Rodionova Elena A, Kuznetsova Alla A, Shakhmatova Elena I, Prutskova Natalia, Nielsen Søren, Holtbäck Ulla, Natochin Yuri, Zelenina Marina
Laboratory of Renal Physiology, IM Sechenov Institute of Evolutionary Physiology and Biochemistry, St. Petersburg, Russia.
Pediatr Nephrol. 2006 Mar;21(3):361-7. doi: 10.1007/s00467-005-2101-8. Epub 2005 Dec 29.
Children with acute pyelonephritis develop polyuria and have reduced maximum urinary concentration capacity. We studied whether these abnormalities are associated with altered urinary excretion of the water channel aquaporin-2 (AQP2) in the renal collecting duct. AQP2 is the main target for antidiuretic action of arginine vasopressin (AVP), and the urinary excretion of this protein is believed to be an index of AVP signaling activity in the kidney. Children with acute pyelonephritis, aged 5-14 years, were examined for urinary flow rate, creatinine clearance, unchallenged urine osmolality, and urinary ion excretion. Urinary excretion of AQP2 was measured by dot immunoblotting technique. Studies were performed in the acute phase of pyelonephritis, in the same children after treatment, and in control patients. At the onset of pyelonephritis, urinary flow rate and solute excretion were increased, but the urinary osmolality was unchanged. The urinary level and urinary excretion of AQP2 was increased in acute pyelonephritis and decreased after treatment. Excretion of aquaporin-3 was unchanged, suggesting that the increase in AQP2 urinary excretion was not due to a shedding of collecting duct cells. The results suggest that a mechanism proximal to the collecting duct may be responsible for the polyuria observed in children with acute pyelonephritis. Increased urinary AQP2 levels suggest that a compensatory activation of apical plasma membrane targeting of AQP2 may occur in pyelonephritis.
急性肾盂肾炎患儿会出现多尿,且最大尿浓缩能力降低。我们研究了这些异常是否与肾集合管中水通道蛋白-2(AQP2)的尿排泄改变有关。AQP2是精氨酸加压素(AVP)抗利尿作用的主要靶点,该蛋白的尿排泄被认为是肾脏中AVP信号传导活性的一个指标。对5至14岁的急性肾盂肾炎患儿进行尿流率、肌酐清除率、基础尿渗透压和尿离子排泄检查。采用斑点免疫印迹技术测定AQP2的尿排泄量。研究在肾盂肾炎急性期、同一患儿治疗后以及对照患者中进行。在肾盂肾炎发作时,尿流率和溶质排泄增加,但尿渗透压未变。急性肾盂肾炎时AQP2的尿水平和尿排泄增加,治疗后降低。水通道蛋白-3的排泄未变,这表明AQP2尿排泄增加并非由于集合管细胞脱落所致。结果表明,集合管近端的一种机制可能是急性肾盂肾炎患儿出现多尿的原因。尿AQP2水平升高表明,肾盂肾炎时可能发生了AQP2顶端质膜靶向的代偿性激活。