Chronic kidney disease after pediatric hematopoietic cell transplant

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.