Abstract
After decades of pioneering and improvement, kidney transplantation is now the renal replacement therapy of choice for most patients with end-stage kidney disease (ESKD). Where focus has traditionally been on surgical techniques and immunosuppressive treatment with prevention of rejection and infection in relation to short-term outcomes, nowadays, so many people are long-living with a transplanted kidney that lifestyle, including diet and exposure to toxic contaminants, also becomes of importance for the kidney transplantation field. Beyond hazards of immunological nature, a systematic assessment of potentially modifiable—yet rather overlooked—risk factors for late graft failure and excess cardiovascular risk may reveal novel targets for clinical intervention to optimize long-term health and downturn current rates of premature death of kidney transplant recipients (KTR). It should also be realized that while kidney transplantation aims to restore kidney function, it incompletely mitigates mechanisms of disease such as chronic low-grade inflammation with persistent redox imbalance and deregulated mineral and bone metabolism. While the vicious circle between inflammation and oxidative stress as common final pathway of a multitude of insults plays an established pathological role in native chronic kidney disease, its characterization post-kidney transplant remains less than satisfactory. Next to chronic inflammatory status, markedly accelerated vascular calcification persists after kidney transplantation and is likewise suggested a major independent mechanism, whose mitigation may counterbalance the excess risk of cardiovascular disease post-kidney transplant. Hereby, we first discuss modifiable dietary elements and toxic environmental contaminants that may explain increased risk of cardiovascular mortality and late graft failure in KTR. Next, we specify laboratory and clinical readouts, with a postulated role within persisting mechanisms of disease post-kidney transplantation (i.e., inflammation and redox imbalance and vascular calcification), as potential non-traditional risk factors for adverse long-term outcomes in KTR. Reflection on these current research opportunities is warranted among the research and clinical kidney transplantation community.
Highlights
Chronic kidney disease (CKD) is a major public health problem, with a current worldwide prevalence of approximately 843 million individuals [1]
In the kidney transplantation field, future advances are expected from amelioration of adverse long-term outcomes by increasing recognition and developing novel, early, and cost-effective risk-management strategies focused on the non-immune aspects of post-kidney transplantation care and optimize long-term health and downturn current rates of premature death in stable kidney transplant recipients (KTR) [11]
Previous studies have demonstrated that cadmium may induce hypertension, which in turn is associated with accelerated kidney function decline and demonstrated in KTR, by shortened allograft survival [80,81,82,83,84]
Summary
Chronic kidney disease (CKD) is a major public health problem, with a current worldwide prevalence of approximately 843 million individuals [1]. Ly half of all kidney allograft losses are due to premature death with a funcItniodneiendg, agprapfrto, xaimloantge-lsytahnadlfinogf paallttkeirdnntehyatalhloags rraefmt laoinsseeds laarregedluyeutnochparnemgeadtuorveedr eraetchenwt iytheaars fu[1n7c,t1io8]n.ing graft, a long-standing pattern that has remained largely unchanged over recent years [17,18]. Laboratory readouts with a proposed involvement in such pathological pathways may point towards non-traditional risk factors and reveal novel targets for clinical intervention [27,28,29,30,31,32]. In the kidney transplantation field, future advances are expected from amelioration of adverse long-term outcomes by increasing recognition and developing novel, early, and cost-effective risk-management strategies focused on the non-immune aspects of post-kidney transplantation care and optimize long-term health and downturn current rates of premature death in stable KTR [11]
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