Thrombocytopenia-Associated Multiple Organ Failure and Acute Kidney Injury

Trung C Nguyen; Miguel A Cruz; Joseph A Carcillo

doi:10.1016/j.ccc.2015.06.004

Thrombocytopenia-Associated Multiple Organ Failure and Acute Kidney Injury

Crit Care Clin. 2015 Oct;31(4):661-74. doi: 10.1016/j.ccc.2015.06.004. Epub 2015 Aug 7.

Authors

Trung C Nguyen¹, Miguel A Cruz², Joseph A Carcillo³

Affiliations

¹ Section of Critical Care Medicine, Department of Pediatrics, Baylor College of Medicine/Texas Children's Hospital, Center for Translational Research on Inflammatory Diseases (CTRID), Michael DeBakey VA Medical Center, Houston, TX 77030, USA. Electronic address: tcnguyen@texaschildrenshospital.org.
² Department of Medicine, Baylor College of Medicine, Center for Translational Research on Inflammatory Diseases (CTRID), Michael DeBakey VA Medical Center, Houston, TX 77030, USA.
³ Department of Critical Care Medicine and Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.

Abstract

Thrombocytopenia-associated multiple organ failure (TAMOF) is a clinical phenotype that encompasses a spectrum of syndromes associated with disseminated microvascular thromboses, such as the thrombotic microangiopathies thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS) and disseminated intravascular coagulation (DIC). Autopsies findings in TTP, HUS, or DIC reveal specific findings that can differentiate these 3 entities. Von Willebrand factor and ADAMTS-13 play a central role in TTP. Shiga toxins and the complement pathway are vital in the development of HUS. Tissue factor is the major protease that drives the pathology of DIC. Acute kidney injury (AKI) is a common feature in patients with TAMOF.

Keywords: ADAMTS-13; AKI; DIC; HUS; Platelet; TAMOF; TTP; VWF.

Publication types

Review

MeSH terms

ADAM Proteins / blood
ADAM Proteins / genetics
ADAMTS13 Protein
Acute Kidney Injury / etiology*
Acute Kidney Injury / metabolism
Antibodies, Monoclonal, Humanized / therapeutic use
Complement Inactivating Agents / therapeutic use
Complement System Proteins / metabolism
Disseminated Intravascular Coagulation / complications*
Disseminated Intravascular Coagulation / metabolism
Disseminated Intravascular Coagulation / therapy
Hemolytic-Uremic Syndrome / complications*
Hemolytic-Uremic Syndrome / genetics
Hemolytic-Uremic Syndrome / microbiology
Hemolytic-Uremic Syndrome / therapy
Humans
Multiple Organ Failure / etiology*
Multiple Organ Failure / metabolism
Multiple Organ Failure / therapy
Purpura, Thrombotic Thrombocytopenic / complications*
Purpura, Thrombotic Thrombocytopenic / genetics
Purpura, Thrombotic Thrombocytopenic / metabolism
Purpura, Thrombotic Thrombocytopenic / therapy
Shiga Toxins / metabolism
Thromboplastin / metabolism
von Willebrand Factor / genetics
von Willebrand Factor / metabolism

Substances

Antibodies, Monoclonal, Humanized
Complement Inactivating Agents
Shiga Toxins
von Willebrand Factor
Complement System Proteins
Thromboplastin
eculizumab
ADAM Proteins
ADAMTS13 Protein
ADAMTS13 protein, human

Abstract

Publication types

MeSH terms

Substances

Grants and funding