Blood Purification

<i>Giới thiệu:</i> Đạt được trạng thái nước bình thường (normohydration) là một vấn đề không đơn giản trong điều trị thẩm phân máu. Ngăn ngừa những tác động có hại của việc quá tải dịch và mất nước thật sự rất khó khăn. Cần có những phương pháp xác định mục tiêu một cách khách quan và có thể áp dụng trong lâm sàng nhằm đại diện cho trạng thái nước bình thường. <i>Phương pháp:</i> Quang phổ bioimpedance toàn thân (50 tần số, 5–1,000 kHz) kết hợp với mô hình mô sinh lý có thể cung cấp một mục tiêu khách quan cho trạng thái nước bình thường dựa trên khái niệm thể tích ngoài tế bào dư thừa. Chúng tôi xem xét hiệu quả của phương pháp này trong một số ứng dụng lâm sàng gần đây. Độ chính xác để xác định thể tích dịch (ví dụ: nước ngoài tế bào), thành phần cơ thể (ví dụ: khối lượng mỡ) và tình trạng quá tải dịch đã được đánh giá ở hơn 1,000 cá nhân khỏe mạnh và bệnh nhân so với các phương pháp tham chiếu tiêu chuẩn vàng sẵn có (ví dụ: bromide, deuterium, cộng hưởng tia X năng lượng kép, plethysmography dịch khí, đánh giá lâm sàng). <i>Kết quả:</i> So sánh với các phương pháp tiêu chuẩn vàng cho thấy sự tương đồng xuất sắc [ví dụ: R² (nước toàn thân) = 0.88; trung vị ± SD (nước toàn thân) = –0.17 ± 2.7 lít]. Sự đồng thuận với đánh giá lâm sàng chất lượng cao về tình trạng dịch đã được chứng minh ở hàng trăm bệnh nhân (trung vị ± SD = –0.23 ± 1.5 lít). Mối liên hệ giữa thể tích siêu lọc và sự thay đổi trong tình trạng quá tải dịch đã được phản ánh tốt bởi phương pháp (trung vị ± SD = 0.015 ± 0.8 lít). Giá trị dự đoán của tình trạng quá tải dịch đối với tỷ lệ tử vong nhấn mạnh tầm quan trọng lâm sàng của mục tiêu nước bình thường, chỉ đứng sau sự hiện diện của bệnh tiểu đường. Mục tiêu nước bình thường khách quan có thể đạt được ở những bệnh nhân thẩm phân máu hiện tại, dẫn đến cải thiện huyết áp và giảm các biến cố bất lợi. <i>Kết luận:</i> Quang phổ bioimpedance toàn thân kết hợp với mô hình mô sinh lý lần đầu tiên cung cấp một mục tiêu khách quan và có liên quan cho việc đánh giá trọng lượng khô lâm sàng.

Both vascular calcification and inflammation are common in patients with chronic kidney disease (CKD). In patients on dialysis, there is increased coronary artery and peripheral artery calcification compared to the general population. Both intimal (atherosclerotic) and medial calcification in CKD patients are associated with increased morbidity and mortality. Vascular calcification is an active cell-mediated process, and likely reflects a transformation of vascular smooth muscle cells to osteoblast-like cells. Pooled uremic serum can induce this transformation, but the mechanism by which it does so is not yet clear. Several mediators of inflammation such as oxidation, carbonyl stress, C-reactive protein, and cytokines may directly stimulate vascular calcification. In addition, inflammation itself reduces fetuin-A, a naturally occurring inhibitor of vascular calcification which binds excess mineral in serum. The combination of the acceleration of vascular calcification together with impaired defense mechanisms creates a uremic milieu primed for extra-osseous calcification.

<b><i>Background:</i></b> Uremia-associated immune deficiency is a well-known complication of loss of renal function and contributes significantly to the overall mortality and morbidity of patients with end-stage renal disease. Chronic inflammation and increased oxidative stress are underlying the uremia-associated immune deficiency. <b><i>Summary:</i></b> In this review, the differential impact of uremia on the cellular immune system is summarized. Virtually all immune cells studied show a combination of an activated status and loss of function. However, uremia preferentially decreases the number and function of lymphoid cells while myeloid cells show normal and/or elevated cell numbers with increased production of inflammatory cytokines and reactive oxygen species. These particular changes are compatible with immunological aging, which is characterized by loss of thymic function, attrition of telomeres and an expanded memory T cell population. Similar to aging in healthy individuals, the proinflammatory and potential cardiotoxic subsets of CD28^null T cells and CD16⁺ monocytes are increased. Epigenetically changed hematopoietic stem cells may be involved in immunological aging as specific DNA regions become hypermethylated. Proinflammatory T cells and monocytes persist after kidney transplantation, which constitutes a persistent cardiovascular risk factor. Possible therapeutic options to reverse or halt uremia-associated immunological aging are discussed. <b><i>Key Messages:</i></b> Premature aging of the immune system is a dominant feature in patients with end-stage renal failure, which corresponds to immunological aging in elderly healthy individuals, which is characterized by preferential loss of cells belonging to the lymphoid cell lineage, inflammation and expansion of proinflammatory immune cells.

<b><i>Background: </i></b>Improvements in the biocompatibility of dialysis membranes have reduced biological responses elicited by blood-membrane interactions. In this article, recent technological developments in dialysis membranes with regard to biocompatibility and recent progress in the evaluation of the biocompatibility of dialysis membranes are reviewed. <b><i>Summary: </i></b>The focus of investigation into dialysis membranes in recent years has focused on not only membrane materials, but also their surface textures, which have been changed, for example, by coating with vitamin E or by changing the amount and type of hydrophilizing agents used. Research and development is directed at altering the chemical and physical properties of membrane surfaces to suppress biological responses that are particularly elicited as a result of platelet activation. To develop membranes with excellent biocompatibility, biocompatibility should be evaluated on a like-for-like basis under conditions that are similar to those in clinical settings. Evaluation using actual dialyzers can be performed using porcine blood, platelet-rich plasma isolated from porcine blood (and platelet-rich plasma with leukocytes), or suspension of neutrophils isolated from porcine blood or cultured human monocytes. <b><i>Key Messages:</i></b> Highly biocompatible dialysis membranes can be developed when the overall correlations among biological reactions are examined by integrating all data on biological responses elicited by blood-membrane interactions or mutual interactions among blood cells.

<b><i>Bối cảnh:</i></b> Hấp thụ miễn dịch (IAS) và trao đổi plasma điều trị (TPE) được coi là an toàn mặc dù fibrinogen bị loại bỏ. Cho đến nay, không có nghiên cứu nào so sánh giảm fibrinogen và nguy cơ chảy máu liên quan trong quá trình tách huyết tương. <b><i>Phương pháp:</i></b> Phân tích hồi cứu của TPE, ba bộ hấp thụ IAS và kết hợp TPE/IAS về giảm fibrinogen và tỷ lệ mắc chảy máu ở 67 bệnh nhân (1.032 liệu pháp). <b><i>Kết quả:</i></b> TPE và TPE/IAS làm giảm fibrinogen lần lượt là 64 ± 11% và 58 ± 9%, dẫn đến nồng độ <100 mg/dl trong 20% và 17% số liệu pháp. IAS làm giảm fibrinogen ít hơn TPE (26 ± 6%, p < 0.0001), dẫn đến nồng độ fibrinogen <100 mg/dl trong 1% số liệu pháp. Thể tích đã xử lý có mối tương quan với sự giảm trong TPE (r = 0.64, p < 0.01), nhưng không có ở IAS. Chảy máu xảy ra trong 1.3% (IAS), 2.3% (TPE) và 3.1% (TPE/IAS) số liệu pháp. <b><i>Kết luận:</i></b> Tình trạng giảm fibrinogen huyết xảy ra ở 20% bệnh nhân sau TPE và TPE/IAS, nhưng hiếm khi xảy ra sau IAS. IAS loại bỏ fibrinogen một cách độc lập với thể tích đã xử lý. Tóm lại, chảy máu là hiếm khi trong quá trình tách huyết tương.

<b><i>Introduction:</i></b> In clinical reports on coronavirus disease 2019 (COVID-19), the incidence of acute kidney injury (AKI) is extremely variable, although AKI is described as an independent risk factor for mortality. A meta-analysis was performed to clarify the incidence and the impact of COVID-19-related AKI on mortality. <b><i>Methods:</i></b> All trials reporting the incidence of AKI in COVID-19 patients were searched using MEDLINE, the Cochrane Library, and EMBASE databases (last update April 26, 2020). <b><i>Results:</i></b> Ten trials with a sample of 5,166 patients were included. AKI occurred in 947 out of 5,166 (18.3%) patients. AKI incidence was higher in severe cases: 62/305 severe patients developed AKI (20%) versus 27/1,268 nonsevere patients (2%) (<i>p</i> = 0.00001). AKI occurred in 475 out of 915 (52%) deceased patients versus 183 out of 2,678 (7%) survivors (<i>p</i> = 0.00001). Continuous renal replacement therapy was significantly more frequent in severe cases and in dead patients. <b><i>Conclusion:</i></b> A significant increase in mortality rate was observed in COVID patients who developed AKI, and AKI incidence was also higher in severe cases. Any supportive strategies to protect kidney could represent valuable intervention to reduce mortality in severe COVID-19 patients.

Hemodialysis (HD) membrane biocompatibility is defined as absence of complement activation. We have recently shown that circulating levels of interleukin (IL) 1 and IL-2 predict death and survival, respectively, of HD patients. Studies have assessed IL-1 in treatments with biocompatible and less biocompatible dialysis membranes, but no study has correlated circulating levels of all these immunoreactants. We assessed these immunoreactants, and temperature as an outcome, during HD in patients treated with different membranes. Twelve stable patients, receiving thrice-weekly chronic bicarbonate HD, were randomly dialyzed with three different types of membranes, composed of: Cuprophan, cuprammonium rayon modified cellulose, and Hemophan. Blood was drawn from the arterial line port before (Pre) and 15, 30, and 60 min during and after (Post) HD. Patients’ temperatures were measured before and after each treatment. The plasma concentrations of IL-1 and IL-2 and factors C3a and C5a were assessed by ELISA. There were no differences between baseline levels of any of the immunoreactants in patients treated with different dialyzers. C3a, C5a, and IL-1 levels increased significantly during HD treatments with all three different membranes. C3a, C5a, and IL-1 levels during Cuprophan and Hemophan treatments were significantly higher than the levels during modified cellulose treatment at 30 and 60 min and Post (p < 0.01). For all the immunoreactants, however, the Post levels were higher than the Pre levels. In contrast to IL-1, there were no differences in mean IL-2 levels during treatments when different membranes were compared. There were few correlations of plasma C3a and C5a levels with plasma IL-1 levels, but there was only one treatment time in one dialyzer group during which IL-2 and any of the other factors were correlated. Pre and Post temperature values and percent change in temperature were not correlated with any of the immunoreactants measured. These data show that C3a, C5a, and IL-1 responses are similar, but not identical, during treatments with different membranes. The response of circulating IL-2 levels to treatments is quite different from that of plasma C3a, C5a and IL-1 levels and suggests that these changes are not solely due to treatment factors. Treatment with modified cellulose membranes is associated with a different immunoreactive profile as compared with patients dialyzed using other cellulose membranes. We suggest that circulating IL-1 levels are good biocompatibility markers.