Key result
Inflammation and a hyperactive immune system play a pivotal role in the pathophysiology of cardiorenal syndrome type I, governing hemodynamics, end-organ dysfunction, and disease severity.
Why the study?
Despite standard of care, mortality, treatment cost, and readmissions remain high in cardiorenal syndrome type I, with critical implications of inflammation warranting further research.
This review highlights the critical role of the immune system and inflammatory pathways in the pathogenesis of Cardiorenal Syndrome Type I, suggesting potential future therapeutic targets.
Immune activation may drive CRS type I progression; leaves open immunomodulatory therapies pending prospective trials.
Physiological organ cross-talk is necessary to maintain equilibrium and homeostasis. Heart and kidney are the essences of this equilibrium. Organ failure in either of these organs can perturb the bidirectional communication between them, impinging this unpleasant vascular and cellular milieu on other distant organs. Cardiorenal syndrome (CRS) type I occurs due to acute deterioration of cardiac function, ultimately causing acute kidney injury (AKI). This syndrome is an intricate condition with neurohormonal and inflammatory aspects. Inflammation creates a vicious circle filled with the innate and adaptive immune systems, pro-inflammatory cytokines, chemokines to actuate hemodynamic compromise in CRS type I patients. Pro-inflammatory cytokines not only aggravate fluid retention and venous congestion but also initiate apoptosis and oxidative stress. The immune response's primary motive is to elicit the heart and kidney to produce cytokines, intensifying the inflammatory process. Despite the possible standard of care, patient mortality, treatment cost, readmissions are extreme in CRS type I, and inflammation certainly has critical inferences warranting future research in humans.
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Peesapati et al. (2020) conducted a review in Cardiorenal Syndrome Type I. Inflammation and immune system activation was evaluated. Inflammation and a hyperactive immune system play a pivotal role in the pathophysiology of cardiorenal syndrome type I, governing hemodynamics, end-organ dysfunction, and disease severity.
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