scholarly journals Coagulation Abnormalities in Renal Pathology of Chronic Kidney Disease: The Interplay between Blood Cells and Soluble Factors

Biomolecules ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1309
Author(s):  
Efthimia G. Pavlou ◽  
Hara T. Georgatzakou ◽  
Sotirios P. Fortis ◽  
Konstantina A. Tsante ◽  
Andreas G. Tsantes ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Coagulation Factors ◽  
Renal Pathology ◽  
Dialysis Session ◽  
Inhibitory System ◽  
Activation Markers ◽  
Soluble Factors ◽  
Coagulation Abnormalities ◽  
Esrd Patients

Coagulation abnormalities in renal pathology are associated with a high thrombotic and hemorrhagic risk. This study aims to investigate the hemostatic abnormalities that are related to the interaction between soluble coagulation factors and blood cells, and the effects of hemodialysis (HD) on it, in end stage renal disease (ESRD) patients. Thirty-two ESRD patients under HD treatment and fifteen healthy controls were included in the study. Whole blood samples from the healthy and ESRD subjects were collected before and after the HD session. Evaluation of coagulation included primary and secondary hemostasis screening tests, proteins of coagulation, fibrinolytic and inhibitory system, and ADAMTS-13 activity. Phosphatidylserine (PS) exposure and intracellular reactive oxygen species (iROS) levels were also examined in red blood cells and platelets, in addition to the platelet activation marker CD62P. Platelet function analysis showed pathological values in ESRD patients despite the increased levels of activation markers (PS, CD62P, iROS). Activities of most coagulation, fibrinolytic, and inhibitory system proteins were within the normal range, but HD triggered an increase in half of them. Additionally, the increased baseline levels of ADAMTS-13 inhibitor were further augmented by the dialysis session. Finally, pathological levels of PS and iROS were measured in red blood cells in close correlation with variations in several coagulation factors and platelet characteristics. This study provides evidence for a complex coagulation phenotype in ESRD. Signs of increased bleeding risk coexisted with prothrombotic features of soluble factors and blood cells in a general hyperfibrinolytic state. Hemodialysis seems to augment the prothrombotic potential, while the persisted platelet dysfunction might counteract the increased predisposition to thrombotic events post-dialysis. The interaction of red blood cells with platelets, the thrombus, the endothelium, the soluble components of the coagulation pathways, and the contribution of extracellular vesicles on hemostasis as well as the identification of the unknown origin ADAMTS-13 inhibitor deserve further investigation in uremia.

scholarly journals Soluble factors from packed red blood cells augmented LPS Induced monocyte production of IL-1Β and caspase-1

Pathology ◽  
2020 ◽  
Vol 52 ◽  
pp. S119
Author(s):  
Robert Flower ◽  
Fenny Chong ◽  
Kelly Rooks ◽  
Melinda Dean
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Soluble Factors ◽  
Packed Red Blood Cells ◽  
Caspase 1

scholarly journals Defective Ca(2+)-induced microvesiculation and deficient expression of procoagulant activity in erythrocytes from a patient with a bleeding disorder: a study of the red blood cells of Scott syndrome

Blood ◽  
1992 ◽  
Vol 79 (2) ◽  
pp. 380-388 ◽  
Author(s):  
EM Bevers ◽  
T Wiedmer ◽  
P Comfurius ◽  
SJ Shattil ◽  
HJ Weiss ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Calcium Ionophore ◽  
Coagulation Factors ◽  
Calcium Ionophore A23187 ◽  
Bleeding Disorder ◽  
Procoagulant Activity ◽  
Ionophore A23187 ◽  
Factor Va ◽  
Resealed Ghosts

The erythrocytes from a patient with Scott syndrome, a bleeding disorder characterized by an isolated defect in expression of platelet procoagulant activity, have been studied. When incubated with the calcium ionophore A23187, Scott syndrome red blood cells (RBCs) expressed less than 10% of the prothrombinase (enzyme complex of coagulation factors Va and Xa) activity of A23187-treated RBCs obtained from normal controls. Consistent with the results from enzyme assay, the ionophore-treated Scott syndrome erythrocytes exhibited diminished membrane vesiculation and decreased exposure of membrane binding sites for factor Va compared with identically treated controls. When examined by scanning electron microscopy, untreated Scott syndrome RBCs were indistinguishable from normal cells. After incubation with A23187, however, the morphology of Scott syndrome RBCs contrasted markedly from normal erythrocytes. Whereas the Ca2+ ionophore induced marked echinocytosis and spiculation of normal RBCs, Scott syndrome RBCs remained mostly discoid under these conditions, with only an occasional echinocyte-like cell observed. These aberrant responses to intracellular Ca2+ were also observed for resealed ghosts prepared from Scott syndrome erythrocytes, indicating that they are related to a defect in the membrane or membrane-associated cytoskeleton. The finding that the erythrocytes of this patient share many of the membrane abnormalities reported previously for Scott syndrome platelets suggests that this defect is common to both cell lines and involves a membrane component required for vesicle formation and for expression of prothrombinase sites.

scholarly journals Defective Ca(2+)-induced microvesiculation and deficient expression of procoagulant activity in erythrocytes from a patient with a bleeding disorder: a study of the red blood cells of Scott syndrome

Blood ◽  
1992 ◽  
Vol 79 (2) ◽  
pp. 380-388 ◽  
Author(s):  
EM Bevers ◽  
T Wiedmer ◽  
P Comfurius ◽  
SJ Shattil ◽  
HJ Weiss ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Calcium Ionophore ◽  
Coagulation Factors ◽  
Calcium Ionophore A23187 ◽  
Bleeding Disorder ◽  
Procoagulant Activity ◽  
Ionophore A23187 ◽  
Factor Va ◽  
Resealed Ghosts

Abstract The erythrocytes from a patient with Scott syndrome, a bleeding disorder characterized by an isolated defect in expression of platelet procoagulant activity, have been studied. When incubated with the calcium ionophore A23187, Scott syndrome red blood cells (RBCs) expressed less than 10% of the prothrombinase (enzyme complex of coagulation factors Va and Xa) activity of A23187-treated RBCs obtained from normal controls. Consistent with the results from enzyme assay, the ionophore-treated Scott syndrome erythrocytes exhibited diminished membrane vesiculation and decreased exposure of membrane binding sites for factor Va compared with identically treated controls. When examined by scanning electron microscopy, untreated Scott syndrome RBCs were indistinguishable from normal cells. After incubation with A23187, however, the morphology of Scott syndrome RBCs contrasted markedly from normal erythrocytes. Whereas the Ca2+ ionophore induced marked echinocytosis and spiculation of normal RBCs, Scott syndrome RBCs remained mostly discoid under these conditions, with only an occasional echinocyte-like cell observed. These aberrant responses to intracellular Ca2+ were also observed for resealed ghosts prepared from Scott syndrome erythrocytes, indicating that they are related to a defect in the membrane or membrane-associated cytoskeleton. The finding that the erythrocytes of this patient share many of the membrane abnormalities reported previously for Scott syndrome platelets suggests that this defect is common to both cell lines and involves a membrane component required for vesicle formation and for expression of prothrombinase sites.

Pro-Coagulant and Pro-Thrombotic Effects of Paclitaxel Mediated by Red Blood Cells

2018 ◽  
Vol 118 (10) ◽  
pp. 1765-1775 ◽  
Author(s):  
Keunyoung Kim ◽  
Youn-Kyeong Chang ◽  
Yiying Bian ◽  
Ok-Nam Bae ◽  
Kyung-Min Lim ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Thrombus Formation ◽  
Case Reports ◽  
Coagulation Factors ◽  
Thrombotic Risk ◽  
Kinase C ◽  
Anti Cancer ◽  
Pkc Ζ

Background Paclitaxel is one of the most widely used anti-cancer drugs, but numerous case reports of thrombotic events in the cancer patients using paclitaxel raise concern over its pro-thrombotic risk. Materials and Methods We investigated whether paclitaxel can elicit pro-thrombotic properties in red blood cells (RBCs) through phosphatidylserine (PS) exposure and microvesicle (MV) release. Results In freshly isolated human RBCs, paclitaxel induced thrombin generation through PS exposure and MV release, whereas either coagulation factors or platelets were unaffected. Paclitaxel-induced PS exposure in RBC was mediated by scramblase activation which was induced by calcium-independent protein kinase C (PKC)ζ activation. Paclitaxel also increased RBC-endothelial cell adhesion and RBC aggregate formation which can also contribute to thrombosis. Indeed, intravenous administration of paclitaxel to rats induced PS exposure and PKCζ activation in RBCs in vivo which ultimately promoted venous thrombus formation. Conclusion These results demonstrated that paclitaxel may elicit pro-thrombotic properties in RBCs through PS exposure and MV release, which can ultimately promote thrombus formation.

Trauma Blood Management: Avoiding the Collateral Damage of Trauma Resuscitation Protocols

Hematology ◽  
2010 ◽  
Vol 2010 (1) ◽  
pp. 463-464 ◽  
Author(s):  
Timothy Hannon
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Damage Control ◽  
Coagulation Factors ◽  
Evidence Based ◽  
Collateral Damage ◽  
Trauma Centers ◽  
Blood Management ◽  
Trauma Resuscitation ◽  
Civilian Trauma

Abstract The use of high ratios of red blood cells to platelets and plasma in trauma resuscitation protocols is quickly gaining favor in civilian trauma centers. The use of higher ratios of coagulation factors to red blood cells has been shown to improve outcomes in both military and civilian centers, but does the evidence support the use of a 1:1:1 ratio, as has been suggested? There is growing evidence that the use of such high ratios may be excessive and potentially harmful, and there has not been enough emphasis on the other components of evidence-based “damage control” resuscitation.

Additive roles of platelets and fibrinogen in whole-blood fibrin clot formation upon dilution as assessed by thromboelastometry

2014 ◽  
Vol 111 (03) ◽  
pp. 447-457 ◽  
Author(s):  
Marisa Ninivaggi ◽  
Gerhardus Kuiper ◽  
Marco Marcus ◽  
Hugo ten Cate ◽  
Marcus Lancé ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Whole Blood ◽  
Blood Cells ◽  
Thrombin Generation ◽  
Prothrombin Complex Concentrate ◽  
Coagulation Factors ◽  
Fibrin Clot ◽  
Clot Formation

SummaryBlood dilution after transfusion fluids leads to diminished coagulant activity monitored by rotational thromboelastometry, assessing elastic fibrin clot formation, or by thrombin generation testing. We aimed to determine the contributions of blood cells (platelets, red blood cells) and plasma factors (fibrinogen, prothrombin complex concentrate) to fibrin clot formation under conditions of haemodilution in vitro or in vivo. Whole blood or plasma diluted in vitro was supplemented with platelets, red cells, fibrinogen or prothrombin complex concentrate (PCC). Thromboelastometry was measured in whole blood as well as plasma; thrombin generation was determined in parallel. Similar tests were performed with blood from 48 patients, obtained before and after massive fluid infusion during cardiothoracic surgery. Addition of platelets or fibrinogen, in additive and independent ways, reversed the impaired fibrin clot formation (thromboelastometry) in diluted whole blood. In contrast, supplementation of red blood cells or prothrombin complex concentrate was ineffective. Platelets and fibrinogen independently restored clot formation in diluted plasma, resulting in thromboelastometry curves approaching those in whole blood. In whole blood from patients undergoing dilution during surgery, elastic clot formation was determined by both the platelet count and the fibrinogen level. Thrombin generation in diluted (patient) plasma was not changed by fibrinogen, but improved markedly by prothrombin complex concentrate. In conclusion, in dilutional coagulopathy, platelets and fibrinogen, but not red blood cells or vitamin K-dependent coagulation factors, independently determine thromboelastometry parameters measured in whole blood and plasma. Clinical decisions for transfusion based on thromboelastometry should take into account the platelet concentration.

T2 Magnetic Resonance to Monitor Hemostasis

2018 ◽  
Vol 45 (03) ◽  
pp. 247-252 ◽  
Author(s):  
Adam Cuker ◽  
Joseph Marturano ◽  
Maria Carinato ◽  
Thomas Lowery ◽  
Douglas Cines
Keyword(s):  
At Risk ◽  
Magnetic Resonance ◽  
Red Blood Cells ◽  
Platelet Function ◽  
Whole Blood ◽  
Blood Cells ◽  
Coagulation Factors ◽  
Fibrin Formation ◽  
Patients At Risk

AbstractThere is a clinical need for pragmatic approaches to measure integrated hemostatic reactions in whole blood rapidly, using small volumes of blood. The authors have applied T2 magnetic resonance (T2MR) to assess coagulation reactions based on partitioning of red blood cells and proteins that occurs during fibrin formation and platelet-mediated clot contraction. T2MR is amenable to measuring clotting times, individual coagulation factors, and platelet function. T2MR also revealed a novel “hypercoagulable” signature characterized by fibrin clots almost insusceptible to fibrinolysis that surround tessellated arrays of polyhedral erythrocytes (“third peak”). This signature, which develops under conditions associated with intense clot formation in vitro, may help identify patients at risk of developing thrombosis and for monitoring antithrombotic therapies in the future.

Hemoglobin crystals of the red blood cells in the human renal cortex: electron microscopic observations of the renal lithiasis

1978 ◽  
Vol 36 (2) ◽  
pp. 480-481
Author(s):  
Kosuke Ueda ◽  
Hiroto Washida ◽  
Nakazo Watari
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Renal Cortex ◽  
Uranyl Acetate ◽  
Osmic Acid ◽  
Renal Lithiasis ◽  
Electron Microscopic ◽  
Hemoglobin C ◽  
First Case ◽  
Ultrathin Sections

IntroductionHemoglobin crystals in the red blood cells were electronmicroscopically reported by Fawcett in the cat myocardium. In the human, Lessin revealed crystal-containing cells in the periphral blood of hemoglobin C disease patients. We found the hemoglobin crystals and its agglutination in the erythrocytes in the renal cortex of the human renal lithiasis, and these patients had no hematological abnormalities or other diseases out of the renal lithiasis. Hemoglobin crystals in the human erythrocytes were confirmed to be the first case in the kidney.Material and MethodsTen cases of the human renal biopsies were performed on the operations of the seven pyelolithotomies and three ureterolithotomies. The each specimens were primarily fixed in cacodylate buffered 3. 0% glutaraldehyde and post fixed in osmic acid, dehydrated in graded concentrations of ethanol, and then embedded in Epon 812. Ultrathin sections, cut on LKB microtome, were doubly stained with uranyl acetate and lead citrate.

Densitometric Identification of Primitive Erythroblasts After Reaction With Diaminobenzidine

1973 ◽  
Vol 31 ◽  
pp. 328-329
Author(s):  
John A. Trotter
Keyword(s):  
Red Blood Cells ◽  
Analytical Method ◽  
Blood Cells ◽  
Guinea Pigs ◽  
Specific Protein ◽  
Visual Examination ◽  
Hemoglobin Synthesis ◽  
Peroxidatic Activity ◽  
Small Density

Hemoglobin is the specific protein of red blood cells. Those cells in which hemoglobin synthesis is initiated are the earliest cells that can presently be considered to be committed to erythropoiesis. In order to identify such early cells electron microscopically, we have made use of the peroxidatic activity of hemoglobin by reacting the marrow of erythropoietically stimulated guinea pigs with diaminobenzidine (DAB). The reaction product appeared as a diffuse and amorphous electron opacity throughout the cytoplasm of reactive cells. The detection of small density increases of such a diffuse nature required an analytical method more sensitive and reliable than the visual examination of micrographs. A procedure was therefore devised for the evaluation of micrographs (negatives) with a densitometer (Weston Photographic Analyzer).

Scanning electron microscopy of erythrophagocytosis by Entamoeba histolytica trophozoites

1992 ◽  
Vol 50 (1) ◽  
pp. 880-881
Author(s):  
Victor Tsutsumi ◽  
Adolfo Martinez-Palomo ◽  
Kyuichi Tanikawa
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Red Blood Cells ◽  
Entamoeba Histolytica ◽  
Causative Agent ◽  
Blood Cells ◽  
Protozoan Parasite ◽  
Complex Phenomenon ◽  
Great Capacity ◽  
Scanning Electron

The protozoan parasite Entamoeba histolytica is the causative agent of amebiasis in man. The trophozoite or motile form is a highly dynamic and pleomorphic cell with a great capacity to destroy tissues. Moreover, the parasite has the singular ability to phagocytize a variety of different live or death cells. Phagocytosis of red blood cells by E. histolytica trophozoites is a complex phenomenon related with amebic pathogenicity and nutrition.

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