Monitoring of renal oxygen supply in critically–ill patients using urinary oxygen tension

Critically-ill patients are at risk of developing renal disorders as a consequence of systemic hypoperfusion. Ischemic acute tubular necrosis and resulting acute renal failure are caused by hypotension or therapeutic management. In this study, we tested the change of O(2) availability induced by fenoldopam mesylate using the continuous measurement of urinary oxygen tension (PuO(2)), a relatively noninvasive technique that could provide potentially important real-time data regarding renal oxygenation in intensive care unit patients. Fenoldopam was administered at different doses (0.03, 0.06, and 0.09 microg x kg(-1) x min(-1)) to 50 stable critically-ill patients. Urine output was collected every hour to assess volume and urinary electrolytes. Heart rate, mean arterial blood pressure, cardiac output, pulmonary artery occlusion pressure, arterial oxygen delivery index, and oxygen consumption index were analyzed after fenoldopam dose modifications and at infusion end. PaO(2) and PuO(2) continuous measurements were obtained through two sensors inserted in the radial artery and in the bladder. After a fenoldopam dose increase, PuO(2) significantly increased (P < 0.05), whereas PaO(2) remained unchanged. During the study, heart rate, mean arterial blood pressure, cardiac output, central venous pressure, pulmonary artery occlusion pressure, arterial oxygen delivery index, and oxygen consumption remained unchanged. Dose-dependent PuO(2) increases, unrelated to indexes of systemic perfusion and cardiac function, demonstrate that fenoldopam affects the balance between renal oxygen supply and demand in stable critically-ill patients.