Chronic kidney disease is an unpleasant condition. There is little that can be done for patients at the present time, though there is hope that senolytic drugs might be able to turn back the fibrosis characteristic of the condition. The kidneys are important to the correct function of tissues throughout the body, and consequently chronic kidney disease accelerates the degenerative aging of many other organs, including the cardiovascular system and brain. Finding ways to restore kidney function in older patients would be a big deal.
Chronic kidney disease (CKD) is a systemic pathology that affects approximately 10% of the population. The prevalence of CKD has increased markedly over the past decades due to aging of the population worldwide and increase in incidence of diabetes mellitus, which has become the primary cause of CKD. Nowadays, CKD is considered a public health problem that causes high rates of mortality in the population due to the association with cardiovascular diseases (CVDs). Multiple studies support the notion that patients with renal disease suffer accelerated aging, which precipitates the appearance of pathologies, including CVDs, usually associated with advanced age.
Considerable efforts have been made to slow the progression of the disease and improve the quality of life in patients with CKD. New pharmacological strategies do slow the progression of CVDs, and reduce the morbidity and mortality of CKD patients. Likewise, methods of renal replacement therapy currently offer increased purification capacity and reduced adverse effects. However, the development of CVDs in patients with CKD has not yet been halted. This may be because when CKD is diagnosed, vascular pathology is already advanced and irreversible.
The causes of vascular damage in CKD are exceptionally complex. Among the theories proposed in recent years to explain the high frequency of CVDs in renal patients, one states that senescence of peripheral blood cells (known as immunosenescence) and vascular cells (known as vascular senescence) may be involved in the initiation and perpetuation of vascular pathology that appears early in patients with CKD.
The aging process that occurs due to uremia is associated with numerous changes at the cellular and molecular level, which coincide with changes observed during the physiological aging process. These changes may explain some of the complications that typically occur in patients with CKD and CKD-associated CVDs. Expanding our understanding of the factors and molecules involved in accelerated senescence will serve to identify possible targets associated with this process. This will lead to improved methods of diagnosis and monitoring of these patients. Understanding the similarities between accelerated senescence and normal physiological aging will help establish new treatments.