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活動內容: 內科部主治醫師教學 題目: Cardiorenal syndrome 心腎症候群 講師: 心臟內科主治醫師 張士琨 醫師 時間: 104 年 02 月 06 日 0730—0830 地點: 國軍高雄總醫院二樓內科會議室 摘要: Acute or chronic dysfunction of the heart or kidneys can induce acute or chronic dysfunction in the other organ. In addition, both heart and kidney function can be impaired by an acute or chronic systemic disorder. The term cardiorenal syndrome (CRS) has been applied to these interactions. In type 1 CRS, acute heart failure (HF) leads to worsening kidney function. In type CRS, chronic HF causes progressive chronic kidney disease. The prevalence of moderate to severe kidney impairment (<60 ml/min per 1.73m2) is approximately 30 to 40 percent in patients with HF. In addition to these baseline observations, patients undergoing treatment for acute or chronic HF frequently develop an increase in serum creatinine, which fulfills criteria for type 1 or type 2 CRS. Among patients with HF who have an elevated serum creatinine and/or a reduced estimated GFR, is is important to distinguish between underlying kidney disease and impaired kidney function due to the CRS. A variety of factors can contribute to a reduction in GFR in patients with HF. The major mechanisms that have been evaluated include neurohumoral adaptations, reduced renal perfusion, increased renal venous pressure, and right ventricular dysfunction. Reduced GFR are common in patients presenting with HF and are associated with increased mortality. A systematic review found that mortality increased by approximately 15 percent for every 10 mL/min reduction in estimated GFR. A fall in GFR during treatment of HF has often been associated with increased mortality in clinical studies in which the mortality risk increased progressively with degree of worsening renal function. However, other evidence suggests that patient outcomes may be improved with aggressive fluid removal even if accompanied by a rise in serum creatinine. Given the limitations imposed by impaired renal function on the ability to correct volume overload and the stron association between impaired or worsening renal function and adverse clinical outcomes in patients with HF, it is possible that effective treatment of the cardiorenal syndrome would improve patient outcomes. On the other hand, the worse prognosis associated with CRS could primarily reflect a reduced GFR being a marker of more severe cardiac disease. In this setting, improving renal function alone would not necessarily improve patient outcomes. There are no medical therapies that have been shown to directly increase GFR in patients with the CRS. On the other hand, improving cardiac function can produce increases in GFR, indicating that types 1 and 2 CRS substantial reversible components.