Acute kidney injury in hematopoietic stem cell transplantation.

PURPOSE OF REVIEW: Acute kidney injury (AKI) in the setting of hematopoietic stem cell transplantation (HSCT) is common in pediatric and adult patients. The incidence ranges from 12 to 66%, and development of AKI in the posttransplant course is independently associated with higher mortality. RECENT FINDINGS: Patients who undergo HSCT have many risk factors for developing AKI, including sepsis, use of nephrotoxic medications, graft versus host disease (GVHD), and veno-occlusive disease (VOD). In addition, engraftment syndrome/cytokine storm, transplant-associated thrombotic microangiopathy (TA-TMA), and less common infections with specific renal manifestations, such as BK and adenovirus nephritis, may lead to kidney injury. There has been significant advancement in the understanding of TA-TMA in particular, especially the role of the complement system in its pathophysiology. The role of early dialysis has been explored in the pediatric population, but not well studied in adult HSCT recipients SUMMARY: This review provides an update on the risk factors, causes, and treatment approaches to HSCT-associated AKI.

Emerging Concepts in Hematopoietic Stem Cell Transplantation-Associated Renal Thrombotic Microangiopathy and Prospects for New Treatments.

Thrombotic microangiopathy associated with hematopoietic stem cell transplantation (HSCT-TMA) is a well-recognized complication of HSCT that has a high risk for death. Even in patients who survive, HSCT-TMA is associated with long-term morbidity and chronic organ injury. HSCT-TMA is a multisystem disease that often affects the kidneys. Renal manifestations of HSCT-TMA include reduced glomerular filtration rate, proteinuria, and hypertension. Understanding of the pathophysiology of HSCT-TMA has expanded in the last decade. Endothelial injury plays a major role. Recent studies also suggest involvement of complement activation. HSCT-TMA has also been considered by some to be an endothelial variant of graft-versus-host disease. Understanding the pathophysiology of HSCT-TMA and its association with activation of the complement system may aid in developing novel therapeutic options. In this review, we summarize current knowledge focusing on epidemiology and prognosis, evidence of complement activation, and endothelial injury; the possible link to graft-versus-host disease; and treatment options for HSCT-TMA.