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Published on: June 2, 2022
Vascular calcifications in uremia: old concepts and new insights
Ulver Derici1, A Meguid El Nahas
1Gazi University, Ankara, Turkey, and Sheffield Kidney Institute, Northern General Hospital, UK.
Insights
Uremic patients face higher mortality, mainly from cardiovascular events linked to vascular calcification. Managing mineral metabolism and avoiding calcium overload are key for prevention and treatment.
Area of Science:
- Nephrology
- Cardiology
- Vascular Biology
Background:
- Uremic patients exhibit significantly higher annual mortality rates than the general population, primarily driven by cardiovascular events.
- Vascular calcification, affecting both intima and media layers, is a critical factor in cardiovascular morbidity and mortality in uremia.
- The precise mechanisms of vascular calcification in uremia are not fully understood.
Purpose of the Study:
- To review the multifaceted pathogenesis of vascular calcification in uremic patients.
- To identify contributing factors beyond traditional cardiovascular risks.
- To highlight the role of mineral metabolism disturbances and calcification inhibitors.
Main Methods:
- Literature review and synthesis of current research on uremia-associated vascular calcification.
- Analysis of factors contributing to vascular calcification, including metabolic derangements and endogenous inhibitors.
- Discussion of therapeutic implications for prevention and treatment.
Main Results:
- Vascular calcification in uremia results from a complex interplay of factors including mineral metabolism disturbances (e.g., phosphate binders, vitamin D therapy), uremia-related risks (e.g., oxidative stress, toxins), and reduced levels of calcification inhibitors (e.g., fetuin-A, MGP).
- Both procalcifying and anticalcifying influences contribute to the dynamic process of vascular calcification.
- Decreased levels of endogenous inhibitors like fetuin-A, matrix Gla protein, osteoprotegerin, and osteopontin are linked to increased extraskeletal calcification.
Conclusions:
- Effective prevention and treatment of vascular calcification in uremic patients require avoiding calcium overload and optimizing metabolic control and dialysis strategies.
- Understanding the balance between procalcifying and anticalcifying factors is crucial for therapeutic interventions.
- Multifactorial approaches addressing mineral metabolism, uremic toxins, and calcification inhibitors are essential.
Abstract:
The annual mortality rate in uremic patients, corrected for age, sex, and race, is significantly higher than in the general population. This is primarily due to cardiovascular events. Vascular calcifications play a vital role in the development of cardiovascular morbidity and subsequent increased mortality. Vascular calcification affects both vascular intima and media layers and its mechanism remains poorly understood. Over the last few years it has been shown that, in addition to traditional cardiovascular risk factors, disturbances in mineral metabolism in the uremic milieu, calcium-containing phosphate binders, and vitamin D treatment of secondary hyperparathyroidism may contribute to the pathogenesis of vascular calcifications. Other uremia-related risk factors (e.g.increased oxidized low-density lipoprotein cholesterol, uremic toxins, increased oxidative stress, dialysis and dialysate-related factors, hemodynamic overload, hyperhomocysteinemia) may also play a role. In uremic patients, apart from these facilitating factors, decreased levels of endogenous calcification inhibitors such as fetuin-Amatrix Gla protein, osteoprotegerin, and osteopontin have also been associated with increased calcium-phosphate precipitation in extraskeletal tissues. Finally, vascular calcification is the outcome of the active and dynamic balance of procalcifying and anticalcifying influences. For the prevention and treatment of vascular calcifications, it is essential to avoid treatment modalities that lead to calcium overload, achieve good metabolic control, and optimize dialysis.
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