ABSTRACT
INTRODUCTION: Severe COVID-19 infections increase the risk of thrombotic events and Intensive Care Units reported increased extracorporeal circuit clotting (ECC) in COVID-19 patients with acute kidney injury. We wished to determine whether hemodialysis (HD) patients with COVID-19 also have increased risk of circuit clotting. METHODS: We reviewed coagulation studies and HD records, 4 weeks before and after COVID-19 polymerase chain reaction detection in HD patients between April 2020 and June 2021. FINDINGS: Sixty-eight (33.5%) of 203 HD patients with COVID-19, 65% male, mean age 64.9 ± 15.3 years, experienced some circuit clotting, and no clotting recorded prior to positive test results. In those who experienced ECC, prothrombin, activated partial thromboplastin or thrombin times were not different, whereas median factor VIII (273 [168-419] vs. 166 [139-225] IU/dl, p < 0.001), D-dimers (2654 [1381-6019] vs. 1351 [786-2334] ng/ml, p < 0.05), and fibrinogen (5.6 ± 1.4 vs. 4.9 ± 1.4 g/L, p < 0.05) were greater. Antithrombin (94 [83-112] vs. 89 [84-103] IU/dl), protein C (102 [80-130] vs. 86 [76-106] IU/dl), protein S (65 [61-75] vs. 65 [52-79] IU/dl) and platelet counts (193 [138-243] vs. 174 [138-229] × 109 /L) did not differ. On multivariable logistic analysis, circuit clotting was associated with log factor VIII (odds ratio [OR] 14.8 (95% confidence limits [95% CL] 1.12-19.6), p = 0.041), fibrinogen (OR 1.57 [95% CL 1.14-21.7], p = 0.006) and log D dimer (OR 4.8 [95% CL 1.16-12.5], p = 0.028). DISCUSSION: Extracorporeal circuit clotting was increased within 4 weeks of testing positive for COVID-19. Clotting was associated with increased factor VIII, fibrinogen and D-dimer, suggesting that the risk of circuit clotting was related to the inflammatory response to COVID-19.
ABSTRACT
BACKGROUND: Patients with COVID-19 infection are at increased risk of thrombosis. We wished to determine whether this was is due to an increase in prothrombotic or reduction in anticoagulant factors and whether heparin would be an appropriate anticoagulant. METHODS: We measured routine coagulation and prothrombotic factors in dialysis patients after a positive COVID-19 test between March 2020 -April 2021. RESULTS: Routine coagulation tests were measured in 227 dialysis patients, 148 males (65.2%), median age 67.5 (53.8-77.0) years. The international normalized ratio was prolonged in 11.5%, activated partial thromboplastin time in 48.5%, thrombin time in 57%. Factor VIII was increased in 59.1%, fibrinogen 73.8%, and D-dimer 95.5%. Protein C was reduced in 15.3%, protein S 28%, and antithrombin (AT) in 12.1%. Two patients were Lupus anticoagulant positive, and two Factor VLeiden positive. Factor VIII levels increased with clinical disease; outpatients 159 (136-179) IU/dl, hospitalized but not ventilated 228 (167-311) IU, ventilated 432 (368-488) IU/dl (p < 0.01). Overall 75% had an AT level ≥ 88 IU/dl (reference range 79-106), but only 11.7% of non-hospitalized patients compared to 45% of those who died, p < 0.01, fibrinogen, D-dimers, and protein S or C did not differ with clinical disease severity, whether patients required hospital admission or not and between survivors and those who died. CONCLUSION: COVID-19 dialysis patients have increased levels of fibrinogen and D-Dimers, but only factor VIII levels in the clotting profile increased with clinical disease severity increasing systemic hypercoagulability. AT concentrations are maintained and as such should not compromise anticoagulation with heparins.