Following transplantation of non-renal solid organs or haematopoietic stem cells, there is a high incidence of both acute and chronic kidney disease (CKD), resulting in increased morbidity and premature mortality (Ojo et al., 2003; Bloom and Reese, 2007; Ojo, 2007; Clajus et al., 2012).
The figure below shows the cumulative incidence of chronic renal failure in non-renal organ transplant patients over a 10-year period (Ojo et al., 2003).
A high proportion of solid organ recipients develop perioperative acute renal failure (defined as a 25% decline; or increase in serum creatinine levels (0.5 mg/dL) above baseline levels; or >2.0 mg/dL serum creatinine): 46–61% in liver, 20–30% in heart, and 5–60% of lung transplant recipients; with 20–25% of liver, 10–15% of heart and 8–10% of lung recipients requiring intermittent or continuous haemodialysis (Ojo, 2007). The 5-year risk of chronic renal failure after transplantation of a non-renal organ ranges from 7% to 21% (Ojo et al., 2003).
Risk factors for the development of CKD following transplantation are pre-existing renal disease, post-transplantation acute kidney injury, pre-transplantation diabetes, pre-transplantation hypertension, hepatitis C infection, age of the recipient, female gender, and thrombotic microangiopathy (Ojo et al., 2003; Bloom and Reese, 2007; Clajus et al., 2012). Obesity was recently identified as a risk factor (independent of diabetes) for adverse renal outcomes following kidney transplantation (Kwan et al., 2016).
Despite improvements in immunosuppression, chronic allograft nephropathy is the main cause of kidney transplant failure. Sequential biopsy specimens taken regularly from the time of kidney transplantation to 10 years follow-up defined the natural history of the condition. During the first-year post transplantation, the key changes were new tubulointerstitial damage accompanied by interstitial fibrosis and tubular atrophy, characterised by rapidly increasing Banff scores. After the first year, microvascular and glomerular damage was more pronounced (Nankivell et al., 2003).
The development of ischaemia/reperfusion injury seen more commonly following deceased kidney transplantation is associated with delayed graft function, graft rejection, chronic rejection and chronic graft dysfunction. The condition develops due to hypoxia and ischaemia during organ procurement (Salvadori et al., 2015).
Guidelines for management of the failing kidney transplant have been published by the British Transplantation Society (Andrews & Standards Committee of the British Transplantation Society, 2014). Much of the post-transplantation renal impairment observed is related to CNI-toxicity and reduction/elimination of CNI exposure is typically performed when a deterioration of renal function is observed. However, it is worth noting that CNI elimination has little effect when a patient’s eGFR is <50 mL/min/1.73 m2 or their renal function is rapidly declining (De Simone et al., 2017b).
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