Background Compensation of contralateral kidney function after living-donor kidney donation is well known, and many predictive factors have been proposed. However, no prediction model has been proposed. This study was performed to establish a tool with which to estimate the degree of compensation of the contralateral kidney after living-donor kidney donation. Methods We retrospectively analyzed 133 living donors for renal transplantation in our institution. We defined a favorable compensation as a post-donation estimated glomerular filtration rate (eGFR) at 1 year (calculated by the Chronic Kidney Disease Epidemiology Collaboration equation) of > 60% of the pre-donation eGFR. We analyzed the living donors’ clinical characteristics and outcomes. Results The median (range) donor age was 59 (24–79) years, median (range) body mass index was 22.9 (16.8–32.7) kg/m 2 , and median (range) body surface area was 1.6 (1.3–2.0) m 2 . All donors were Japanese, and 73% of the donors were biologically related. The median (range) donor pre-donation eGFR was 108.7 (82–144) ml/min/1.73 m 2 , and the median (range) post-donation eGFR at 1 year was 86.9 (43–143) ml/min/1.73 m 2 . Eighty-six percent of donors had compensatory hypertrophy. In the univariate analysis, age, female sex, history of hypertension, body surface area, and pre-donation eGFR were significantly associated with hypertrophy ( p < 0.05). In the multivariate analysis, age, female sex, history of hypertension, and ratio of the remnant kidney volume to body weight were significantly associated with hypertrophy ( p < 0.05). Based on these results, we created a compensation prediction score (CPS). The median (range) CPS was 8.7 (1.1–17.4). Receiver operating characteristic analysis showed strong diagnostic accuracy for predicting favorable compensation (area under the curve, 0.958; 95% confidence interval, 0.925–0.991, p < 0.001). The optimal cut-off value of the CPS was 5.0 (sensitivity, 92.0%; specificity, 89.5%). The CPS had a strong positive correlation with the post-donation eGFR (R = 0.797, p < 0.001). Conclusion The CPS might be useful tool with which to predict a favorable compensation of the contralateral kidney and remnant kidney function. If the CPS is low, careful management and follow-up might be necessary. Further investigations are needed to validate these findings in larger populations.

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We previously reported that allografts from living donors may have pre-existing histopathological damages, defined as the combination of interstitial fibrosis (ci), tubular atrophy (ct), and arteriolar hyalinosis (ah) scores of ≧1, according to the Banff classification. We examined preoperative characteristics to identify whether the degree of these damages was related to metabolic syndrome-related factors of donors. We conducted a single-center cross-sectional analysis including 183 living kidney donors. Donors were divided into two groups: chronic change (ci + ct ≧ 1 ∩ ah ≧ 1, n = 27) and control (n = 156). Preoperative characteristics, including age, sex, blood pressure, hemoglobin A1c (HbA1c), aortic calcification index (ACI), and psoas muscle index (PMI), were analyzed. Comparing the groups, the baseline estimated glomerular filtration rate was not significantly different; however, we observed a significant difference for ACI (p = 0.009). HbA1c (p = 0.016) and ACI (p = 0.006) were independent risk factors to predict pre-existing histopathological damages, whereas PMI was not. HbA1c correlated with ct scores (p = 0.035), and ACI correlated with ci (p = 0.005), ct (p = 0.021), and ah (p = 0.017). HbA1c and ACI may serve as preoperative markers for identifying pre-existing damages on the kidneys of living donors.

Due to atrophic bladder, patients undergoing long-term dialysis experience vesicoureteral reflux and complicated urinary tract infections after kidney transplantation. A 58-year-old woman underwent living donor kidney transplantation after 41 years of dialysis. She had no contraindications, with good cardiac function and minimal artery calcification despite the long history of hemodialysis. Immunosuppression was initiated with tacrolimus, mycophenolate mofetil, prednisolone, and basiliximab. Ureteroneocystostomy with an antireflux technique was carefully conducted as her bladder volume was 15 mL. The postoperative clinical course was uneventful with immediate graft function. The bladder volume gradually increased to 81 mL at discharge, 3 weeks postoperatively. The patient was initially depressed due to frequent urination early post-transplant but recovered soon after as the bladder volume gradually increased to 400 mL. The patient has not yet reported a urinary tract infection episode. This case highlights living donor kidney transplantation-induced recovery of bladder function with careful ureteroneocystostomy, despite the long dialysis history.