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Kidney Week

Abstract: PO0183

Thrombotic Microangiopathy as a Complication of Malignant Hypertension

Session Information

  • AKI Mechanisms - 2
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Report

  • 103 AKI: Mechanisms

Author

  • Eskarous, Hany, Easton Hospital, Easton, Pennsylvania, United States
Introduction

Thrombotic microangiopathies (TMA) are defined as disorders characterized by the presence of microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and microthrombi. Of all the known causes of TMAs, malignant hypertension is one of the most underreported ones.

Case Description

A 23-year-old African American male patient presented to the emergency department with a 2-week history of nausea, vomiting, diarrhea, and abdominal pain. His past medical history is significant for hypertension treated with lisinopril, but the patient is noncompliant with his medication. He had a blood pressure of 245/176 mmHg. Laboratory tests revealed hemoglobin of 10.7g/dl, platelet count of 88,000/microliter, white blood count of 14,300/microliter, blood urea nitrogen of 29 mg/dl, creatinine of 4.7 mg/dl (unknown prior creatinine levels ), lactate dehydrogenase of 900 units/l, low haptoglobin, serum potassium of 2.1mg/dl and normal coagulation profile. With control of blood pressure, the platelet counts improved. ADAMTS13 test and stool Shiga toxin were negative. Peripheral blood smear showed schistocytes. Workup for secondary hypertension were all negative. A diagnostic CT guided left kidney biopsy revealed active and chronic TMA.

Discussion

In our patient presenting with renal TMA and severe hypertension, TTP was thought to be less likely as the patient did not have the classical presentation of fever and neurological symptoms. In addition, thrombocytopenia and LDH levels normalized with aggressive control of blood pressure. Hence, plasma exchange was deferred. Since the patient presented with diarrhea, HUS was high on the differential, but a negative Shiga toxin PCR ruled out the possibility. Renal biopsy revealed acute and chronic TMA in renal blood vessels with focal severe arteriolosclerosis, fibrin, and onion skinning of arteries supporting the diagnosis of malignant nephrosclerosis as the cause of TMA.

Arteriolar narrowing with fibrin