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Kidney Week

Abstract: FR-PO069

Rare Presentation of Renal Infarction Due to Protein S Deficiency

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

  • Soe, Thin Thin, New York City Health and Hospitals Corporation, New York, New York, United States
  • Amjad, Arfa, New York City Health and Hospitals Corporation, New York, New York, United States
  • Puri, Isha, New York City Health and Hospitals Corporation, New York, New York, United States
  • Azhar, Muhammad, New York City Health and Hospitals Corporation, New York, New York, United States
  • Mallappallil, Mary C., New York City Health and Hospitals Corporation, New York, New York, United States
Introduction

Protein S deficiency is a rare hematologic disorder which can be hereditary or acquired. Protein S deficiency is associated with increased risk of venous thromboembolism. However, there is no clear evidence of PS deficiency and arterial thromboembolic.

Case Description

We present the case of a 55-year-old female patient with no significant medical history who presented with 3 days of left sided flank pain, nausea and vomiting. She had mild leukocytosis, normal hemoglobin, unremarkable metabolic profile and with RBCs in urine microscopy, but no pyuria or bacteria. CAT scan of abdomen and pelvis with intravenous contrast revealed large well demarcated hypodensity in the upper pole of the left kidney, read as renal infarct (see image). CT angiogram of abdomen and pelvis was done to confirm thromboembolism, which revealed the occlusion of peripheral distal segmental branch of the distal left renal artery supplying upper pole of the kidney. She has 2 children, no history of spontaneous fetal losses. There is no family history of blood clotting disorders. She is a smoker 1 pack of cigarette for more than 30 years ( >30 pack years). Hypercoagulable work up revealed very Low protein S levels – 26%, normal protein C, antithrombin III assay, Factor V Leiden mutation, Lupus anticoagulants, Cardiolipin, Beta 2 Glycoprotein 1 ab, no PNH clone, or JAK 2 mutation. We ruled out cardiac embolic source by echocardiogram and electrocardiogram did not show any Atrial fibrillation, flutter or other arrhythmias. She was treated with oral Apixaban for 6 months, and counseled about smoking cessation.

Discussion

In literature reviews, smoking nicotine can increase risk of thrombotic events such as stroke and myocardial infarction. There are studies that prove free protein S is significantly lower in smokers, and it contributes to thrombotic complications.