Ectopic Calcification in Uremia: Where Do We Stand?

Cozzolino, Mario; Ciceri, Paola

doi:10.1159/000506178

Cited by 4 publications

(4 citation statements)

References 9 publications

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“…(v) Osteochondral transdifferentiation is induced in SMCs, ECs, stem cells, etc., which may subsequently release extracellular vesicles (EVs) to participate in and regulate calcification. (vi) Elastin is degraded, and the mineralized matrix is re‐established 11–14 . CKD, with the pathological conditions of hypercalcaemia, hyperphosphataemia, hyperthyroidism, oxidative stress, inflammation, α‐Klotho deficiency and the accumulation of uraemic toxins, such as indoxyl sulphate (IS) and advanced‐glycation end products (AGEs), will amplify these effects.…”

Section: Vc In Ckdmentioning

confidence: 99%

“…[8][9][10] Elastin is degraded, and the mineralized matrix is re-established. [11][12][13][14] CKD, with the pathological conditions of hypercalcaemia, hyperphosphataemia, hyperthyroidism, oxidative stress, inflammation, α-Klotho deficiency and the accumulation of uraemic toxins, such as indoxyl sulphate (IS) and advanced-glycation end products (AGEs), will amplify these effects.…”

Section: Vc In Ck Dmentioning

confidence: 99%

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Role of crosstalk between endothelial cells and smooth muscle cells in vascular calcification in chronic kidney disease

et al. 2021

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Chronic kidney disease (CKD) is an extremely serious health problem that causes poor health outcomes and substantial social and economic burdens worldwide. The high cardiovascular morbidity and mortality in the CKD population are mainly caused by extensive and progressive vascular calcification (VC). 1,2 Notably, in CKD patients, severe intimal calcification (known as atherosclerotic calcification and thought to originate from atherosclerosis) and medial calcification (known as Mönckeberg's sclerosis) are both prominent and can occur simultaneously, and both are accelerated with decreasing kidney function. 2,3 However, there are currently no effective treatment measures for VC. Although progress has been made in understanding the pathogenesis of VC, it is still largely assumptive and needs to be clarified. VC was previously regarded as a passive, degenerative disease. With further in-depth research, calcification has been found to be an active and adjustable process, analogous to bone formation, in

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Section: Vc In Ckdmentioning

confidence: 99%

Section: Vc In Ck Dmentioning

confidence: 99%

Role of crosstalk between endothelial cells and smooth muscle cells in vascular calcification in chronic kidney disease

et al. 2021

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“…advanced glycation end products, indoxyl-sulfate, and p-cresyl sulfate) are crucial risk factors of endothelial dysfunction prevalent in CKD or uremia patients, and endothelial dysfunction is the principal hallmark of VC [ 5 , 6 ]. Besides, the drug treatment, such as Ca-containing phosphate binders, exacerbates VC in hemodialysis patients [ 7 ]. However, the precise mechanism of VC has not been illustrated.…”

Section: Introductionmentioning

confidence: 99%

Clinical significance of serum CDC42 in the prediction of uremic vascular calcification incidence and progression

Pan

et al. 2023

Libyan Journal of Medicine

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Vascular calcification (VC) is prevalent in uremia patients, lacking effective molecular biomarkers. This study was conducted to explore the role of serum cell division cycle 42 (CDC42) in the diagnosis of uremic VC incidence and progression. We enrolled 104 uremia patients and selected arcus aortae calcification (AAC) as the outcome phenotype. Levels of CDC42, 1,25-dihydroxy vitamin D (1,25(OH) 2 -D), fibroblast growth factor-23 (FGF-23), and other laboratory parameters in the blood were measured. The receiver operator characteristic curve, the Pearson test, and the multivariate Logistic regression were used for the analysis of CDC42 diagnostic values, correlation analysis, and screening of VC risk factors, respectively. CDC42 was higher in the serum of uremia patients with VC and elevated with the increase in AAC level. Serum CDC42 level>1.025 was predictive of VC incidence with 83.58% sensitivity and 56.76% specificity, and CDC42 level>1.280 was predictive of VC progression with 73.33% sensitivity and 68.18% specificity. Serum CDC42 was positively correlated with 1,25(OH) 2 -D and FGF-23. Uremia patients with higher serum CDC42 had a higher probability of VC incidence and progression. Generally, serum CDC42 helped the diagnosis of uremic VC incidence and progression and was an independent risk factor for uremic VC progression.

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“…By contrast, ectopic calcification in other organs, such as muscles, is rare, apart from systemic calciphylaxis [ 4 , 5 ]. Although there have been reported cases so far, diffuse liver calcification is an extremely rare disorder; however, we experienced the case of a patient who developed diffuse liver calcification over a short period.…”

Section: Introductionmentioning

confidence: 99%

Hemodialysis Patient with Diffuse Liver Calcification After Septic Shock

et al. 2021

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Patient: Female, 82-year-old Final Diagnosis: Diffuse liver calcification Symptoms: Shock Medication:— Clinical Procedure: — Specialty: Nephrology Objective: Rare coexistence of disease or pathology Background: Calcification in arteries is sometimes observed in patients undergoing hemodialysis; however, ectopic calcification in other organs is uncommon. In particular, diffuse liver calcification is very rare. We report a case of rapidly developing diffuse liver calcification in a patient undergoing hemodialysis. Case Report: An 82-year-old woman started hemodialysis because of diabetic nephropathy, and her renal function worsened due to acute coronary syndrome. Percutaneous coronary intervention was conducted, and she was referred to our hospital. However, she subsequently contracted various infections, including a urinary tract infection and pneumonia. On day 43 of hospitalization, she developed septic shock and liver dysfunction due to catheter-induced infection. Although she did not have any medical history of liver disease, hypoperfusion of the liver resulted in liver dysfunction, and a computed tomography scan conducted 3 months later showed diffuse calcification in her liver. Despite recovering from septic shock, she ultimately died of multiple organ failure 21 months after admission to our hospital. Conclusions: Diffuse liver calcification is extremely rare; however, it can be observed in patients undergoing hemodialysis who experience liver hypoperfusion. The precise mechanisms underlying this disorder remain unknown, but a critically ill status and specific characteristics of hemodialysis patients may play important roles in liver calcification.

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Ectopic Calcification in Uremia: Where Do We Stand?

Cited by 4 publications

References 9 publications

Role of crosstalk between endothelial cells and smooth muscle cells in vascular calcification in chronic kidney disease

Role of crosstalk between endothelial cells and smooth muscle cells in vascular calcification in chronic kidney disease

Clinical significance of serum CDC42 in the prediction of uremic vascular calcification incidence and progression

Hemodialysis Patient with Diffuse Liver Calcification After Septic Shock

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