Abstract

In clinical practice, heart failure (HF) and renal impairment are coexisting illness which is linked with one another. Heart and kidney have bidirectional inter-relationships, and it has been suggested that the kidney is the most significant organ involved in acute HF. The "cardio-renal syndrome" (CRS) is defined as acute or chronic malfunction of one organ causing acute or chronic dysfunction of the other [1, 2]. Furthermore, renal failure in HF can lead to decreased diuretic efficacy, diuretic resistance, congestion worsening, and further deterioration of renal function, creating a vicious cycle. In patients with acute HF, renal impairment is also a powerful independent predictor of short-term and long-term prognosis [3 - 9]. Renal hypoperfusion caused by inadequate cardiac output and over diuresis has long been thought to be the etiology of CRS. However, research has progressively shown a relationship between venous congestion and CRS, rather than inadequate cardiac output, correlating the failing right heart to CRS in recent decades. Indeed, both RHF and CRS have complicated and intertwined pathophysiologies that may affect several organs and systems in addition to isolated heart and kidney disease. This study focuses on the pathophysiology of RHF and cardio-centric phenotypes of CRS ("Type 1" and "Type 2"), as well as treatment options.

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