POS-013 THROMBOTIC MICROANGIOPATHY AFTER COVID-19: LACK OF EVIDENCE OF COMPLEMENT ACTIVATION? A CASE REPORT

ABSTRACT

Introduction: Evidence regarding thrombotic microangiopathy related to covid-19 is reported in the literature, particularly in severe cases. We describe a case recovered from previous asymptomatic covid-19, presenting with acute renal failure, hemolytic anemia, and low platelets. Thrombotic microangiopathy (TMA) was confirmed by renal biopsy, without immunofluorescence staining for C3c and C1q, suggesting this case is not complement-mediated. Anticoagulant therapy led to kidney function improvement. Methods: Case report. Results: A 72-year-old women with a past medical history of primary hypertension was referred to the hospital for the diagnosis of acute renal failure. Three days prior to admission, she suffered abdominal pain, decreased urine output, her blood test revealed elevated serum creatinine of 393 umol/L, and low platelets of 43.6 K/uL. She denied history of hematologic or renal disorders, yet mentioned that she found asymptomatic covid-19 one month before admission. On admission, the vital signs was significant for a blood pressure of 140/80 mmHg. Physical examination was noted with facial oedema, upper abdominal pain, otherwise unremarkable. Laboratory test confirmed acute renal failure with the ongoing increase of serum urea 30.4 mmol/L and creatinine 575 umol/L. Her total blood count discovered thrombocytopenia and anemia, with the platelet count of 50 k/uL, and the hemoglobin of 94 g/L. Lactate dehydrogenase was in upper limit of 434 U/L, and the bilirubin level was in normal range. The peripheral blood smear showed “fragmented” RBCs. Coombs’ test was negative for both direct and indirect method. Stool examination failed to detect either red or white blood cell. Haptoglobin level was 1.14 g/L, which was in normal range (0.41-2.58 g/L). Ddimer was elevated 1376 ng/mL, and the fibrinogen 6.37 g/L. Immunology investigation was conducted with the result of normal level for both complement C3 and C4, negative reaction for anti-cardiolipin IgM and IgG, anti MPO, anti PR3, RF, anti-streptolysin O. Bone marrow aspiration did not show abnormalities. There were Forrest III gastric ulcers found by gastric endoscopy (two ulcers with diameter of 9mm and 10mm, with pseudo-membrane covered). Initially she was treated symptomatically with amlodipin, intravenous PPI, and IV furosemide. As the kidney function was getting worse, hemodialysis was initiated at day 1, day 3, day 6, and day 10 of admission. Renal biopsy was performed and showed active thrombotic microangiopathy. Given the normal complement profile, and negative C3c staining on immunofluorescence of renal biopsy investigation, complement mediated TMA may not be the pathogenesis of this case. The patient was started for anticoagulant therapy, initially subcutaneous low molecular weight heparin and then oral anti-vitamin K. She obtained dramatic recovery with dialysis off, increased urine output, normalized platelets and red cell count, and serum urea and creatinine back to nearly normal range at discharge. Conclusions: Complement related thrombotic microangiopathy is a rare and severe condition. This case of TMA after covid-19 reveals a non-complement mediated pathogenesis, with different treatment. Anticoagulation is an effective therapy in hypercoagulation induced TMA. No conflict of interest