Markers of increased cardiovascular risk in elderly patients with chronic kidney disease: A preliminary study

Like other organ systems, the kidneys also go through process of normal senescence, including both anatomical and physiological changes. Normal physiological aging is characterized by the expected age-related changes in the kidneys. With age, the kidneys are subject to structural changes, for example, there is a decrease in the number of functional glomeruli due to an increase in the prevalence of nephrosclerosis (atherosclerosis, glomerulosclerosis, atrophy of the tubules with interstitial fibrosis) and to some extent compensatory hypertrophy of the remaining nephrons. Older age is also associated with reduced cortical volume, increased medullary, and larger and more numerous renal cysts. Changes in normal aging are important in clinical practice. Against the background of suppression of reparative capabilities, the elderly are more prone to acute damage and chronic kidney disease, aggravation of the course of chronic kidney disease. The elderly have less renal functional reserve when they do actually develop chronic kidney disease and they are also at higher risk for acute kidney injury. Cardiovascular disease is a leading cause of death and a common comorbidity among patients with kidney disease. In this review, we have identified the most characteristic structural and functional changes in the kidneys in elderly patients and their impact on cardiovascular risk.

Download Full-text

207 FGF-23 and Cardiovascular Risk Factors in Patients with Chronic Kidney Disease: An Indian Perspective

American Journal of Kidney Diseases ◽

10.1053/j.ajkd.2018.02.213 ◽

2018 ◽

Vol 71 (4) ◽

pp. 567

Keyword(s):

Risk Factors ◽

Chronic Kidney Disease ◽

Cardiovascular Risk ◽

Kidney Disease ◽

Cardiovascular Risk Factors ◽

Fgf 23 ◽

Indian Perspective

Download Full-text

Faculty Opinions recommendation of Reduction of cardiovascular risk in chronic kidney disease by mineralocorticoid receptor antagonism.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.725835891.793510469 ◽

2015 ◽

Author(s):

Luis Ruilope ◽

Enrique Morales

Keyword(s):

Chronic Kidney Disease ◽

Cardiovascular Risk ◽

Kidney Disease ◽

Mineralocorticoid Receptor ◽

Receptor Antagonism ◽

Mineralocorticoid Receptor Antagonism

Download Full-text

Biochemical and Paraclinical Evaluation of Organ Damage in Arterial Hypertension with Associated Chronic Kidney Disease

Revista de Chimie ◽

10.37358/rc.20.6.8183 ◽

2020 ◽

Vol 71 (6) ◽

pp. 194-204

Author(s):

Teim Baaj ◽

Ahmed Abu-Awwad ◽

Mircea Botoca ◽

Octavian Marius Cretu ◽

Elena Ardeleanu ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Cardiovascular Risk ◽

Kidney Disease ◽

Ventricular Hypertrophy ◽

Ankle Brachial Index ◽

Intima Media Thickness ◽

Organ Damage ◽

Left Ventricular ◽

Study Group ◽

Group A

Organ damages, which contribute to the overall cardiovascular risk of hypertensive patients, should be early detected, prevented and treated. The study evaluated organ damage in a hypertensive study group with chronic kidney disease (CKD), compared with a study group of hypertension without CKD. Albuminuria was present in 41.2% and reduced estimated glomerular filtration rate [60 ml/min/m2 was present in 72.5% of hypertensive with CKD. The comparison of organ damage revealed in the CKD group a statistical significant higher prevalence of organ damage as follows: intima-media thickness ]0.9 mm in 39.9% vs 10.5%, carotid plaques in 28.2% vs 12.6%, left ventricular hypertrophy in 39.9% vs 31%, ankle brachial index in 6.2% vs 3.5%. Early detection and treatment of additional cardiovascular risk factors as dyslipidaemia and hyperglycaemia, that have significant role in the pathogenesis of organ damage, contribute to the better prevention of cardiovascular and renal complications in hypertension with CKD.

Download Full-text

Atorvastatin treatment does not abolish inflammatory mediated cardiovascular risk in subjects with chronic kidney disease

Scientific Reports ◽

10.1038/s41598-021-83273-2 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Renate M. Hoogeveen ◽

Simone L. Verweij ◽

Yannick Kaiser ◽

Jeffrey Kroon ◽

Hein J. Verberne ◽

...

Keyword(s):

Cardiovascular Disease ◽

Chronic Kidney Disease ◽

Cardiovascular Risk ◽

Kidney Disease ◽

Arterial Wall ◽

Ldl Cholesterol ◽

Statin Treatment ◽

Receptor Expression ◽

Disease Stage ◽

Cellular Inflammation

AbstractIndividuals with chronic kidney disease are at an increased risk for cardiovascular disease. This risk may partially be explained by a chronic inflammatory state in these patients, reflected by increased arterial wall and cellular inflammation. Statin treatment decreases cardiovascular risk and arterial inflammation in non-CKD subjects. In patients with declining kidney function, cardiovascular benefit resulting from statin therapy is attenuated, possibly due to persisting inflammation. In the current study, we assessed the effect of statin treatment on arterial wall and cellular inflammation. Fourteen patients with chronic kidney disease stage 3 or 4, defined by an estimated Glomerular Filtration Rate between 15 and 60 mL/min/1.73 m2, without cardiovascular disease were included in a single center, open label study to assess the effect of atorvastatin 40 mg once daily for 12 weeks (NTR6896). At baseline and at 12 weeks of treatment, we assessed arterial wall inflammation by 18F-fluoro-deoxyglucose positron-emission tomography computed tomography (18F-FDG PET/CT) and the phenotype of circulating monocytes were assessed. Treatment with atorvastatin resulted in a 46% reduction in LDL-cholesterol, but this was not accompanied by an attenuation in arterial wall inflammation in the aorta or carotid arteries, nor with changes in chemokine receptor expression of circulating monocytes. Statin treatment does not abolish arterial wall or cellular inflammation in subjects with mild to moderate chronic kidney disease. These results imply that CKD-associated inflammatory activity is mediated by factors beyond LDL-cholesterol and specific anti-inflammatory interventions might be necessary to further dampen the inflammatory driven CV risk in these subjects.

Download Full-text