Cardiorenal syndrome (CRS) type 1 is a subtype within a broader group of disorders characterized by an aberrant, bidirectional interaction between the heart and kidneys, where acute kidney injury occurs following acute heart failure (AHF) due to a complex interplay of hemodynamic alterations, neurohormonal activation, and immune-mediated injury. Another mechanism in inflammation has emerged as a central contributor to the maladaptive "crosstalk" along this cardiorenal axis. Previous studies have identified elevated circulating cytokines, immune cell infiltration, and oxidative stress as potential drivers of renal dysfunction following cardiac injury. Recently, there has been a push toward exploring molecular imaging (MI) as a compelling noninvasive approach to visualizing these inflammatory responses in vivo, given its use in uncovering the pathophysiology of other cardiovascular and renal diseases. Modalities such as positron emission tomography, magnetic resonance imaging, and emerging optical technology have demonstrated the ability to detect immune cell activity, chemokine expression, and tissue-level inflammation. Interestingly, investigations using CXCR4-targeted radiotracers and magneto-fluorescent nanoparticles have shown concurrent inflammatory activation in cardiac and renal tissues after AHF, underscoring a possible mechanistic link between these organs. While the direct application of MI in CRS remains limited, early findings support its utility in characterizing this post-AHF inflammatory crosstalk. Consequently, this chapter aims to review the molecular and cellular pathways underlying inflammation in acute CRS and examine the current state of MI as it pertains to this disorder, given that improved imaging of cardiorenal inflammation may facilitate earlier diagnosis and more targeted therapeutic strategies for those who develop CRS.