Girolami J P, Bascands J L, Vega Vidalle C, Pecher C, Moatti J P, Adam A, Suc J M
Inserm U 133, Centre de Recherche en Biologie cellulaire humaine, Faculté de Médecine Rangueil, Toulouse, France.
Nephron. 1991;59(1):51-6. doi: 10.1159/000186517.
Urinary kallikrein excretion (UKE) was measured in 20 patients before and after hemodialysis (HD). When compared to the values of normal subjects (136 +/- 56 micrograms/24 h, n = 100), UKE was decreased in all patients before HD (6.6 +/- 5.8 micrograms/24 h, p less than 0.001, n = 20). After HD a significant increase in 24-hour UKE was observed in all patients (18.6 +/- 7.2 micrograms/24 h, p less than 0.05, n = 20). Expressed as the individual percent increase, the UKE enhancement ranged from 16 to 670%. It was due to an enhancement in the excretion of the active form which represented 52 +/- 6.8% before HD and reached 76.3 +/- 7.5% of the total form after HD (p less than 0.01). The excretion of the inactive form remained unchanged. The increase in UKE was found to be significantly correlated with reductions in urinary sodium, potassium, and osmolality (r = -0.826, r = -0.568, r = -0.847, respectively, p less than 0.01, n = 20). The increase in UKE following HD could not be explain by an increase in aldosterone as urinary aldosterone decreased. A transient improvement in intracellular homeostasis (removal of inhibitory toxins and normalization of osmotic pressure) could be evoked. The increase in UKE 24 h after HD points out a new situation confirming the relations of UKE with changes in osmolality and extracellular volume.
在20例患者进行血液透析（HD）前后测量了尿激肽释放酶排泄量（UKE）。与正常受试者的值（136±56微克/24小时，n = 100）相比，所有患者在HD前UKE均降低（6.6±5.8微克/24小时，p<0.001，n = 20）。HD后，所有患者24小时UKE均显著增加（18.6±7.2微克/24小时，p<0.05，n = 20）。以个体增加百分比表示，UKE增强范围为16%至670%。这是由于活性形式排泄增加，活性形式在HD前占52±6.8%，HD后占总形式的76.3±7.5%（p<0.01）。非活性形式的排泄保持不变。发现UKE的增加与尿钠、钾和渗透压的降低显著相关（分别为r = -0.826，r = -0.568，r = -0.847，p<0.01，n = 20）。HD后UKE的增加不能用醛固酮增加来解释，因为尿醛固酮降低。可以引起细胞内稳态的短暂改善（去除抑制性毒素和渗透压正常化）。HD后24小时UKE的增加指出了一种新情况，证实了UKE与渗透压和细胞外液变化的关系。
