Rhabdomyolysis-Associated Acute Kidney Injury: From Pathogenic Mechanisms to the Therapeutic Use of Sorbents.

BACKGROUND

Rhabdomyolysis is a pathological process that results from the breakdown of skeletal muscle fibers, leading to the release of intracellular contents such as myoglobin, creatine kinase, potassium, and phosphate into the systemic circulation. One of the most critical and life-threatening complications of rhabdomyolysis is acute kidney injury (RA-AKI), which occurs in 10-50% of patients with severe rhabdomyolysis.

SUMMARY: The mechanisms of RA-AKI include myoglobin-induced oxidative injury, tubular obstruction by casts, renal vasoconstriction, hypoperfusion, and triggering of the inflammatory response. The mainstay of therapy is fluid resuscitation and early conservative interventions to prevent myoglobin precipitation in the tubular lumen. Emerging interventions using renal replacement therapy (RRT) using selected types of membranes represent a significant advancement in the management of the most severe forms of RA-AKI. Hemoadsorption alone or in series with an RRT circuit (sequential therapies) offers a promising approach for a more efficient and faster removal of myoglobin, addressing one of the primary drivers of kidney injury. Furthermore, cytokine adsorption could offer a dual beneficial effect by reducing the systemic inflammatory response that exacerbates kidney damage during rhabdomyolysis.

KEY MESSAGES: The aim of this narrative review is to analyze the causes and the pathogenic mechanisms of RA-AKI and to explore the therapeutic role of specific RRT modalities and sorbent-based extracorporeal therapies.