Worsening renal function (WRF) in patients with acute heart failure (AHF) is defined as an increase in blood creatinine level of 25% or 0.3 mg/dl or more at any time during the patient’s hospitalization compared to the baseline level at admission. This is similar to the current definition of acute kidney injury (AKI) but is broader in time. From this, we concluded that WRF in AHF patients without comorbid chronic kidney disease (CKD) manifests mainly as acute cardiorenal syndrome (type I), while WRF in AHF patients with comorbid CKD manifests as different types and complexities of cardiorenal syndromes, depending on the stage and severity of CKD. The incidence of WRF in AHF patients is high, such as the results of the ARIC study, which showed that the incidence of renal failure in patients with acute decompensated heart failure before hospitalization was 14%, and the incidence of renal failure in patients with acute decompensated heart failure after hospitalization was as high as 27%, with a significant difference between the two. Moreover, the concomitant rate of CKD in AHF patients was high, and the results of the ARCS study in the United States showed that the concomitant rate of CKD was 66.1% in all patients with acute decompensated heart failure, and the concomitant rate of CKD in patients with new-onset acute decompensated heart failure was also as high as 63.8%. The mechanism of WRF in patients with AHF is mainly related to volume overload, congestive changes in the venous system and hormonal activation of the neuroendocrine system. When AHF occurs, cardiac output decreases, renal venous pressure increases, vascular resistance increases, etc., which can ultimately lead to a significant decrease in renal perfusion, causing WRF; and renal insufficiency can cause sodium retention, hypertension, anemia, and urinary toxins, etc., which can further aggravate the damage of cardiac function, triggering a vicious circle. In addition, during the clinical treatment of AHF, the effects of certain medications, such as inappropriate use of NSAIDs, iodine-containing contrast agents, RAS blockers, aldosterone receptor antagonists, vasopressin receptor antagonists, and diuretics, may also lead to WRF. WRF has an important impact on the prognosis of AHF. It has been found that the grading and degree of AKI significantly affects all-cause mortality in patients with AHF, especially in patients with AHF who develop AKI on admission compared to those who develop AKI after admission.The more severe the degree of AKI grading, the worse the clinical prognosis of the patient. The diagnosis of WRF in AHF patients is that both AHF and AKI should be accurately determined. Diagnosis of AHF is mainly through clinical examination, blood BNP measurement, central venous pressure measurement and cardiac ultrasonography. The diagnosis of AKI is made by means of blood creatinine, cystatin C, and estimated glomerular filtration rate (eGFR) assessment. Glomerular injury is assessed by urinary microalbumin and urinary cystatin C, while tubular injury is measured by urinary N-acetyl-β-D-glucosidase (NAG), urinary cystatin C, and urinary a1-microglobulin. It is worth noting that blood creatinine is not a real-time indicator of glomerular filtration rate (GFR) changes, which can be delayed for 48-72 hours, and its normal value varies greatly with age and gender, so it is best to use the eGFR formula to assess GFR. It was found that the CKD-EPI formula was more accurate in patients with AHF and provided a better prognosis for patients than the MDRD formula, and that the use of the CKD-EPI formula, which contains cystatin C as a variable, better predicted the occurrence of WRF in patients with AHF. NT-proBNP is now more commonly used in the diagnosis of AHF because it is more sensitive and stable than BNP in the detection of early or mild heart failure, and is less affected by renal function, but special attention should be paid to the fact that its appropriate cut-off value for the diagnosis of AHF is different in different ages, e.g., 450 pg/ml for <50 years old, 900 pg/ml for 50-75 years old and 1800 pg/ml for those >75 years old. In clinical diagnosis and treatment, it is important to monitor the cardiac and renal changes simultaneously to prevent WRF. It has been found that changes in blood creatinine and BNP after treatment in patients with AHF can clearly determine the prognosis, and the prognosis is poorer if the NT-proBNP level does not decrease by more than 30% and the blood creatinine increases by more than 0.3 mg/dl after treatment. Current advances in marker detection methods, such as devices that can rapidly measure neutrophil gelatinase-associated lipid transport protein and BNP simultaneously in a single drop of blood, can better assist physicians in clinical monitoring. The occurrence of WRF in AHF patients is mostly related to conditions such as volume overload, decreased cardiac output, decreased effective circulating volume, and improper clinical management. In the case of volume overload, diuretics can improve symptoms more rapidly and effectively than other drugs for heart failure. Although 65% of patients with congestive AHF are hypervolumic, another 30% are isovolumic and 5% are hypovolumic conditions, which may lead to WRF if the patient’s volume status is not carefully assessed prior to the use of diuretics.In addition, the therapeutic window for water loading is significantly narrower in the AHF condition compared with the normal condition, e.g., insufficient use of diuretics, fluid retention that makes the body less responsive to treatment such as angiotensin-converting enzyme inhibitors, and use of β-receptor inhibitors. therapeutic response is reduced, and the risk of using beta-blockers is increased; if diuretics are overused, blood volume insufficiency tends to occur, leading to an increased risk of hypotension with angiotensin-converting enzyme inhibitors, and a significantly greater risk of causing WRF. Diuretic resistance occurs more often in patients with AHF, when attention should be paid to find and improve the possible causes, such as excessive sodium intake, concomitant use of NSAIDs, blood volume insufficiency, accompanied by hypotension, etc., and do not increase the dose of diuretics and lead to the occurrence or aggravation of WRF. When diuretics are ineffective, blood ultrafiltration therapy can be considered. Currently, there are clinical devices that can use peripheral vein as vascular access, treat at a blood flow rate of 40 ml/min and ultrafiltration rate of less than 500 ml/h, which can provide safe treatment without the need of renal specialist supervision. However, the efficacy of hemofiltration alone is short-term, mainly to buy time and opportunity for comprehensive clinical management, and should not be neglected for the treatment of etiology and causative factors, in addition, hemofiltration alone does not have renoprotective effect, and its improper use may aggravate the renal injury, so it is preferable to choose the treatment of continuous hemodialysis or hemofiltration in the occurrence of WRF in patients with AHF. Hemodiafiltration can isotonically remove excessive volume load, remove urinary toxins and “myocardial inhibitory factor”, and reduce plasma levels of renin, aldosterone and norepinephrine. In the development of WRF in AHF patients with CKD, attention should be paid to the correction of risk factors for the progression of CKD, such as proteinuria, hypertension, anemia, dyslipidemia, smoking, continuous use of nephrotoxic drugs, iron deficiency, malnutrition, and disorders of calcium and phosphorus metabolism, and so on. It has been found that, for AHF patients with CKD, there is insufficient active intervention for cardio-renal disease risk factors due to doctors’ frequent fear of toxic reactions caused by drug accumulation, etc., such as not daring to reasonably use aspirin, β-blockers, RAS-blockers, and statins for treatment.Kdigo’s 2012 guideline on the treatment of cardiovascular disease in combination with CKD clearly states that CKD with CKD with cardiovascular disease is basically the same as that of cardiovascular high-risk patients, except that more monitoring and close attention to adverse drug reactions are required. In conclusion, AHF patients are prone to develop WRF, therefore, AHF patients should be carefully evaluated for their renal function after admission to the hospital, and special attention should be paid to the major risk factors affecting the prognosis, such as blood pressure, blood urea, creatinine, and NT-proBNP, etc., after the development of WRF, and the patients with CKD are more prone to WRF, and the management of WRF in patients with CKD should be paid special attention to the effects of drugs, and the treatment of WRF should be given to patients with CKD, and the treatment of WRF should be carried out in the same way as that of CKD. The effect of medications should be given along with adequate treatment.