Cardio-renal syndrome type 3: epidemiology, pathophysiology, and treatment

Abstract

A complex pathophysiology, cardio-renal syndrome (CRS), has been redefined in recent years. One subtype is acute renocardiac CRS, or CRS type 3. This syndrome is intended to comprise situations in which acute kidney injury (AKI) results in acute cardiac injury or dysfunction. The pathophysiology of CRS type 3 is not well understood. Existing evidence suggests a bidirectional link between these two organ systems. The mechanisms whereby AKI leads to cardiac dysfunction have been proposed to include two categories: direct effects of AKI on the heart, and effects of AKI on remote organ function with indirect effects on the heart. AKI has been shown to cause inflammation in experimental renal ischemic models, which then induced cytokine expression, leukocyte infiltration into the heart, cell death by apoptosis, and impaired cardiac function. Combined with this finding is the well-known significant physiological derangements, such as fluid and electrolyte imbalance and uremia, that underpin remote organ failure and finally affect cardiac function, which in turn causes further kidney injury. This vicious cycle is fundamental to cardio-renal syndromes. The high morbidity and mortality is likely a result of this adverse synergy. A standard definition and diagnostic criteria are important first steps to approach this syndrome. Results obtained from studies using a standard definition of AKI can lead us to the next step of early recognition, prevention, therapeutic intervention, and improved quality of care. Novel biomarkers and therapeutic interventions for primary and secondary disorders are being developed and tested. The hope is that improved outcomes will follow.