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Transcript
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.