The Accelerated Aging Produced by Chronic Kidney Disease

Many lines of evidence point to kidney function as being particularly important to the health of organs throughout the body. To pick one example, one of the better known longevity-associated genes, klotho, appears to act in the kidney, and yet is well known for producing improvements in cognitive function. Here, researchers discuss much of the other evidence related to the accelerated aging observed in chronic kidney disease patients. Once the kidney starts to decline, near everything else in the body follows, with cardiovascular issues being a particularly prominent part of the problem.

The characteristics of chronic kidney disease (CKD) are similar to those of the aging process; therefore, it has been hypothesized that CKD promotes premature aging associated with related diseases. Furthermore, chronic diseases usually observed in aging, such as cardiovascular disease (CVD), inflammation, vascular calcification, mineral, and bone disorders, and chronodisruption (chronic alteration of circadian rhythms), are markedly frequent in patients with CKD.

CVD is the most clinically relevant comorbidity associated with CKD. The coexistence of both diseases could be explained by the following: (1) patients with CKD have a higher prevalence of non-traditional cardiovascular risk factors, (2) many cardiovascular risk factors exacerbate CKD progression, and (3) CKD itself can be considered a risk factor for CVD. According to 2013 data from the U.S. Renal Data System, an estimated 43% and 15% of patients with CKD experience heart failure and acute myocardial infarction in their lifetime (versus healthy persons: 18.5% and 6.4%, respectively).

The development of CVD in patients with CKD is due primarily to endothelial dysfunction. Endothelial cells in patients with renal disorders experience premature senescence due to received stress signals, which may lead to apoptosis. Under physiological conditions, endothelial cells have a non-adherent and anticoagulant surface; however, molecules expressed on the surface of damaged endothelial cells may be altered, increasing cell adhesion capacity. Platelets bind to the damaged surface, triggering the onset of coagulation with consequent inflammation and thrombosis, thereby causing cardiovascular accidents.

Several factors, such as inflammation, oxidative stress, primary diseases such as hypertension or diabetes, and hyperlipidemia, contribute to endothelial deterioration in CKD. Another example is hyperphosphatemia, which is present in many patients with renal disorders. High phosphate concentrations increase oxidative stress and reduce the concentration of nitric oxide, which the endothelial cells release to relax and avoid the rigidity of the arteries and regulate endothelial permeability.


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