Kidney has ability to compensate its size and function against the nephron loss for maintaining total renal function, for example, in both donor and recipient in renal transplantation. However, the factors that regulate this compensation have not been fully clarified yet. It has been reported that approximately 70% of renal transplantation recipients suffer from anemia. Hereby we examined the effects of anemia on the compensatory renal hypertrophy in the mice lacking erythropoietin production. The anemic mice showed disrupted compensation after UNX compared to normoxemic mice. The disruption was accompanied by the sustained phosphorylation of ribosomal protein S6, a marker of mTOR activation, and by the sustained activation of YAP, a key transcriptional factor for the organ development; both of which had been normalized after successful compensation in the normal mice. There were no difference in the numbers of Ki67- and TUNEL-positive cells and in the capillary blood flow between anemic and normoxemic mice. In conclusion, anemia disrupted compensatory renal hypertrophy after UNX despite the activated tissue growth signals.