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Kidney Week

Abstract: PO0542

Evaluation of Thromboelastometry and Multiple Electrode Aggregometry in ESRD

Session Information

Category: CKD (Non-Dialysis)

  • 2102 CKD (Non-Dialysis): Clinical, Outcomes, and Trials

Authors

  • Abdelmaguid, Alyaa, King’s Kidney Care, King’s College Hospital, London, United Kingdom
  • Roberts, Lara N., King’s Thrombosis Centre, Department of Haematological Medicine, King’s College Hospital NHS Foundation Trust, London, United Kingdom
  • Joslin, Jennifer R., King’s Kidney Care, King’s College Hospital, London, United Kingdom
  • Hunt, Beverley, Thrombosis and Haemostasis Centre, Guy’s and St Thomas’ NHS Foundation Trust, London, United Kingdom
  • Parmar, Kiran H., Thrombosis and Haemostasis Centre, Guy’s and St Thomas’ NHS Foundation Trust, London, United Kingdom
  • Bramham, Kate, King’s Kidney Care, King’s College Hospital, London, United Kingdom
Background

Bleeding and thrombosis rates are paradoxically increased in chronic kidney disease (CKD), but risk assessment for both is not possible with routine laboratory tests. We aimed to evaluate haemostatic changes in CKD stage 5 patients with modern techniques; using thromboelastometry (TEM), multiple electrode aggregometry (MEA), markers of thrombogenesis, fibrinolysis and endothelial activation.

Methods

TEM, MEA, thrombin antithrombin (TAT), alpha-2 antiplasmin, d-dimer and Intercellular Adhesion Molecule-1 (ICAM-1) were quantified in 50 CKD Stage 5 patients (including 20 haemodialysis patients) and 30 healthy controls. Patients taking antiplatelet agents were excluded from MEA analysis.

Results

TEM parameters showed hypercoagulability, with increased maximal clot firmness (MCF) & shorter clot formation time (CFT); and D-dimer, TAT and ICAM-concentrations were also increased in CKD Stage 5 patients compared to HC (Table 1).
Platelet dysfunction was evident in CKD Stage 5 with lower aggregation in ADPtest and TRAPtest compared to HC.

Conclusion

Our study shows that the prothrombotic changes in CKD Stage 5 are due to increased coagulation and endothelial activation. Bleeding tendency may relate to platelet dysfunction and possibly increased fibrinolytic activation.

Table (1): Comparison of TEM, MEA, Alpha-2 Antiplasmin, D-dimer, Thrombin Antithrombin and ICAM-1 between Healthy Controls and CKD Stage 5 (Median and Interquartile Range (IQR))
 Healthy Controls
n=30
CKD Stage 5
n=50
p-value
TEM   
EXTEM CT (42-74 sec)56 (52,60)58 (55,62)p=0.056
EXTEM CFT (46-148 sec)68 (62,81)49 (40,66)p<0.001
EXTEM MCF (49-71 mm)67 (65,70)72 (67,74)p<0.001
FIBTEM MCF (9-25mm)18 (15, 21)25 (20, 32)p=0.004
MEA   
ADPtest (57-113 U)61 (41,78)37 (20,61)p=0.005
ASPItest (71-115 U)75 (56,89)64 (48,100)p=0.904
TRAPtest (84-128 U)112 (84,121)78 (53,116)p=0.012
Alpha-2 Antiplasmin ug/L2173 (994,3641)3075 (622,8000)p=0.266
D-dimer µg/mL FEU0.22 (0.14, 0.30)0.76 (0.39, 1.52)p<0.001
Thrombin Antithrombin ug/L1.65 (1.01,2.49)2.26 (1.58,3.82)p=0.019
ICAM-1 ug/L222 (191,248)288 (249,326)p<0.001

TEM: Thromboelastometry, CT: Clot Time, CFT: Clot Firmness Time, MCF: Maximum Clot Firmness, MEA: Multiple Electrode Aggregometry, ICAM-1: Intercellular Adhesion Molecule-1