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Cited by 363

The DOI matches its Crossref record; 174 of the 174 references it cites were found in a registry or an index.

Cardiovascular complications in chronic kidney disease: a review from the European Renal and Cardiovascular Medicine Working Group of the European Renal Association

Open access
Zoccali, Carmine, Mallamaci, Francesca, Adamczak, Marcin, de Oliveira, Rodrigo Bueno, Massy, Ziad A, Sarafidis, Pantelis, Agarwal, Rajiv, Mark, Patrick B, Kotanko, Peter, Ferro, Charles J, Wanner, Christoph, Burnier, Michel, Vanholder, Raymond, Wiecek, Andrzej·2023·Cardiovascular Research

Abstract

Chronic kidney disease (CKD) is classified into five stages with kidney failure being the most severe stage (stage G5). CKD conveys a high risk for coronary artery disease, heart failure, arrhythmias, and sudden cardiac death. Cardiovascular complications are the most common causes of death in patients with kidney failure (stage G5) who are maintained on regular dialysis treatment. Because of the high death rate attributable to cardiovascular (CV) disease, most patients with progressive CKD die before reaching kidney failure. Classical risk factors implicated in CV disease are involved in the early stages of CKD. In intermediate and late stages, non-traditional risk factors, including iso-osmotic and non-osmotic sodium retention, volume expansion, anaemia, inflammation, malnutrition, sympathetic overactivity, mineral bone disorders, accumulation of a class of endogenous compounds called ‘uremic toxins’, and a variety of hormonal disorders are the main factors that accelerate the progression of CV disease in these patients. Arterial disease in CKD patients is characterized by an almost unique propensity to calcification and vascular stiffness. Left ventricular hypertrophy, a major risk factor for heart failure, occurs early in CKD and reaches a prevalence of 70–80% in patients with kidney failure. Recent clinical trials have shown the potential benefits of hypoxia-inducible factor prolyl hydroxylase inhibitors, especially as an oral agent in CKD patients. Likewise, the value of proactively administered intravenous iron for safely treating anaemia in dialysis patients has been shown. Sodium/glucose cotransporter-2 inhibitors are now fully emerged as a class of drugs that substantially reduces the risk for CV complications in patients who are already being treated with adequate doses of inhibitors of the renin-angiotensin system. Concerted efforts are being made by major scientific societies to advance basic and clinical research on CV disease in patients with CKD, a research area that remains insufficiently explored.

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Registry

Crossref · 10.1093/cvr/cvad083

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Metadata

Authors
Zoccali, C., Mallamaci, F., Adamczak, M., de Oliveira, R. B., Massy, Z. A., Sarafidis, P., Agarwal, R., Mark, P. B., Kotanko, P., Ferro, C. J., Wanner, C., Burnier, M., Vanholder, R., & Wiecek, A.
Venue
Cardiovascular Research
Published
2023-05-30
Volume
119
Issue
11
Pages
2017-2032
ISSN
  • 0008-6363 (ISSN-L)
  • 1755-3245
OpenAlex
W4378745282
Cited by
363
References
174
FWCI
59.55
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Cardiovascular complications in chronic kidney disease: a review from the European Renal and Cardiovascular Medicine Working Group of the European Renal Association. https://app.cochat.ai/papers/10.1093/cvr/cvad083
The paper
Zoccali, C., Mallamaci, F., Adamczak, M., de Oliveira, R. B., Massy, Z. A., Sarafidis, P., Agarwal, R., Mark, P. B., Kotanko, P., Ferro, C. J., Wanner, C., Burnier, M., Vanholder, R., & Wiecek, A. (2023). Cardiovascular complications in chronic kidney disease: a review from the European Renal and Cardiovascular Medicine Working Group of the European Renal Association. Cardiovascular Research. https://doi.org/10.1093/cvr/cvad083

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.