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With a mean worldwide prevalence of 13%, chronic kidney disease imposes a massive health burden on our society. In addition to reduced kidney function, patients with chronic kidney disease increasingly suffer from cardiovascular diseases affecting the heart and vasculature. Cardiovascular diseases account for around half of the deaths of patients with advanced chronic kidney disease. However, therapeutic options are highly insufficient. The pathological mechanisms that underlie increased cardiovascular risk in patients with chronic kidney disease remain largely unknown. This Special Issue provides insights into comorbidities in CKD patients, mainly focused on increased cardiovascular risk, and summarizes current knowledge of underlying pathophysiological mechanisms.

arterial stiffness --- carotid–femoral pulse wave velocity --- hemodialysis --- p-cresyl sulfate --- uremic toxins --- arterial calcification --- lipid metabolism --- inflammation --- coagulation --- endothelial dysfunction --- epigenetics --- chronic kidney disease --- uremic cardiopathy --- left ventricular hypertrophy --- phosphate --- PTH --- FGF23 --- klotho --- sclerostin --- chronodisruption --- chronodisruptor --- circadian rhythm --- internal clock --- uremia --- uremic cardiomyopathy --- organ crosstalk --- cardiorenal syndrome --- left-ventricular hypertrophy --- heart failure --- cardiac fibrosis --- cardiovascular disease --- vascular calcification --- experimental rodent models --- FGFG23 --- Klotho --- Wnt/β-catenin --- CKD --- parathyroid hormone --- secondary hyperparathyroidism --- uremic toxin --- ageing --- end-stage kidney disease --- premature ageing --- senescence --- bone --- gut --- cardiovascular --- CKD–MBD --- comorbidity --- fibrosis --- calcification

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• Reference Manager
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With a mean worldwide prevalence of 13%, chronic kidney disease imposes a massive health burden on our society. In addition to reduced kidney function, patients with chronic kidney disease increasingly suffer from cardiovascular diseases affecting the heart and vasculature. Cardiovascular diseases account for around half of the deaths of patients with advanced chronic kidney disease. However, therapeutic options are highly insufficient. The pathological mechanisms that underlie increased cardiovascular risk in patients with chronic kidney disease remain largely unknown. This Special Issue provides insights into comorbidities in CKD patients, mainly focused on increased cardiovascular risk, and summarizes current knowledge of underlying pathophysiological mechanisms.

Medicine --- arterial stiffness --- carotid–femoral pulse wave velocity --- hemodialysis --- p-cresyl sulfate --- uremic toxins --- arterial calcification --- lipid metabolism --- inflammation --- coagulation --- endothelial dysfunction --- epigenetics --- chronic kidney disease --- uremic cardiopathy --- left ventricular hypertrophy --- phosphate --- PTH --- FGF23 --- klotho --- sclerostin --- chronodisruption --- chronodisruptor --- circadian rhythm --- internal clock --- uremia --- uremic cardiomyopathy --- organ crosstalk --- cardiorenal syndrome --- left-ventricular hypertrophy --- heart failure --- cardiac fibrosis --- cardiovascular disease --- vascular calcification --- experimental rodent models --- FGFG23 --- Klotho --- Wnt/β-catenin --- CKD --- parathyroid hormone --- secondary hyperparathyroidism --- uremic toxin --- ageing --- end-stage kidney disease --- premature ageing --- senescence --- bone --- gut --- cardiovascular --- CKD–MBD --- comorbidity --- fibrosis --- calcification --- arterial stiffness --- carotid–femoral pulse wave velocity --- hemodialysis --- p-cresyl sulfate --- uremic toxins --- arterial calcification --- lipid metabolism --- inflammation --- coagulation --- endothelial dysfunction --- epigenetics --- chronic kidney disease --- uremic cardiopathy --- left ventricular hypertrophy --- phosphate --- PTH --- FGF23 --- klotho --- sclerostin --- chronodisruption --- chronodisruptor --- circadian rhythm --- internal clock --- uremia --- uremic cardiomyopathy --- organ crosstalk --- cardiorenal syndrome --- left-ventricular hypertrophy --- heart failure --- cardiac fibrosis --- cardiovascular disease --- vascular calcification --- experimental rodent models --- FGFG23 --- Klotho --- Wnt/β-catenin --- CKD --- parathyroid hormone --- secondary hyperparathyroidism --- uremic toxin --- ageing --- end-stage kidney disease --- premature ageing --- senescence --- bone --- gut --- cardiovascular --- CKD–MBD --- comorbidity --- fibrosis --- calcification

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Arterial hypertension affects about 1 billion people worldwide and it is the strongest modifiable risk factor for cardiovascular disease and related disability. Since the initial discovery of rare monogenic disorders with large effects, the role of genomics has evolved into large genome-wide association studies detecting common variants with a modest effect size. Similarly, pharmacogenomics has emerged as a new tool for understanding variability in drug response, to maximize efficacy and reduce toxicity. This book presents the most recent advances in the field of genetics and genomics of arterial hypertension and their potential impact on clinical management. The book is a useful tool for clinicians but also to the research community and those who want to be updated in the field.

Research & information: general --- Biology, life sciences --- atrial natriuretic peptide --- T2238C variant --- endothelial dysfunction --- smooth muscle cells contraction --- platelet aggregation --- epigenetics --- cardiovascular diseases --- renin --- low-renin --- hypertension --- mineralocorticoid receptor --- genetics --- aldosterone --- essential hypertension --- blood pressure --- genome-wide association studies --- exome microarray --- next-generation sequencing --- rare variants --- rare-variants association testing --- burden test --- sequence kernel association test --- hypokalemia --- low renin hypertension --- monogenic hypertension --- Liddle syndrome --- SCNN1A --- SCNN1B --- SCNN1G --- non-coding RNA --- micro RNA --- primary aldosteronism --- aldosterone-producing adenoma --- transcriptome profiing --- DNA methylation --- histone modifications --- vascular smooth muscle cells --- endothelial cells --- Kruppel-like factor 15 --- left ventricular hypertrophy --- cardiac hypertrophy --- heart failure --- genetics of left ventricular hypertrophy --- fibromuscular dysplasia --- non atherosclerotic vascular stenosis --- PHACTR1 --- genetic association --- cervical artery dissection --- spontaneous coronary arteries dissection --- CRY1 --- CRY2 --- HSD3B1 --- HSD3B2 --- cardio-tonic steroids --- endogenous ouabain --- adducin --- renal damage --- African American --- ARMC5 --- GRK4 --- CACNA1D --- endocrine hypertension --- atrial natriuretic peptide --- T2238C variant --- endothelial dysfunction --- smooth muscle cells contraction --- platelet aggregation --- epigenetics --- cardiovascular diseases --- renin --- low-renin --- hypertension --- mineralocorticoid receptor --- genetics --- aldosterone --- essential hypertension --- blood pressure --- genome-wide association studies --- exome microarray --- next-generation sequencing --- rare variants --- rare-variants association testing --- burden test --- sequence kernel association test --- hypokalemia --- low renin hypertension --- monogenic hypertension --- Liddle syndrome --- SCNN1A --- SCNN1B --- SCNN1G --- non-coding RNA --- micro RNA --- primary aldosteronism --- aldosterone-producing adenoma --- transcriptome profiing --- DNA methylation --- histone modifications --- vascular smooth muscle cells --- endothelial cells --- Kruppel-like factor 15 --- left ventricular hypertrophy --- cardiac hypertrophy --- heart failure --- genetics of left ventricular hypertrophy --- fibromuscular dysplasia --- non atherosclerotic vascular stenosis --- PHACTR1 --- genetic association --- cervical artery dissection --- spontaneous coronary arteries dissection --- CRY1 --- CRY2 --- HSD3B1 --- HSD3B2 --- cardio-tonic steroids --- endogenous ouabain --- adducin --- renal damage --- African American --- ARMC5 --- GRK4 --- CACNA1D --- endocrine hypertension