SHARE @ Advocate Health - Midwest - Scientific Day: Drug Induced Microangiopathy: The Vascular Consequences of Abuse
 

Affiliations

Advocate Christ Medical Center

Abstract

Introduction/Background:

Thrombotic microangiopathy (TMA) is a syndrome causing thrombocytopenia and microangiopathic hemolytic anemia. It can be induced by drugs, pathogens, or the immune system. Drug-induced TMA is most often caused by chemotherapy agents, while cocaine-induced TMA is rare. A case of a patient with TMA, acute renal failure, thrombocytopenia, and MAHA after crack cocaine use is presented.

Description:

A 50-year-old male with COPD, hypertension, and crack cocaine use was initially hospitalized at an outside hospital for bloody diarrhea, shortness of breath, hematuria, fever, and chills after smoking crack cocaine. Initially treated for COPD exacerbation with antibiotics and steroids, he developed acute urinary retention, worsening creatinine (2.23 to 11.93 mg/dL), and metabolic acidosis requiring bicarbonate infusion. His hemoglobin dropped from 10.3 to 7.0 g/dL, and platelets from 123 to 10 K/mcL. Transferred to our hospital for suspected thrombotic microangiopathy (TMA) and plasmapheresis, he presented with elevated creatinine (12.80 mg/dL), severe anemia, low C3, schistocytes, and normal ADAMTS13. Testing for autoimmune and infectious causes was negative. Hemodialysis and plasmapheresis sessions were initiated. After treatment, kidney function gradually improved, and weekly eculizumab infusions were done. Nephrology and hematology advised continued hemodialysis and eculizumab with outpatient follow-up.

Discussion:

TMA is caused by various factors, including drug-induced, complement-mediated, hemolytic uremic syndrome (HUS), and thrombotic thrombocytopenic purpura (TTP). Our patient's TMA was likely due to crack cocaine use given the symptom onset after consumption, presence of schistocytes, low C3 levels, and normal ADAMTS13. Cocaine-induced TMA can result from activating the complement cascade, vasoconstriction, vascular damage, and platelet activation. Reports show cocaine depletes platelets by triggering the alternative complement pathway, leading to low C3 and normal C4, mirroring our patient’s findings. Cocaine-induced vasoconstriction impairs renal blood flow, leading to acute tubular necrosis and renal failure. Although renal biopsy could confirm TMA, it is unnecessary for diagnosis and contraindicated in acute kidney injury (AKI). In TMA cases, obtaining a thorough medical history, including drug use, is essential. Treating drug-induced TMA involves stopping the offending agent and providing supportive care. When TTP or TMA is suspected, initiating anti-complement therapy like eculizumab is prudent.

Presentation Notes

Presented at Scientific Day; May 21, 2025; Park Ridge, IL.

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May 21st, 11:41 AM May 21st, 1:15 PM

Drug Induced Microangiopathy: The Vascular Consequences of Abuse

Introduction/Background:

Thrombotic microangiopathy (TMA) is a syndrome causing thrombocytopenia and microangiopathic hemolytic anemia. It can be induced by drugs, pathogens, or the immune system. Drug-induced TMA is most often caused by chemotherapy agents, while cocaine-induced TMA is rare. A case of a patient with TMA, acute renal failure, thrombocytopenia, and MAHA after crack cocaine use is presented.

Description:

A 50-year-old male with COPD, hypertension, and crack cocaine use was initially hospitalized at an outside hospital for bloody diarrhea, shortness of breath, hematuria, fever, and chills after smoking crack cocaine. Initially treated for COPD exacerbation with antibiotics and steroids, he developed acute urinary retention, worsening creatinine (2.23 to 11.93 mg/dL), and metabolic acidosis requiring bicarbonate infusion. His hemoglobin dropped from 10.3 to 7.0 g/dL, and platelets from 123 to 10 K/mcL. Transferred to our hospital for suspected thrombotic microangiopathy (TMA) and plasmapheresis, he presented with elevated creatinine (12.80 mg/dL), severe anemia, low C3, schistocytes, and normal ADAMTS13. Testing for autoimmune and infectious causes was negative. Hemodialysis and plasmapheresis sessions were initiated. After treatment, kidney function gradually improved, and weekly eculizumab infusions were done. Nephrology and hematology advised continued hemodialysis and eculizumab with outpatient follow-up.

Discussion:

TMA is caused by various factors, including drug-induced, complement-mediated, hemolytic uremic syndrome (HUS), and thrombotic thrombocytopenic purpura (TTP). Our patient's TMA was likely due to crack cocaine use given the symptom onset after consumption, presence of schistocytes, low C3 levels, and normal ADAMTS13. Cocaine-induced TMA can result from activating the complement cascade, vasoconstriction, vascular damage, and platelet activation. Reports show cocaine depletes platelets by triggering the alternative complement pathway, leading to low C3 and normal C4, mirroring our patient’s findings. Cocaine-induced vasoconstriction impairs renal blood flow, leading to acute tubular necrosis and renal failure. Although renal biopsy could confirm TMA, it is unnecessary for diagnosis and contraindicated in acute kidney injury (AKI). In TMA cases, obtaining a thorough medical history, including drug use, is essential. Treating drug-induced TMA involves stopping the offending agent and providing supportive care. When TTP or TMA is suspected, initiating anti-complement therapy like eculizumab is prudent.

 

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