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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-creatinine1.3 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 values130/80 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.

The determination of serum procalcitonin (PCT) was tested for its utility in detecting invasive bacterial infection and acute rejection during the first 6 wk after kidney transplantation. Fifty-seven kidney graft recipients were prospectively included in the study. In 13/57 patients, 16 episodes of acute biopsy-proven rejection occurred and were treated with high-dose steroids (n = 14) or with OKT3 (n = 2). Seventeen out of 57 patients experienced 19 invasive bacterial infections; 2/57 had partial graft necrosis due to malperfusion. Twenty-five out of 57 graft recipients experienced an uncomplicated postoperative course. A total of 116 samples were analyzed and the following data obtained: PCT, C-reactive protein (CRP), white blood cell (WBC) count, corresponding body temperature and serum creatinine. Procalcitonin values for patients with rejection did not differ significantly from those of the healthy transplant recipients (p = 0.47). In contrast, PCT was clearly elevated with invasive bacterial infection or partial graft necrosis (p0.01). OKT3 treatment of rejection led to a more than 10-fold increase in PCT. C-reactive protein, unlike PCT, was elevated to a variable extent in patients with graft rejection, though CRP values were significantly more elevated in patients with infection than in those with rejection (p0.01). The specifity for detection of invasive bacterial infection was 0.7 for PCT and 0.43 for CRP, whereas sensitivity was 0.87 for PCT and 1.0 for CRP. There was no correlation between PCT and serum creatinine (r = 0.06). Haemodialysis did not lower PCT serum concentrations. Procalcitonin values rose postoperatively to peak levels on the first and second days and mostly declined to normals within 1 wk. In conclusion PCT, not being influenced by acute kidney graft rejection but serving as a specific indicator of systemic bacterial infection, could help to discriminate between both types of inflammation.