Mubarak M, Raza A, Rashid R, Sapna F, Shakeel S. Thrombotic microangiopathy after kidney transplantation: Expanding etiologic and pathogenetic spectra. World J Transplant 2024; 14(1): 90277 [PMID: 38576763 DOI: 10.5500/wjt.v14.i1.90277]
Corresponding Author of This Article
Muhammed Mubarak, MD, Professor, Department of Pathology, Sindh Institute of Urology and Transplantation, Chand Bibi Road, Karachi 74200, Sindh, Pakistan. drmubaraksiut@yahoo.com
Research Domain of This Article
Transplantation
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Transplant. Mar 18, 2024; 14(1): 90277 Published online Mar 18, 2024. doi: 10.5500/wjt.v14.i1.90277
Thrombotic microangiopathy after kidney transplantation: Expanding etiologic and pathogenetic spectra
Muhammed Mubarak, Amber Raza, Rahma Rashid, Fnu Sapna, Shaheera Shakeel
Muhammed Mubarak, Rahma Rashid, Shaheera Shakeel, Department of Histopathology, Sindh Institute of Urology and Transplantation, Karachi 74200, Sindh, Pakistan
Amber Raza, Department of Nephrology, Sindh Institute of Urology and Transplantation, Karachi 74200, Sindh, Pakistan
Fnu Sapna, Department of Pathology, Montefiore Medical Center, The University Hospital for Albert Einstein School of Medicine, Bronx, NY 10461, United States
Author contributions: Mubarak M, Raza A, Rashid R, Sapna F, Shakeel S contributed equally to this work; Mubarak M and Raza A designed the research study; Mubarak M, Raza A, Rashid R, Sapna F, Shakeel S performed the research; Mubarak M and Raza A wrote the manuscript; Mubarak M, Raza A, Rashid R, Sapna F, Shakeel S have read and approve the final manuscript.
Conflict-of-interest statement: All authors have no conflict-of-interest to declare.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Muhammed Mubarak, MD, Professor, Department of Pathology, Sindh Institute of Urology and Transplantation, Chand Bibi Road, Karachi 74200, Sindh, Pakistan. drmubaraksiut@yahoo.com
Received: November 29, 2023 Peer-review started: November 29, 2023 First decision: January 15, 2024 Revised: January 28, 2024 Accepted: March 4, 2024 Article in press: March 4, 2024 Published online: March 18, 2024
Abstract
Thrombotic microangiopathy (TMA) is an uncommon but serious complication that not only affects native kidneys but also transplanted kidneys. This review is specifically focused on post-transplant TMA (PT-TMA) involving kidney transplant recipients. Its reported prevalence in the latter population varies from 0.8% to 14% with adverse impacts on both graft and patient survival. It has many causes and associations, and the list of etiologic agents and associations is growing constantly. The pathogenesis is equally varied and a variety of pathogenetic pathways lead to the development of microvascular injury as the final common pathway. PT-TMA is categorized in many ways in order to facilitate its management. Ironically, more than one causes are contributory in PT-TMA and it is often difficult to pinpoint one particular cause in an individual case. Pathologically, the hallmark lesions are endothelial cell injury and intravascular thrombi affecting the microvasculature. Early diagnosis and classification of PT-TMA are imperative for optimal outcomes but are challenging for both clinicians and pathologists. The Banff classification has addressed this issue and has developed minimum diagnostic criteria for pathologic diagnosis of PT-TMA in the first phase. Management of the condition is also challenging and still largely empirical. It varies from simple maneuvers, such as plasmapheresis, drug withdrawal or modification, or dose reduction, to lifelong complement blockade, which is very expensive. A thorough understanding of the condition is imperative for an early diagnosis and quick treatment when the treatment is potentially effective. This review aims to increase the awareness of relevant stakeholders regarding this important, potentially treatable but under-recognized cause of kidney allograft dysfunction.
Core Tip: Thrombotic microangiopathy (TMA) is a pattern of microvascular injury characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and multi-organ dysfunction. It is not a specific disease but rather a clinicopathological syndrome associated with numerous causes and conditions. It can also involve kidney allograft and can lead to graft dysfunction and loss. Posttransplant-TMA is distinct from native kidney TMA in certain respects and poses significant diagnostic and therapeutic challenges. A thorough understanding of the condition and the development of consensus-based diagnostic criteria are imperative for an early diagnosis and timely treatment to achieve best patient outcomes.
