Abstract：
The relief of the impediment to urinary flow is the treatment of acute kidney failure due to urinary tract obstruction. However, there is a risk of inducing massive polyuria, which can be self-limited or produce severe contraction of the intravascular volume with pre-renal acute kidney failure and alterations in the internal environment. Polyuria, urine output > 3 L/d or > 200 mL/min for more than 2 hours, can have multiple causes, and can be classified as osmotic, aqueous or mixed. Post-obstructive polyuria obeys different pathogenic mechanisms, which overlap and vary during a patient\'s evolution. Initially, there is a decrease in vasoconstrictor factors and an increase in renal blood flow, which, added to the excess of urea accumulated, will cause intense osmotic diuresis (osmotic polyuria due to urea). Added to these factors are the positive sodium and water balance during acute renal failure, plus the contributions of crystalloid solutions to replace diuresis (ionic osmotic polyuria). Finally, there may be tubular dysfunction and decreased solutes in the renal medullary interstitium, adding resistance to the action of vasopressin. The latter causes a loss of free water (mixed polyuria). We present the case of a patient with post-obstructive polyuria where, by analyzing the clinical symptoms and laboratory alterations, it was possible to interpret the mechanisms of polyuria and administer appropriate treatment for the pathogenic mechanism.
摘要：
排尿障碍的缓解是由于尿路梗阻引起的急性肾衰竭的治疗。然而,有诱发大量多尿的风险，这可能是自我限制的或导致血管内体积严重收缩，伴有肾前急性肾衰竭和内环境改变。多尿,尿量>3L/d或>200mL/min超过2小时，可能有多种原因，可以归类为渗透，水性或混合。梗阻性多尿症遵循不同的致病机制，在患者的进化过程中重叠和变化。最初，血管收缩因子减少，肾血流量增加，which,添加到积累的过量尿素中，会引起强烈的渗透性利尿（由于尿素引起的渗透性多尿）。这些因素增加了急性肾衰竭期间钠和水的正平衡，加上晶体溶液替代利尿（离子渗透性多尿）的贡献。最后,肾髓质间质可能有肾小管功能障碍和溶质减少，增加对加压素作用的抵抗力。后者导致游离水的损失(混合多尿)。我们介绍了一例阻塞性多尿症患者，通过分析临床症状和实验室改变，有可能解释多尿症的发病机制,并对其发病机制给予适当的治疗.
