with simultaneous development of local initiatives that may allow us to better understand and face local conditions. Reprint requests to Ricardo Correa-Rotter, M.D., Head, Department of Nephrology and Mineral Metabolism, Instituto Nacional de Ciencias Medicas y Nutrici ´ on Salvador Zubir ´ an, Vasco de Quiroga 15, Tlalpan ´ 14000, Mexico, DF Mexico. E-mail: correarotter@prodigy.net.mx REFERENCES 1. OMRAN AR: The epidemiologic transition: A key of the epidemiology of population change. Milibank Mem Fund Q 49:509–538, 1971 2. REDDY KS, YUSUF SL: Emerging epidemic of cardiovascular disease in developing countries. Circulation 97:596–601, 1998 3. WORLD BANK: World Development Report: Investing in Health, New York, Oxford University Press, 1993 4. RIVERA JA, BARQUERA S, CAMPIRANO F, TOVAR V, et al: Epidemiological and nutritional transition in Mexico: Rapid increase of non-communicable chronic diseases and obesity.Public Health Nutr 5:113–122, 2002 5. 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Nutr Rev 52:285–298, 1994 11. LANG T: The public health impact of globalization of food trade, in Diet, Nutrition and Chronic Disease: Lessons from Contrasting Worlds, edited by Shetty PS, McPherson K, Chichester, United Kingdom, Wiley, 1997, pp 173–187 12. DREWNOWSKI A, POPKIN BM: The nutrition Special Issue “Diabetic Nephropathy: Diagnosis, Prevention and Treatment” Marta Ruiz-Ortega 1,2,* , Raul R. Rodrigues-Diez 1,2, Carolina Lavoz 3 and Sandra Rayego-Mateos 4 1 Molecular and Cellular Biology in Renal and Vascular Pathology, IIS-Fundación Jiménez Díaz-UniversidadAutónoma Madrid, 28040 Madrid, Spain; rrodrigues@fjd.es 2 Red de Investigación Renal (REDINREN), Instituto de Salud Carlos III, 28029 Madrid, Spain 3 Division of Nephrology, School of Medicine, Universidad Austral de Chile, 5090000 Valdivia, Chile; carolina.lavoz@uach.cl 4 Vascular and Renal Translational Research Group. Institut de Recerca Biomèdica de Lleida (IRBLleida), 25198 Lleida, Spain; srayego@fjd.es * Correspondence: mruizo@fjd.es Received: 11 March 2020; Accepted: 13 March 2020; Published: 17 March 2020 Abstract: Diabetic nephropathy (DN) is the main cause of end-stage renal disease. DN is a complex disease mediated by genetic and environmental factors, and many cellular and molecular mechanisms are involved in renal damage in diabetes. There are no biomarkers that reflect the severity of the underlying renal histopathological changes and can effectively predict the progression of renal damage and stratify the risk of DN among individuals with diabetes mellitus. Current therapeutic strategies are based on the strict control of glucose and blood pressure levels and, although there are new anti-diabetic drugs, these treatments only retard renal damage progression, being necessary novel therapies. In this Special Issue, there are several comprehensive reviews and interesting original papers covering all these topics, which would be of interest to the growing number of readers of the Journal of Clinical Medicine. Keywords: chronic kidney disease; diabetic nephropathy; biomarkers; treatment Chronic kidney disease (CKD) is a major health problem because of its association with a high cardiovascular risk, and most CKD patients progress to end-stage renal disease (ESRD), requiring dialysis or transplantation. Type 2 diabetes mellitus is one of the most important risk factors in the development of CKD, around 30%–50% of ESRD patients worldwide come from a diabetic origin. Diabetic nephropathy (DN) has been classically considered as a metabolic disease; however, increasing data support the important role of immune response in the pathogenesis of this disease. Here, we provide the reader with four comprehensive reviews about the molecular mechanisms involved in renal damage in diabetes, pointing out novel therapeutic options for this disease that would be of interest to general medical readers as well as specialists in diabetes. The article of Donate-Correa et al. [1] delves into the pathogenesis of proinflammatory molecules and mechanisms related to the