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Vascular calcification in chronic kidney disease: an update

Georg Schlieper1, Leon Schurgers2, Vincent Brandenburg3

  • 1Department of Nephrology, RWTH University of Aachen, Aachen, Germany.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|April 29, 2015
PubMed

Insights

Cardiovascular calcification, a risk factor for disease and death, accelerates in patients with chronic kidney disease or diabetes. Preventing this calcification by balancing promoters and inhibitors is key, as reversing it is difficult.

Area of Science:

  • Cardiovascular research
  • Nephrology
  • Endocrinology

Background:

  • Cardiovascular calcification contributes significantly to morbidity and mortality.
  • Patients with chronic kidney disease and/or diabetes experience accelerated calcification in various cardiovascular tissues.
  • Calcific uraemic arteriolopathy (calciphylaxis) is a rare but severe manifestation.

Purpose of the Study:

  • To review the pathomechanisms of cardiovascular calcification, particularly in chronic kidney disease and diabetes.
  • To discuss current therapeutic strategies focusing on prevention.
  • To highlight the challenges and current research in the therapeutic regression of established calcifications.

Main Methods:

  • Review of existing literature on cardiovascular calcification.
  • Analysis of pathomechanistic pathways involving promoters and inhibitors.
  • Examination of cellular processes in vascular calcification.
  • Overview of therapeutic approaches and clinical trials.

Main Results:

  • An imbalance of calcification promoters (calcium, phosphate) and inhibitors (fetuin-A, matrix Gla protein) is central to pathogenesis.
  • Cellular processes, including vascular smooth muscle cell osteochondrogenesis and senescence, play a role.
  • Preventive measures targeting the promoter-inhibitor balance are essential.
  • Therapeutic regression of established cardiovascular calcification in humans is rarely reported.

Conclusions:

  • Preventing cardiovascular calcification by correcting biochemical and cellular imbalances is crucial.
  • Effective therapeutic strategies for reversing existing calcification are limited.
  • Ongoing clinical trials are investigating secondary prevention in patients with established cardiovascular calcification.

Keywords:
MGPVSMCcardiovascular diseasesphenotype switchvitamin K

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