Abstract
Type-1 cardiorenal syndrome refers to acute kidney injury induced by acute worsening cardiac function. Worsening renal function is a strong and independent predictive factor for poor prognosis. Currently, several problems of the type-1 cardiorenal syndrome have not been fully elucidated. The pathogenesis mechanism of renal dysfunction is unclear. Besides, the diagnostic efficiency, sensitivity, and specificity of the existing biomarkers are doubtful. Furthermore, the renal safety of the therapeutic strategies for acute heart failure (AHF) is still ambiguous. Based on these issues, we systematically summarized and depicted the research actualities and predicaments of the pathogenesis, diagnostic markers, and therapeutic strategies of worsening renal function in type-1 cardiorenal syndrome.
Highlights
Acute heart failure (AHF), characterized by acute or subacute worsening symptoms and signs of heart failure (HF), is an intractable clinical and public health problem with high morbidity, mortality, and economic burden
Depending upon the chief culprit of the pernicious and bidirectional insufficiency of both organs, cardiorenal syndrome” (CRS) can be categorized into five clinical subtypes and acute worsening renal function (WRF) caused by the acute deterioration of cardiac function is termed as type-1 CRS (CRS-1 or acute CRS) [4, 5]
We summarized the latest findings of WRF in CRS-1, including the pathogenesis, clinical parameters facilitating diagnosis, and treatment strategies
Summary
Acute heart failure (AHF), characterized by acute or subacute worsening symptoms and signs of heart failure (HF), is an intractable clinical and public health problem with high morbidity, mortality, and economic burden. The term WRF is commonly regarded as an acute and/or sub-acute change that occurs to kidney function, exhibiting an increase of serum creatinine concentration or a decline of the estimated glomerular filtration rate (eGFR) during AHF, a precise and unified definition of WRF in CRS-1 has not been given for that different renal injury biomarkers and different amplitude of variation which is considered significant were adopted in different studies. The vasoconstriction and sodium-retaining neurohormones, including angiotensin II and renin, will be over-generated and over-secreted as an autocompensatory mechanism [20] This hypothesis is oversimplified and can only partially explain WRF in CRS1, especially for patients with AHF with obviously impaired left ventricular systolic function and decreased cardiac output. The Acute Kidney Injury N-gal Evaluation of Symptomatic
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