Kidney Injury after Rhabdomyolysis: What Is New?

Abstract

Severe damage of skeletal muscle, referred to as rhabdomyolysis, is the cause of 10% of acute kidney injury (AKI) cases and AKI complicates 13–50% of traumatic or nontraumatic rhabdomyolysis. Hypovolemia and the direct nephrotoxic effect of myoglobin are thought to be the main factors involved in rhabdomyolysis-induced AKI. Myoglobin promotes kidney injuries through vasoconstrictive properties, proximal tubular injuries, and distal obstruction. Recently, we demonstrated that macrophages influence the long-term prognosis of this disease by exerting proinflammatory as well as profibrotic properties. Clinical management relies on early diagnosis (creatine kinase > 5,000 UI/l) and fluid resuscitation using isotonic sodium chloride. Despite optimal rehydration, patients can develop AKI and require renal replacement therapy (RRT). Severe hyperkalemia or metabolic acidosis is the main cause of RRT. Thus, intermittent hemodialysis rather than continuous RRT should be used as frontline RRT, if available. To date, alkalinization, as well as prophylactic intermittent hemodialysis with high cut-off membrane, did not demonstrate superiority on long-term renal function compared to conventional approach. While global prognosis is depending upon the cause of rhabdomyolysis, mortality increases from 22% to 59% as soon as patients develop AKI. Long-term prognosis is unknown. Animal models demonstrated that rhabdomyolysis can lead to renal fibrosis after several months of follow-up. This suggests that patients with rhabdomyolysis should be considered as at high risk to develop chronic kidney disease and therefore referred to nephrologists to minimize long-term consequences of chronic kidney disease.