Abstract:

Cardiorenal syndrome type 1 (CRS1) is defined as acute kidney injury (AKI) caused by acute cardiac function deterioration. Its pathological mechanism is complex and clinical manifestations are diverse. Early diagnosis and prevention of AKI are crucial to improving the prognosis of CRS1 patients. The traditional method for AKI diagnosis mainly relies on the assessment of serum creatinine (SCr) and urine volume, which may lead to delayed diagnosis of AKI and increased hospital admission and mortality. This article described the subtypes and pathophysiology of CRS1, and discussed important potential biomarkers for early diagnosis of CRS1, including B-type natriuretic peptide (BNP), N-terminal proBNP (NT-proBNP), cardiac troponin (cTn), soluble stromelysin 2 (sST2), galectin 3 (Gal-3), cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1), fatty acid-binding protein (FABP), the product of tissue inhibitor of metalloproteinase 2 (TIMP-2) and insulin-like growth factor-binding protein 7 (IGFBP7), N-acetyl-β-D-glucosaminidase (NAG), fibroblast growth factor 23 (FGF-23), interleukin-18 (IL-8), and microRNA (miRNA), etc, in order to provide a reference for the early clinical diagnosis, risk assessment, and prognosis improvement of CRS1 patients.

Key words: Cardiorenal syndrome type 1, Pathophysiology, Early diagnosis, Biomarker