Eberhard O K, Kliem V, Offner G, Oldhafer K, Fangmann J, Pichlmay R, Koch K M, Brunkhorst R
Department of Nephrology, Medizinische Hochschule Hannover, Germany.
Clin Transplant. 1997 Oct;11(5 Pt 1):415-9.
Our aim was to assess the long-term risks for kidney donors of developing arterial hypertension and hypertension-associated diseases or hyperfiltration injury of the remaining solitary kidney. We conducted a cross-sectional study in which 29 donors who were nephrectomized at our center between October 1973 and March 1990 were enrolled. At the time of evaluation median age was 54 (37-70) yr. Since kidney donation an average time interval of 11.1 +/- 3.8 yr had elapsed. Body weight, casual blood pressure, S-creatinine and proteinuria were recorded. In 28/29 donors 24-h blood pressure monitoring was performed; all 29 were tested for microalbuminuria (MAU). The patient history was checked for treatment with antihypertensives, coronary heart disease and diabetes mellitus. From all 29 kidney donors surveyed up to 19.8 yr none developed marked renal insufficiency: median S-creatinine was 1.0 mg/dl (range 0.7-1.6), only 3 donors had a S-creatinine > 1.3 mg/dl. Glomerular filtration rate (GFR) decreased in an age-dependent manner. While all donors had been normotensive without an antihypertensive treatment at time of nephrectomy, actually 29% proved to be hypertensive with average values > 130/80 mmHg in the 24-h assessment. 5/29 donors received antihypertensives, 3 of whom nevertheless were hypertensive. Day-night profile was lost in 2 patients. After donation one patient developed coronary heart disease. 7/29 donors (24%) displayed positive testing for MAU, furthermore one had proteinuria (approx. 300 mg/l). MAU was associated in one case with slightly elevated S-creatinine (1.3 mg/dl) and in 3 cases with arterial hypertension. In the long-term course living related kidney donors do not seem to be at risk for developing hypertensive disorders more often than the general population. The prevalence of MAU in the 29 cases studied was higher than so far described for healthy subjects. This may reflect subclinical hyperfiltration damage of the glomerulus. Progressive renal insufficiency with clinical relevant function loss of the remaining solitary organ, however, was not observed up to 19.8 yr after kidney donation.
我们的目的是评估肾供体发生动脉高血压、高血压相关疾病或剩余孤立肾超滤损伤的长期风险。我们进行了一项横断面研究，纳入了1973年10月至1990年3月在我们中心接受肾切除术的29名供体。评估时的中位年龄为54（37 - 70）岁。自肾脏捐献后，平均时间间隔为11.1±3.8年。记录了体重、偶测血压、血清肌酐和蛋白尿情况。28/29名供体进行了24小时血压监测；所有29名供体均检测了微量白蛋白尿（MAU）。检查患者病史，了解其是否接受过抗高血压治疗、是否患有冠心病和糖尿病。在接受调查的所有29名肾供体中，长达19.8年无一例发生明显肾功能不全：血清肌酐中位数为1.0mg/dl（范围0.7 - 1.6），只有3名供体的血清肌酐>1.3mg/dl。肾小球滤过率（GFR）呈年龄依赖性下降。虽然所有供体在肾切除时血压正常且未接受抗高血压治疗，但在24小时评估中，实际有29%的供体血压升高，平均值>130/80mmHg。29名供体中有5名接受了抗高血压治疗，其中3名仍患有高血压。2例患者的昼夜血压模式消失。捐献后1例患者发生了冠心病。29名供体中有7名（24%）MAU检测呈阳性，此外1名有蛋白尿（约300mg/l）。1例MAU与血清肌酐轻度升高（1.3mg/dl）相关，3例与动脉高血压相关。从长期来看，活体亲属肾供体发生高血压疾病的风险似乎并不比普通人群更高。在研究的29例中，MAU的患病率高于迄今报道的健康受试者。这可能反映了肾小球的亚临床超滤损伤。然而，在肾脏捐献后长达19.8年，未观察到剩余孤立器官出现具有临床相关功能丧失的进行性肾功能不全。
