Background: The relationship between oral activated charcoal (OAC) and hyperphosphatemia and vascular calcification is not completely clear. We observed and recorded the effects of OAC on hyperphosphatemia and vascular calcification in stage 3-4 chronic kidney disease (CKD).
Methods: In a randomized controlled study, we included 97 patients with stage 3-4 CKD. In the first phase of the experiment, the patients were randomly divided into the OAC group and placebo group. The endpoint of this phase was the development of hyperphosphatemia. The patients with hyperphosphatemia were selected into the second phase of the study. These patients underwent coronary artery multidetector computed tomography (MDCT) and were randomly divided into three groups: the OAC group, the calcium carbonate (CC) group and the lanthanum carbonate (LC) group.
Results: The first and second phases of the experiment were followed for 12 months. In the first phase of the experiment, there was a statistically significant difference in the proportion of patients with hyperphosphatemia between the OAC and placebo groups (28.57% vs. 79.17%, X = 24.958, P = 0.000). In the second phase, the differences in coronary calcification score (CACS) between the OAC group, the CC group and the LC group were statistically significant (525.5 ± 104.2 vs 688.1 ± 183.7 vs 431.4 ± 122.5, P < 0.01).
Conclusion: Oral activated charcoal effectively delays the onset of hyperphosphatemia in patients with chronic kidney disease. OAC appears to delay the development of vascular calcifications in stage 3-4 CKD patients.
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http://dx.doi.org/10.1007/s40620-018-00571-1 | DOI Listing |
Sci Adv
January 2025
Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, P. R. China.
It is urgent for patients with chronic kidney disease (CKD) to develop a robust and facile therapy for effective control of serum phosphate and reasonable regulation of gut microbiota, which are aiming to prevent cardiovascular calcification and reduce cardiovascular complications. Here, bioinspired by intestinal microstructures, we developed biomimetic wrinkled prebiotic-containing microspheres with enhanced intestinal retention and absorption for reducing hyperphosphatemia and vascular calcification of CKD model rats. The resultant CSM@5 microspheres exhibited favorable phosphate binding capacity in vitro and could effectively reduce serum concentration of phosphorous in vivo.
View Article and Find Full Text PDFNephrol Dial Transplant
January 2025
Division of Nephrology and Section of Mineral Metabolism, Department of Medicine, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, AL, USA.
Elevations in systemic phosphate levels, also called hyperphosphatemia, occur in chronic kidney disease (CKD) and during the normal aging process and are associated with various pathologies, such as cardiovascular injury. Experimental studies suggest that at high serum concentrations, phosphate can induce osteogenic differentiation of vascular smooth muscle cells and contribute to vascular calcification. However, the precise underlying mechanism leading to cardiovascular injury is not well understood.
View Article and Find Full Text PDFJ Med Case Rep
December 2024
Liver Cancer Institute, National Clinical Research Center for Interventional Medicine, Zhongshan Hospital, Fudan University, 136 Yi Xue Yuan Road, Shanghai, 200032, People's Republic of China.
Background: Tumor lysis syndrome is a life-threatening complication in the treatment of cancer. However, it rarely occurs in solid tumors, especially in hepatocellular carcinoma.
Case Presentation: We present a 52-year-old male Asian patient with advanced hepatocellular carcinoma treated with hepatic artery infusion chemotherapy that resulted in tumor lysis syndrome.
FASEB J
December 2024
Xinxiang Key Laboratory of Metabolism and Integrative Physiology, School of Forensic Medicine, Xinxiang Medical University, Xinxiang, Henan, China.
Vascular calcification (VC), associated with high cardiovascular mortality in patients with chronic kidney disease (CKD), involves osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs). O-GlcNAcylation, a dynamic post-translational modification, is closely linked to cardiovascular diseases, including VC. However, the exact role and molecular mechanism of O-GlcNAc signaling in abnormal mineral metabolism-induced VC remain unclear.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Medical and Surgical Sciences, "Magna Grecia" University, 88100 Catanzaro, Italy.
Vascular calcification (VC) is a biological phenomenon characterized by an accumulation of calcium and phosphate deposits within the walls of blood vessels causing the loss of elasticity of the arterial walls. VC plays a crucial role in the incidence and progression of chronic kidney disease (CKD), leading to a significant increase in cardiovascular mortality in these patients. Different conditions such as age, sex, dyslipidemia, diabetes, and hypertension are the main risk factors in patients affected by chronic kidney disease.
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