Laboratory of Nephrology, Department of Microbiology and Immunology, KU Leuven, Leuven, Belgium.
Department of Nephrology and Renal Transplantation, University Hospitals Leuven, Leuven, Belgium.
Diabetes Care. 2019 Apr;42(4):625-634. doi: 10.2337/dc18-1936. Epub 2019 Feb 14.
The kinetics and risk factors of diabetic nephropathy after kidney transplantation remain unclear. This study investigated the posttransplant occurrence of diabetic nephropathy and the contribution of posttransplant glycemic control.
We performed a single-center prospective cohort study of 953 renal allograft recipients and 3,458 protocol-specified renal allograft biopsy specimens up to 5 years after transplantation. The effects of pretransplant diabetes and glycemic control (glycated hemoglobin levels) on the posttransplant histology were studied.
Before transplantation, diabetes was present in 164 (17.2%) renal allograft recipients, primarily type 2 ( = 146 [89.0%]). Despite intensive glycemic control (glycated hemoglobin 7.00 ± 1.34% [53 ± 14.6 mmol/mol], 6.90 ± 1.22% [52 ± 13.3 mmol/mol], and 7.10 ± 1.13% [54 ± 12.4 mmol/mol], at 1, 2, and 5 years after transplantation), mesangial matrix expansion reached a cumulative incidence of 47.7% by 5 years in the pretransplant diabetes group versus 27.1% in patients without diabetes, corresponding to a hazard ratio of 1.55 (95% CI 1.07-2.26; = 0.005). Mesangial matrix expansion was not specific for diabetic nephropathy and associated independently with increasing age. Pretransplant diabetes was associated with posttransplant proteinuria but not with estimated glomerular filtration rate, graft failure, or any other structural changes of the glomerular, vascular, or tubulointerstitial renal compartments. The occurrence of diabetic nephropathy was independent of posttransplant glycated hemoglobin levels.
Mesangial matrix expansion, an early indicator of diabetic nephropathy, can occur rapidly in patients with diabetes before transplantation, despite intensive glycemic control. Prevention of diabetic nephropathy requires more than pursuing low levels of glycated hemoglobin.
肾移植后糖尿病肾病的动力学和危险因素仍不清楚。本研究调查了移植后糖尿病肾病的发生情况以及移植后血糖控制的作用。
我们对 953 例肾移植受者和 3458 例符合方案的肾移植活检标本进行了单中心前瞻性队列研究，这些标本在移植后 5 年内进行。研究了移植前糖尿病和血糖控制（糖化血红蛋白水平）对移植后组织学的影响。
移植前，164 例（17.2%）肾移植受者存在糖尿病，主要为 2 型（=146 [89.0%]）。尽管进行了强化血糖控制（糖化血红蛋白 7.00±1.34%[53±14.6mmol/mol]、6.90±1.22%[52±13.3mmol/mol]和 7.10±1.13%[54±12.4mmol/mol]，分别在移植后 1、2 和 5 年），但在移植前糖尿病组中，系膜基质扩张在 5 年内累积发生率达到 47.7%，而无糖尿病患者为 27.1%，相应的危险比为 1.55（95%CI 1.07-2.26；=0.005）。系膜基质扩张并非糖尿病肾病特异性，且与年龄增长独立相关。移植前糖尿病与移植后蛋白尿有关，但与估算肾小球滤过率、移植失败或肾小球、血管或肾小管间质肾区的任何其他结构变化无关。糖尿病肾病的发生与移植后糖化血红蛋白水平无关。
尽管进行了强化血糖控制，但移植前糖尿病患者的系膜基质扩张（糖尿病肾病的早期指标）仍可能迅速发生。预防糖尿病肾病需要的不仅仅是追求低水平的糖化血红蛋白。
