Chronic renal failure after liver transplantation (LT) is significantly more frequent than after lung or heart transplantation and it results in an increased short and long-term mortality. Renal impairment may occur before LT (functional or due to preexisting parenchymal kidney disease), in the peri-operative period or later after LT. The number of patients with renal failure after LT has increased due to the liver allocation based on MELD and to the more liberal use of higher risk grafts. Calcineurin inhibitor (CNI) nephrotoxicity is the most important cause of renal dysfunction but is a modifiable factor. Strategy to prevent CNI-associated nephrotoxicity is post-op CNI minimization by induction therapy and reduced dose and/or delayed introduction of CNI in combination with mycophenolate mofetil (MMF) or everolimus with no penalty in term of rejection. With everolimus, usually started one month after LT, a drastic minimization of CNI is possible and this results in superior kidney function until at least 3 years follow up. At the moment of renal impairment a drastic reduction of CNI dose together with the introduction of MMF results in an improvement in GFR at 6 to 2 years with a low rate of acute rejection. However, secondary prevention fails to normalize renal function in most of the patients once e GFR <60 ml/min/1.73m²ml.

肝移植（LT）后的慢性肾功能衰竭比肺或心脏移植后的频率明显更高，并且导致短期和长期死亡率的增加。肾功能不全可能发生在LT前（功能性或由于先前存在的实质性肾脏疾病），围手术期或LT之后。LT后肾功能衰竭的患者人数有所增加，这是由于基于MELD的肝脏分配以及对高风险移植物的更宽松使用所致。钙调神经磷酸酶抑制剂（CNI）的肾毒性是肾功能不全的最重要原因，但也是可改变的因素。预防与CNI相关的肾毒性的策略是通过诱导治疗将CNI降至最低，并与霉酚酸酯（MMF）或依维莫司联用，降低剂量和/或延迟引入CNI，而不会因排斥反应而受到任何惩罚。对于通常在LT后一个月开始的依维莫司，可以将CNI大大减至最小，这将导致肾脏功能优越，直到至少随访3年。在肾功能不全的时刻，CNI剂量的急剧减少以及MMF的引入导致6至2年时GFR的改善，急性排斥率低。然而，一旦e GFR <60 ml / min / 1.73m，二级预防不能使大多数患者的肾功能正常化 可以最大限度地减少CNI，这将导致优越的肾脏功能，直到至少随访3年。在肾功能不全的时刻，CNI剂量的急剧减少以及MMF的引入导致6至2年时GFR的改善，急性排斥率低。然而，一旦e GFR <60 ml / min / 1.73m，二级预防不能使大多数患者的肾功能正常化 可以最大限度地减少CNI，这将导致优越的肾脏功能，直到至少随访3年。在肾功能不全的时刻，CNI剂量的急剧减少以及MMF的引入导致6至2年时GFR的改善，急性排斥率低。然而，一旦e GFR <60 ml / min / 1.73m，二级预防不能使大多数患者的肾功能正常化²毫升