부산대학교 도서관

Lack of increased urine calcium-oxalate supersaturation in long-term kidney transplant recipients. Nephrolithiasis is uncommon after kidney transplantation. However, calcium (Ca) supplementation, which has been proposed as a treatment of post-transplant osteopenia, might increase calciuria and bolster Ca stone formation. Therefore, in 24-hour urine of 82 normocalcemic long-term renal transplant recipients (RT) and in 82 healthy subjects (HS), we assessed some Ca nephrolithiasis risk factors and the Ca-salt saturation estimated by the ion-activity product index (AP) and relative supersaturation (RS). In RT, calciuria was lower (mean ± SD, 3.20 ± 2.25 vs. 4.61 ± 1.71 mmol/day; P < 0.001), urinary volume higher (2.41 ± 0.83 vs. 1.39 ± 0.53 liter/day; P < 0.001), oxaluria higher (419 ± 191 vs. 311 ± 79 µmol/day; P < 0.001) and citraturia lower (1.40 ± 1.36 vs. 3.77 ± 1.36 mmol/day;P < 0.001) than in HS. As a result, Ca-oxalate supersaturation was lower in RT than HS (AP, 1.07 ± 0.69 vs. 2.07 ± 1.13,P < 0.001; and RS, 0.62 ± 0.26 vs. 0.94 ± 0.21, P < 0.001), and was similar in subgroups of RT(N = 37) and HS (N = 37) matched for urinary volume, demonstrating that even without any larger urinary volume, Ca-oxalate saturation was not higher in RT than HS, and suggesting that opposite changes in Ca and oxalate in RT likely canceled their effects on lithogenic risk. In RT which had similar urinary pH and phosphate (P) than HS, Ca-P supersaturation was lower than in HS for brushite (AP, 3.25 ± 6.67 vs. 6.01 ± 4.85, P < 0.001; RS, -0.33 ± 0.76 vs. 0.48 ± 0.53, P < 0.001) and octacalcium phosphate (RS,-0.95 ± 0.72 vs. 0.21 ± 0.85, P < 0.001), and similar for apatite. Finally, fasting calciuria and calciuric response to a single oral Ca load were similar in RT (N = 19) and HS (N= 8). Together, these results argue strongly against a higher risk of Ca stone formation in RT than HS, even in case of Ca supplementation.