JS-NG-5: THROMBOTIC MICROANGIOPATHY OR MALIGNANT HYPERTENSION: WHICH COMES FIRST? A CASE REPORT FROM A TERTIARY CARE HOSPITAL

Abstract

A 66-year-old woman with a history of arterial hypertension was admitted to the emergency department (ED) due to disorientation. She reported a severe headache, nausea, vomiting in the evening prior the admission; her blood pressure (BP) when the ambulance arrived was 220/100 mmHg. During admission, BP was 158/91 mmHg, pulse 95 beats/minute, oxygen saturation 88% on room air, body temperature 36.6°C. The urine examination showed that urine protein was 3+, red blood cell count 10 mg/L. The whole blood cell analysis revealed neutrophilic leukocytosis, thrombocytopenia (Table). There was 1 schistocyte seen in the peripheral blood smear. The serum creatinine and urea values were raised (Table) with elevated level of D-dimers (1690 mcg/L (< 250 mcg/L)). Head CT showed no signs of hemorrhage or ischemia. Ceftriaxone, ampicillin, and acyclovir were initiated for suspected neuro-infection, she also underwent transfusion with 4 units of platelets due to thrombocytopenia. Patients GCS fell from 11 to 9 over 13 hours, therefore she was transferred to the intensive care unit (ICU). Cerebrospinal fluid analysis showed cytosis 15 cells/mcL (predominance of lymphocytes) and protein level of 1,073 g/L; PCR panel for the most common bacterial and viral meningitis agents came back negative. On day 2, lactate dehydrogenase level was raised at 3086 U/L (125–243 U/L), haptoglobin was < 0.08 g/L (0.3–2.0 g/L) and Coombs test was negative. Due to worsening renal function (Table) hemodialysis was initiated. The differential diagnosis included thrombotic thrombocytopenic purpura, atypical hemolytic-uremic syndrome (HUS), secondary thrombotic microangiopathy (TMA), immune thrombocytopenic purpura (ITP) and disseminated intravascular coagulation (DIC). ADAMTS-13, CH50, SC5b-9 levels were tested (0.53 TV/ml (0.40–1.50 TV/ml), 60 U Eq/ml (55–75 U Eq/ml), 4689 ng/ml (200–325 ng/ml), respectively). The patient started on plasmapheresis. On day 3, fundoscopy showed cotton wool spots (ischemia) with hemorrhages and soft exudates next to the optic nerve disc; intravenous methylprednisolone pulse therapy was administered (1 g daily for three days followed by oral methylprednisolone 32 mg daily). Renal biopsy on day 5 revealed active TMA damaging the glomeruli and acute tubular necrosis. After 15 days in the ICU, she remained hypertensive and anuric despite given treatment. Moreover, pulmonary edema occurred on day 15. Malignant hypertension (MH) is characterized by severe hypertension and multi-organ ischemic complications. It can cause TMA and the overall presentation may imitate primary TMA. The approach of renal TMA in MH remains challenging. Herein, we reported a case of MHT with biopsy-proven TMA in the kidney.