of Bioengineering and Food Technology, Faculty of Applied Sciences and Biotechnology, Shoolini University, Himachal Pradesh, India

*Corresponding Author: Dibyajyoti Banerjee, Department of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India.

Received: October 21, 2025; Published: January 01, 2026

Abstract

Diabetes mellitus has emerged as one of the most formidable global health challenges of the 21st century, affecting over 500 million adults worldwide, with projections suggesting that this number may exceed 850 million by 2050 [1]. Diabetes imposes a significant metabolic burden and serves as a precursor to a wide spectrum of chronic complications affecting nearly every organ system, including retinopathy, neuropathy, cardiovascular disease, and nephropathy [2]. Among these, diabetic kidney disease (DKD), also known as diabetic nephropathy (DN), stands out as the most serious and life-limiting complication, accounting for up to 40% of people living with diabetes being affected by chronic kidney disease (CKD) globally [1,2]. DKD is poised to become an even greater contributor to the global CKD burden as the prevalence of diabetes continues to rise, challenging both developed and developing healthcare systems in the coming decades [1]. Diabetic nephropathy remains the prototypical microvascular complication of diabetes and one of the foremost causes of CKD and end-stage renal disease (ESRD) globally [2]. The first descriptions of renal changes in diabetes date back to the mid-20th century, when clinicians correlated proteinuria in long-standing diabetic patients with progressive renal failure. Landmark work by Mogensen and colleagues subsequently identified microalbuminuria as an early harbinger of overt nephropathy, revolutionizing the paradigm of DN monitoring and prevention [3]. In classical teaching, DN is conceptualized as a progressive sequence from glomerular hyperfiltration to microalbuminuria, overt proteinuria, declining glomerular filtration, and ultimately ESRD [3,4]. However, growing evidence indicates that structural and molecular injury may precede measurable albuminuria, and that some patients progress without the canonical microalbuminuric stage [4,5]. Despite decades of research, DN continues to impose a heavy toll on patients and health systems, largely because it is often detected only after irreversible nephron loss has occurred [2,5]. In the earliest or “silent” phase, glomeruli undergo adaptive changes in response to chronic hyperglycemia, hypertension, and metabolic stress, including glomerular basement membrane thickening, mesangial expansion, and podocyte stress or detachment [5]. Tubular epithelial cells also sustain subclinical injury due to glucose toxicity, oxidative stress, and local inflammation [5]. These changes, though initially compensatory, can evolve into irreversible injury if the metabolic and hemodynamic insults persist. Histologic studies have shown that even normoalbuminuric diabetic kidneys may harbour early mesangial expansion and nodular lesions [5]. Over time, the compensatory reserve is overwhelmed, and microalbuminuria develops as glomerular.

References

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Citation

Citation: Dibyajyoti Banerjee., et al. “Need for Early Diagnosis of Diabetic Nephropathy: From Silent Beginnings to Therapeutic Opportunity". 10.2 (2026): 01-04

Copyright

Copyright: © 2026 Dibyajyoti Banerjee., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.