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Chronic kidney disease after pediatric hematopoietic cell transplant
1University of Washington, Children's Hospital and Regional Medical Center, 4800 Sandpoint Way NE, A-7931, Seattle, WA 98105, USA. sangeeta.hingorani@seattlechildrens.org.
Insights
Kidney disease (CKD) is common after hematopoietic stem cell transplant (HCT). Further research should focus on graft-versus-host disease (GVHD) and inflammation to prevent CKD and end-stage renal disease.
Area of Science:
- Nephrology
- Oncology
- Hematology
Background:
- Hematopoietic stem cell transplantation (HCT) is increasingly used worldwide.
- Kidney disease (CKD) is a common complication following HCT, presenting as distinct clinical entities like thrombotic microangiopathy (TMA), idiopathic CKD, and nephrotic syndrome.
- The rising number of HCT procedures necessitates a better understanding of post-transplant kidney complications.
Purpose of the Study:
- To investigate the role of graft-versus-host disease (GVHD) and chronic inflammation in the development and progression of idiopathic CKD post-HCT.
- To identify patients at risk for CKD after HCT for potential intervention and prevention strategies.
- To re-evaluate the focus on total body irradiation (TBI) and explore alternative prevention strategies for CKD.
Main Methods:
- Observational study analyzing clinical data of HCT recipients.
- Review of patient records to identify causes of CKD, including GVHD, calcineurin inhibitor use, and conditioning regimens.
- Correlation analysis between specific HCT-related factors and the incidence/progression of CKD.
Main Results:
- CKD is a significant complication after HCT, with TMA, idiopathic CKD, and nephrotic syndrome being distinct entities.
- Factors beyond TBI and conditioning regimens, such as acute GVHD (aGVHD), chronic GVHD (cGVHD), and prolonged calcineurin inhibitor use, contribute to CKD.
- The independent role of GVHD and chronic inflammation in idiopathic CKD requires further investigation.
Conclusions:
- CKD management post-HCT requires collaborative efforts between nephrologists and oncologists, focusing on renal function, blood pressure, and urinalysis.
- Preventing CKD may involve reducing the inflammatory and cytokine effects of GVHD and minimizing calcineurin inhibitor exposure, rather than solely focusing on TBI reduction.
- Early identification of at-risk patients is crucial for implementing interventions to prevent CKD and progression to end-stage renal disease.
Abstract:
There are 3 clearly distinct clinical entities that occur after HCT: TMA, idiopathic CKD, and nephrotic syndrome. The potentially independent role of GVHD and chronic inflammation in the development and progression of idiopathic CKD warrants further investigation. CKD after HCT is a relatively common occurrence. As the indications for and number of transplants performed world wide increases, so will the burden of kidney disease. Identifying those patients at risk for the development of CKD will be important for potential intervention and prevention of CKD and progression to end-stage renal disease in this patient population. There are those patients who will develop CKD that is not related to TBI or the conditioning regimen but rather to complications and/or therapy that occur after HCT, specifically aGVHD and cGVHD and prolonged calcinuerin inhibitor use. The burden of management will fall not only to the nephrologists but the oncologist as well to ensure close monitoring of renal function, blood pressure, and urinalyses posttransplant. It may be that our energies have been misdirected in trying to reduce exposure to TBI, and rather we should try to decrease the inflammatory and cytokine effects of GVHD and reduce exposure to calcineurin inhibitors to prevent CKD in this population of patients.
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