Sami SeungMi Jin, Anushree Dugar, Andrew N Hoofnagle, Amber P Sanchez, David M Ward, Joachim H Ix, Charles Ginsberg
{"title":"Therapeutic Plasma Exchange and Changes in Calcium, Phosphate, Parathyroid Hormone, and Fibroblast Growth Factor-23.","authors":"Sami SeungMi Jin, Anushree Dugar, Andrew N Hoofnagle, Amber P Sanchez, David M Ward, Joachim H Ix, Charles Ginsberg","doi":"10.1210/clinem/dgaf400","DOIUrl":null,"url":null,"abstract":"<p><strong>Context: </strong>Therapeutic plasma exchange (TPE) removes plasma proteins and other unwanted substances, causing non-specific alterations of plasma components. A previous study showed ∼70% reduction in vitamin D metabolites following a single TPE treatment, prompting further investigation into TPE's effects on vitamin D regulators and metabolites: calcium, phosphate, parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF-23).</p><p><strong>Objective: </strong>This study examined changes in plasma and effluent levels of total calcium, phosphate, PTH, and FGF-23 in persons undergoing TPE.</p><p><strong>Methods: </strong>Measurements were taken immediately before, immediately after, and at follow-up. Paired t-tests compared the percent changes in metabolites from pre- to post-TPE.</p><p><strong>Results: </strong>Study participants (N=42) had a mean age of 55 ± 16 years, 28 (67%) were female and 32 (76%) were white. TPE led to acute changes in calcium [-9%, (95% CI -11%, -8%)], phosphate [-14%, (-18%, -11%)], and FGF-23 [-12%, (-18%, -6%)] concentrations. In contrast, PTH levels increased [91% (63%, 119%)] from baseline to post-TPE. While most metabolites returned to baseline by the follow-up visit (median 4 [IQR 3,7] days), nearly 25% of patients experienced persistent asymptomatic hypocalcemia. This persistent calcium deficit was not fully corrected by continuous IV calcium gluconate infusions administered during the study, nor by the endogenously increased PTH levels.</p><p><strong>Conclusions: </strong>These findings underscore the need for improved care protocols and vigilant monitoring of mineral metabolism TPE patients, especially those receiving long-term treatment. Further research is warranted to understand the enduring effects of TPE on mineral metabolism and develop strategies to prevent complications.</p>","PeriodicalId":520805,"journal":{"name":"The Journal of clinical endocrinology and metabolism","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Journal of clinical endocrinology and metabolism","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1210/clinem/dgaf400","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Context: Therapeutic plasma exchange (TPE) removes plasma proteins and other unwanted substances, causing non-specific alterations of plasma components. A previous study showed ∼70% reduction in vitamin D metabolites following a single TPE treatment, prompting further investigation into TPE's effects on vitamin D regulators and metabolites: calcium, phosphate, parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF-23).
Objective: This study examined changes in plasma and effluent levels of total calcium, phosphate, PTH, and FGF-23 in persons undergoing TPE.
Methods: Measurements were taken immediately before, immediately after, and at follow-up. Paired t-tests compared the percent changes in metabolites from pre- to post-TPE.
Results: Study participants (N=42) had a mean age of 55 ± 16 years, 28 (67%) were female and 32 (76%) were white. TPE led to acute changes in calcium [-9%, (95% CI -11%, -8%)], phosphate [-14%, (-18%, -11%)], and FGF-23 [-12%, (-18%, -6%)] concentrations. In contrast, PTH levels increased [91% (63%, 119%)] from baseline to post-TPE. While most metabolites returned to baseline by the follow-up visit (median 4 [IQR 3,7] days), nearly 25% of patients experienced persistent asymptomatic hypocalcemia. This persistent calcium deficit was not fully corrected by continuous IV calcium gluconate infusions administered during the study, nor by the endogenously increased PTH levels.
Conclusions: These findings underscore the need for improved care protocols and vigilant monitoring of mineral metabolism TPE patients, especially those receiving long-term treatment. Further research is warranted to understand the enduring effects of TPE on mineral metabolism and develop strategies to prevent complications.