Author(s): Christian Perez Calvo*, Michel Perez Marrugo, Emerson Javier García Ballesteros, Alejandro Alberto Nuñez Ospino, Luis Saray Ricardo, Gabriel Padilla Vega, Carlos José Brito Jacome, José María Mejía Barrera, Julio Contreras Pasimino, Jhohanna María Parra Pizarro, Felipe Herrera Lozano
Diabetic kidney disease is one of the microvascular complications with the greatest impact on morbidity and mortality in patients with diabetes. Previously thought to be a linear series of events consisting of ultrafiltration, glomerular hypertension, albuminuria, and successive decreases in GFR, it is now known to be affected by multiple metabolic and hemodynamic pathophysiological mechanisms, leading to cell signaling pathways, oxidative stress, dysregulated autophagy, triggering structural damage and functional alterations leading to disease. There are also recognized risk factors for the disease that trigger pathophysiological mechanisms that contribute to its development, such as obesity, smoking, poor metabolic control, arterial hypertension, ethnicity, among others. Although current therapies have not completely halted the development of the disease, current efforts are focused on developing new therapies that can positively influence its onset and progression, with both SGLTi and AR-GLP1 playing a leading role, improving cardiovascular and renal outcomes, independently of their effect on the control of hyperglycemia, which is why they are currently a fundamental pillar of management. Finerenone, a mineralocorticoid receptor antagonist, is another current therapy that has been shown to have an impact on cardiovascular and renal outcomes, playing a complementary role to ACEI and ARB II in the management of albuminuria.
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