Cardiorenal syndrome(CRS) has been defined as a state in which therapy to relieve heart failure(HF) symptoms is limited by further worsening renal function. Currently, there is no widely accepted standard for the diagnosis of CRS syndrome. But some researchers have suggested that CRS can be diagnosed when renal function worsens with creatinine elevation＞3-5 mg/L or glomerular filtration rate decrement＞9-15 ml/min. Nowadays, the exact prevalence of CRS remains unclear. Some studies revealed that the incidence of CRS in case of HF reached as high as 30%. The mechanisms behind CRS are complex. Central venous congestion, neuroendocrine hyperactivity, anemia, oxidative stress and renal sympathetic nerve hyperactivity have been demonstrated to be important reasons causing cardiorenal syndrome. The treatment for CRS remains a big challenge. The first principle of the treatment is to correct the reversible risk factors. Stable renal perfusion is also needed by sustaining systolic blood pressure over 80 mmHg or mean blood pressure over 60 mmHg. For those with low cardiac output, nitrates might be helpful. Further, medications with renal toxicity should be withdrawn timely. Diuretics, angiotensin converting enzyme inhibitor/angiotensin receptor blocker, hemofiltration, recombinant human B-type natriuretic peptide can be used as appropriate choice.