Abstract
Hypouricemia in kidney transplant (KT) recipients is rare since they usually have subnormal kidney function which raises serum uric acid level. Recently, interests in pathogenesis of hypouricemia have been increasing due to the understanding of the role of uric acid transporter in renal hypouricemia (RHUC). We herein report the case of RHUC consequently developed in a KT recipient from a living donor with RHUC diagnosed by the detailed urinary and genetic test. A 73-year-old Japanese man underwent KT, and the donor was his wife who had hypouricemia [serum uric acid (S-UA) 0.6 mg/dL]. Nine months after KT, the recipient's S-UA was low (1.5 mg/dL) with serum creatinine (S-Cr) of 1.56 mg/dL, and fractional excretion of UA (FEUA) was high (59.7%; normal < 10%), indicating RHUC. Regarding the donor's information, S-Cr, S-UA, and FEUA were 0.95 mg/dL, 1.0 mg/dL, and 54.5%, respectively. To investigate further on the pathogenesis of RHUC in both the recipient and the donor, we performed genetic tests. The donor had a homozygous mutation of W258X in the SLC22A12 gene and the recipient had a wild type of W258X. Finally, we reviewed the previous literature on RHUC among KT recipients and discussed the strategy of follow-up for these patients.