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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Features of Lipid Disorders in Cardiovascular–Kidney–Metabolic Syndrome

  • Alexandr Ceasovschih1
  • Yusuf Ziya Şener2,3
  • Mustafa Arici4
  • Mariia Cherska5
  • Vanessa Bianconi6
  • Malik Ejubović7,8
  • Stanislav Kotlyarov9
  • Vladimir Ristovski10
  • Ahmet Yetkin11
  • Pelin Golforoush12
  • Tatyana Storozhenko13,14
  • Fotios Barkas15
6 more authors
  • Alexandru Corlateanu16
  • Pradeesh Sivapalan17,18
  • Tea Gamezardashvili19,20
  • Antonio M. Gotto21
  • Laurentiu Sorodoc1
  • Victorita Sorodoc1
21 affiliations
  1. 1Grigore T. Popa University of Medicine and Pharmacy, 700115 Iasi, Romania
  2. 2Department of Cardiology, Thoraxcentrum, Erasmus MC, 3015 CE Rotterdam, The Netherlands
  3. 3Department of Internal Medicine, Yavuzeli District State Hospital, 27907 Gaziantep, Türkiye
  4. 4Department of Nephrology, Hacettepe University, 06800 Ankara, Türkiye
  5. 5State Institution “V.P. Komisarenko Institute of Endocrinology and Metabolism of the National Academy of Medical Sciences of Ukraine”, 04114 Kyiv, Ukraine
  6. 6Department of Medicine and Surgery, University of Perugia, 06132 Perugia, Italy
  7. 7Department of Internal Medicine, Cantonal Hospital Zenica, 72000 Zenica, Bosnia and Herzegovina
  8. 8University of Zenica, 72000 Zenica, Bosnia and Herzegovina
  9. 9Department of Nursing, Ryazan State Medical University, 390026 Ryazan, Russia
  10. 10Department for Invasive and Interventional Cardiology, City General Hospital “8th of September”, 1000 Skopje, North Macedonia
  11. 11Department of Cardiology, Suşehri District State Hospital, 58600 Sivas, Türkiye
  12. 12The Francis Crick Institute, 1 Midland Rd, London NW1 1AT, UK
  13. 13Cardiovascular Center Aalst, 9300 Aalst, Belgium
  14. 14Department of Prevention and Treatment of Emergency Conditions, L.T. Malaya Therapy National Institute NAMSU, 61039 Kharkiv, Ukraine
  15. 15Department of Internal Medicine, Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110 Ioannina, Greece
  16. 16Department of Respiratory Medicine and Allergology, State University of Medicine and Pharmacy “Nicolae Testemitanu”, 2004 Chisinau, Moldova
  17. 17Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, DK-2200 Copenhagen, Denmark
  18. 18Copenhagen Respiratory Research, Department of Medicine, Copenhagen University Hospital—Herlev and Gentofte, DK-2900 Copenhagen, Denmark
  19. 19Remedical Hospital, 9/16’ Tsinandali Str., 1044 Tbilisi, Georgia
  20. 20Georgian Atherosclerosis Association, 9’ L. Managadze Str., 0144 Tbilisi, Georgia
  21. 21Weill Medical College, Cornell University, New York, NY 10065, USA
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Abstract

Cardiovascular–kidney–metabolic (CKM) syndrome is driven by the interplay of visceral adiposity, insulin resistance, chronic inflammation, oxidative stress, and progressive kidney dysfunction. These mechanisms generate a distinct atherogenic dyslipidaemic phenotype characterised by elevated triglycerides (TG), reduced high-density lipoprotein-cholesterol (HDL-C), increased apolipoprotein B (apoB)-containing lipoproteins, remnant cholesterol (RC) accumulation, small dense low-density lipoprotein (LDL) particles, and frequently elevated lipoprotein(a) [Lp(a)]. Such lipid abnormalities contribute to accelerated atherosclerosis and early renal deterioration. In turn, kidney dysfunction further amplifies lipid abnormalities. These pathways underscore the need for a timely and comprehensive lipid assessment using apoB, non-HDL-C, RC, and Lp(a) within the CKM framework. Effective lipid management is crucial for CKM syndrome treatment, with the potential to reduce residual cardiovascular and renal risk and improve long-term clinical outcomes. In this narrative review, we examine current evidence on the pathophysiological mechanisms underlying CKM-related dyslipidaemia and provide a practical framework for its assessment and management. Management requires a multimodal approach tailored to the patient’s lipid phenotype and overall cardiovascular risk, incorporating a range of lipid-lowering strategies including statins, ezetimibe, PCSK9 inhibitors, bempedoic acid, fibrates, icosapent ethyl, and emerging therapies targeting apoC-III, ANGPTL3, and Lp(a). Beyond lipid lowering, lifestyle interventions and cardiometabolic therapies such as glucagon-like peptide-1 receptor agonists, sodium-glucose cotransporter 2 inhibitors, and finerenone may provide complementary cardiometabolic and renal protection.

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Cite

BibTeXRIS
BibTeX
@article{ceasovschih2026features,
  title = {{Features of Lipid Disorders in Cardiovascular–Kidney–Metabolic Syndrome}},
  author = {Alexandr Ceasovschih and Yusuf Ziya Şener and Mustafa Arici and Mariia Cherska and Vanessa Bianconi and Malik Ejubović and Stanislav Kotlyarov and Vladimir Ristovski and Ahmet Yetkin and Pelin Golforoush and Tatyana Storozhenko and Fotios Barkas and Alexandru Corlateanu and Pradeesh Sivapalan and Tea Gamezardashvili and Antonio M. Gotto and Laurentiu Sorodoc and Victorita Sorodoc},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = sep,
  doi = {10.3390/ijms27188317},
  url = {https://www.mdpi.com/1422-0067/27/18/8317},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Features of Lipid Disorders in Cardiovascular–Kidney–Metabolic Syndrome
AU  - Alexandr Ceasovschih
AU  - Yusuf Ziya Şener
AU  - Mustafa Arici
AU  - Mariia Cherska
AU  - Vanessa Bianconi
AU  - Malik Ejubović
AU  - Stanislav Kotlyarov
AU  - Vladimir Ristovski
AU  - Ahmet Yetkin
AU  - Pelin Golforoush
AU  - Tatyana Storozhenko
AU  - Fotios Barkas
AU  - Alexandru Corlateanu
AU  - Pradeesh Sivapalan
AU  - Tea Gamezardashvili
AU  - Antonio M. Gotto
AU  - Laurentiu Sorodoc
AU  - Victorita Sorodoc
PY  - 2026
DA  - 2026/09/18
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27188317
UR  - https://www.mdpi.com/1422-0067/27/18/8317
AB  - Cardiovascular–kidney–metabolic (CKM) syndrome is driven by the interplay of visceral adiposity, insulin resistance, chronic inflammation, oxidative stress, and progressive kidney dysfunction. These mechanisms generate a distinct atherogenic dyslipidaemic phenotype characterised by elevated triglycerides (TG), reduced high-density lipoprotein-cholesterol (HDL-C), increased apolipoprotein B (apoB)-containing lipoproteins, remnant cholesterol (RC) accumulation, small dense low-density lipoprotein (LDL) particles, and frequently elevated lipoprotein(a) [Lp(a)]. Such lipid abnormalities contribute to accelerated atherosclerosis and early renal deterioration. In turn, kidney dysfunction further amplifies lipid abnormalities. These pathways underscore the need for a timely and comprehensive lipid assessment using apoB, non-HDL-C, RC, and Lp(a) within the CKM framework. Effective lipid management is crucial for CKM syndrome treatment, with the potential to reduce residual cardiovascular and renal risk and improve long-term clinical outcomes. In this narrative review, we examine current evidence on the pathophysiological mechanisms underlying CKM-related dyslipidaemia and provide a practical framework for its assessment and management. Management requires a multimodal approach tailored to the patient’s lipid phenotype and overall cardiovascular risk, incorporating a range of lipid-lowering strategies including statins, ezetimibe, PCSK9 inhibitors, bempedoic acid, fibrates, icosapent ethyl, and emerging therapies targeting apoC-III, ANGPTL3, and Lp(a). Beyond lipid lowering, lifestyle interventions and cardiometabolic therapies such as glucagon-like peptide-1 receptor agonists, sodium-glucose cotransporter 2 inhibitors, and finerenone may provide complementary cardiometabolic and renal protection.
SN  - 1422-0067
ER  -