Case Report: Prevention of Rhabdomyolysis-Associated Acute Kidney Injury by Extracorporeal Blood Purification With Cytosorb®.

Simon Rauch,Matthias Bock,Carlo Leggieri,Ewald Gruber,Andrea Borgato,Paolo Mario Enrico Seraglio

doi:10.3389/fped.2021.801807

Simon Rauch, Matthias Bock + Show 4 more

Open Access

https://doi.org/10.3389/fped.2021.801807

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Abstract

Acute kidney injury (AKI) is a severe complication of rhabdomyolysis. The pathophysiology of rhabdomyolysis-associated AKI is complex, but myoglobin related damage plays a major role. Extracorporeal removal of myoglobin is therefore an appealing target to prevent AKI, however, attempts to remove myoglobin with standard dialysis membranes have so far been disappointing. Here we report the case of a 12-year-old boy with severe trauma-related rhabdomyolysis where we successfully utilized continuous renal replacement therapy in combination with Cytosorb® to eliminate myoglobin and prevent AKI. The early use of extracorporeal myoglobin removal with Cytosorb® after severe rhabdomyolysis might be an option and should be further investigated as a tool to prevent the development of AKI.

Highlights

Rhabdomyolysis is a clinical syndrome caused by damage to skeletal muscle and release of its breakdown products into the circulation
We report the case of a child with severe traumarelated rhabdomyolysis without established Acute kidney injury (AKI) where we initiated continuous renal replacement therapy combined with a Cytosorb R cartridge as a measure to prevent rhabdomyolysisassociated AKI
Twelve hours after initiation of continuous veno-venous hemodiafiltration (CVVHDF) plus Cytosorb R, creatinine kinase (CK) and myoglobin had substantially decreased (Figure 1), yet, during the subsequent 12 h of extracorporeal treatment an Rhabdomyolysis is a pathogenetic cause of AKI [1, 2], and myoglobin plays an essential role in the development of AKI [8, 13]

Summary

Introduction

Rhabdomyolysis is a clinical syndrome caused by damage to skeletal muscle and release of its breakdown products into the circulation. Most studies on the risk of and outcome after rhabdomyolysis-associated AKI in children were done after natural disasters, especially earthquakes. The pathophysiology of rhabdomyolysis-associated AKI is complex, and different mechanisms such as tubular damage by oxidative injury, tubular obstruction by precipitated Tamm-Horsfall protein-myoglobin complexes, and renal vasoconstriction have been described [8,9,10].

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Conclusion